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Old 1st February 2009, 02:38 PM   #1
Baby Nemesis
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Latest Alzheimer's research?

Do you know of any promising new research into drugs that might help reverse or cure Alzheimer's disease, or into lifestyle changes that might be preventative to some extent?

Here are some findings that seem interesting, from the past several months. If anyone has any more information on them or related things, it could be interesting:

Brain Plaques Blocked By Anti-Inflammatory Drug

Quote:
Brain destruction in Alzheimer's disease is caused by the build-up of a protein called amyloid beta in the brain, which triggers damaging inflammation and the destruction of nerve cells. Scientists had previously shown that preventing individual amyloid beta proteins from sticking to one another minimized brain lesions and protected nerve cells against damage.

The new study - a collaborative effort by researchers in Germany and the US - shows that an anti-inflammatory drug (called CNI-1493) may have the same effect. ...

In mice prone to developing an Alzheimer's-like disease, the drug decreased brain inflammation and improved memory and cognitive function.

Other anti-inflammatory drugs, such as ibuprofen, have been shown to reduce Alzheimer's disease lesions in the brains of rodents, but CNI-1493 appears to be faster and more effective. If these results hold up in humans, CNI-1493 may provide a more effective alternative to current Alzheimer's therapies, which temporarily prolong the function of nerve cells but do not prevent their destruction.
Common Medication Associated With Cognitive Decline In Elderly

Quote:
A study published in Journal of the American Geriatrics Society suggested that the use of certain medications in elderly populations may be associated with cognitive decline. The study examined the effects of exposure to anticholinergic medications, a type of drug used to treat a variety of disorders that include respiratory and gastrointestinal problems, on over 500 relatively healthy men aged 65 years or older with high blood pressure. ...

The findings show that chronic use of medications with anticholinergic properties may have detrimental effects on memory and the ability to perform daily living tasks, such as shopping and managing finances. Participants showed deficits in both memory and daily function when they took these medications over the course of a year. The degree of memory difficulty and impairment in daily living tasks also increased proportionally to the total amount of drug exposure, based on a rating scale the authors developed to assess anticholinergicity of the drugs.

"This study extends our previous findings on acute cognitive impairment following recent anticholinergic exposure in older medical inpatients," says Han.
"Prescribing for older adults who take multiple prescription and over-the-counter medications requires careful attention to minimize the risk of potential harms of the drugs while maximizing their health benefits." ...
Yale Researchers Clear Up Alzheimer's Plaques In Mice

Quote:
Blocking a common immune system response cleared up plaques associated with Alzheimer's Disease and enabled treated mice to recover some lost memory, Yale University researchers report Friday in the journal Nature Medicine.

Researchers hope the new approach may one day overcome one of the biggest obstacles to development of new dementia medications - the difficulty in finding drugs that can safely cross the blood-brain barrier. ...

When TGF- was blocked, the immune system seemed to unleash immune cells known as peripheral macrophages. The macrophages passed through the blood-brain barrier and surrounded the neurons and plaques in the brains of mice.

"If results from our study in mice engineered to develop Alzheimer's-like dementia are supported by studies in humans, we may be able to develop a drug that could be introduced into the bloodstream to cause peripheral immune cells to target the amyloid plaques,'' said Terrence Town, lead author of the study. ...
Gene/Stress Interaction Increases Cognitive Decline In Elderly

Quote:
... Researchers from the Baltimore Memory Study report in The American Journal of Psychiatry (AJP), the official journal of the American Psychiatric Association, that a high level of the stress hormone cortisol in study participants aged 50 to 70 years was associated with worsened cognitive abilities. The researchers
also found that the effect was greater among those with a common form of the gene for apolipoprotein E (APOE), which has been shown to increase the risk for Alzheimer's disease. ...

The effect appears to increase as the number of copies of a specific APOE gene in the individual increases. Everyone inherits two versions of the APOE gene, known as alleles - one from each parent. The most common APOE alleles are epsilon-2, -3, and -4. Having at least one epsilon-4 allele increases an individual's risk of late-onset Alzheimer's disease. Individuals with two copies of the epsilon-4 version of the gene are particularly susceptible to the damaging effects of cortisol in the brain.

"Our findings indicate that the APOE epsilon-4 allele may increase vulnerability of the aging brain to elevated cortisol levels," said lead author Lee, a doctoral student in epidemiology at the Johns Hopkins Bloomberg School of Public Health. "While our results remain to be replicated, the observed cortisol-APOE interaction is intriguing since both cortisol and APOE have been implicated in cognitive decline associated with aging as well as in Alzheimer's disease." ...
Socially Active And Not Easily Stressed? You May Not Develop Dementia

Quote:
... The lifestyle questionnaire determined how often each person regularly participated in leisure or organizational activities and the richness of their social network. Participants were followed for six years. During that time, 144 developed dementia.

The study found that people who were not socially active but calm and relaxed had a 50 percent lower risk of developing dementia compared with people who were isolated and prone to distress. The dementia risk was also 50 percent lower for people who were outgoing and calm compared to those who were outgoing
and prone to distress.

"In the past, studies have shown that chronic distress can affect parts of the brain, such as the hippocampus, possibly leading to dementia, but our findings suggest that having a calm and outgoing personality in combination with a socially active lifestyle may decrease the risk of developing dementia even further,"
says study author Hui-Xin Wang, PhD, with the Karolinska Institute in Stockholm, Sweden.

"The good news is, lifestyle factors can be modified as opposed to genetic factors which cannot be controlled. But these are early results, so how exactly mental attitude influences risk for dementia is not clear," said Wang. ...
Researchers Link Memory Loss To Poor Diet

Quote:
... Collaboration between two laboratories at MUSC and one at Arizona State University led researchers to discover that rodents that were fed a diet high in cholesterol and saturated fat displayed impairment in working memory. This memory loss is associated with inflammation in the brain, as well as the impairment of structural proteins that affect how a nerve cell functions. As inflammation is associated with a poor diet, the failure of functions in other key organs such as the eye and the ear also could be expected.

Assuming that the same phenomenon occurs in human beings, the study suggests that as humans age, memory may be preserved and brain functions improved by restricting the consumption of cholesterol and saturated fats. ...
Apple Juice Delays Onset Of Alzheimer's Disease In Mouse Model

Quote:
A growing body of evidence demonstrates that we can take steps to delay age-related cognitive decline, including in some cases that which accompanies Alzheimer's disease, according to a study published in the January 2009 issue of the Journal of Alzheimer's Disease.

Thomas B. Shea, PhD, of the Center for Cellular Neurobiology; Neurodegeneration Research University of Massachusetts, Lowell and his research team have carried out a number of laboratory studies demonstrating that drinking apple juice helped mice perform better than normal in maze trials, and prevented the decline in performance that was otherwise observed as these mice aged.

In the most recent study Shea and his team demonstrated that mice receiving the human equivalent of 2 glasses of apple juice per day for 1 month produced less of a small protein fragment, called "beta-amyloid" that is responsible for forming the "senile plaques" that are commonly found in brains of individuals suffering from Alzheimer's disease. ...
Brain Starvation As We Age Appears To Trigger Alzheimer's - Improving Blood Flow To Brain Is A Preventive Strategy

Quote:
... "This finding is significant because it suggests that improving blood flow to the brain might be an effective therapeutic approach to prevent or treat Alzheimer's," said Vassar, a professor of cell and molecular biology at the Feinberg School.

A simple preventive strategy people can follow to improve blood flow to the brain is getting exercise, reducing cholesterol and managing hypertension. ...
Is The Next Treatment For Alzheimer's Already Out There?

Quote:
New Alzheimer's Society research will investigate whether curcumin, found in the popular Indian spice turmeric, and a number of drugs for other conditions, could benefit people with Alzheimer's.

Researchers at Southampton University will examine whether the drugs could counteract some of the brain changes that are characteristic of the disease. ...

Indian communities that regularly eat curcumin have a surprisingly low incidence of Alzheimer's, but we do not know why. Part of our research will investigate how curcumin may help protect the brain and prevent the disease. ...
Vaccine Triggers Immune Response, Prevents Alzheimer's

Quote:
A vaccine created by University of Rochester Medical Center scientists prevents the development of Alzheimer's disease-like pathology in mice without causing inflammation or significant side effects.

Vaccinated mice generated an immune response to the protein known as amyloid-beta peptide, which accumulates in what are called "amyloid plaques" in brains of people with Alzheimer's. The vaccinated mice demonstrated normal learning skills and functioning memory in spite of being genetically designed to develop an aggressive form of the disease. ...

Bowers expects the vaccine eventually to be tested in people, but due to the number of studies required to satisfy regulatory requirements, it could be three or more years before human trials testing this type of Alzheimer's vaccine occur.
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Old 2nd February 2009, 09:16 AM   #2
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Here are a couple more:

Alzheimer's Symptoms, Lesions Reduced By Vitamin B3

Quote:
An over-the-counter vitamin in high doses prevented memory loss in mice with Alzheimer's disease, and UC Irvine scientists now are conducting a clinical trial to determine its effect in humans.

Nicotinamide, a form of vitamin B3, lowered levels of a protein called phosphorylated tau that leads to the development of tangles, one of two brain lesions associated with Alzheimer's disease. The vitamin also strengthened scaffolding along which information travels in brain cells, helping to keep neurons alive and further preventing symptoms in mice genetically wired to develop Alzheimer's. ...

Nicotinamide is a water-soluble vitamin sold in health food stores. It generally is safe but can be toxic in very high doses. Clinical trials have shown it benefits people with diabetes complications and has anti-inflammatory properties that may help people with skin conditions. ...
I wonder if anything will come of it.

As with this:

The Emerging Role Of Infection In Alzheimer's Disease

Quote:
... Alzheimer's disease (AD), the most frequent cause of dementia, is a form of amyloidosis. It has been known for a century that dementia, brain atrophy and amyloidosis can be caused by chronic bacterial infections, namely by Treponema pallidum in the atrophic form of general paresis in syphilis. Bacteria and viruses are powerful stimulators of inflammation. It was suggested by Alois Alzheimer and his colleagues a century ago that microorganisms may be contributors in the generation of senile plaques in AD.

The fact that pathogens may suppress, subvert or evade host defenses and establish chronic or latent infection has received little attention in the past.

During infection, active oxygen and nitrogen species generated by inflammatory cells may cause DNA damage, induce apoptosis, and modulate enzyme activities and gene expression. Depending upon the biology of the pathogen and the host defense mechanisms the organism can persist in the infected tissues and cause chronic inflammation and amyloid deposition. The outcome of infection is as much determined by the genetic predisposition of the patient as by the virulence and biology of the infecting agent. Environmental factors and nutrition are critical determinants of disease expression as well. ...
A bit technical for me, but I could just about cope. Isn't it amazing that something so tiny can do so much damage to people. It'll be interesting to find out how that research develops.
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Old 5th February 2009, 10:18 AM   #3
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Get into that sunshine!

If you can find any.

A research project claims to have discovered a link between lack of vitamin D and cognitive impairment in older people that could lead to dementia. But it actually says that as older people's skin isn't so good at absorbing vitamin D from sunshine, the researchers want to investigate whether food supplements might be the way to go.

Link Between Vitamin D And Cognitive Impairment

Quote:
... The study was based on data on almost 2000 adults aged 65 and over who participated in the Health Survey for England in 2000 and whose levels of cognitive function were assessed. The study found that as levels of Vitamin D went down, levels of cognitive impairment went up. Compared to those with optimum levels of Vitamin D, those with the lowest levels were more than twice as likely to be cognitively impaired. ...
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Old 25th February 2009, 07:12 PM   #4
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http://news.bbc.co.uk/1/hi/health/4286435.stm

Quote:
The active ingredient in marijuana may stall decline from Alzheimer's disease, research suggests.
Scientists showed a synthetic version of the compound may reduce inflammation associated with Alzheimer's and thus help to prevent mental decline.
google :
Alzheimer's disease cannabis

449 000 entries.
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Old 25th February 2009, 08:06 PM   #5
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A recent (small) Oxford study negatively correlated serum B-12 levels with dementia and Alzheimer's disease. http://ageing.oxfordjournals.org/cgi...short/13/2/101

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Old 26th February 2009, 03:56 AM   #6
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Oh. I've found a news article that gives a lot more detail on that: Low Vitamin B12 Levels Linked to a Shrinking Brain

Quote:
*Study participants were divided into three groups, based on their B12 levels. The group with the lowest levels of vitamin B12 at the start of the study lost twice as much brain volume as those with the highest levels. The difference was significant, even after researchers considered such factors as initial brain size, age, sex, education and cognitive test scores.

*“Many factors that affect brain health are thought to be out of our control, but this study suggests that simply adjusting our diets to consume more vitamin B12 through eating meat, fish, fortified cereals or milk may be something we can easily adjust to prevent brain shrinkage and so perhaps save our memory,” said study author Anna Vogiatzoglou of Oxford University.

*Research shows that vitamin B12 deficiency is common among seniors, who are less able to absorb the nutrient effectively through their gut. “More vitamin B12 intake could help reverse this problem,” said Vogiatzoglou.

*However, the study did not look at whether taking vitamin B12 supplements would have similar benefits for the brain. David Smith, another author of the study, said the work established an association between low B12 levels and a shrinking brain, but it’s not clear if the nutrient deficiency actually caused the shrinkage.

*“This doesn’t mean you should go out and buy vitamin B12 tablets tomorrow,” he said. “We need to know the results of a clinical trial in which we’re testing whether B12 does actually prevent brain shrinkage.”

Last edited by Baby Nemesis; 26th February 2009 at 03:57 AM.
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Old 8th March 2009, 10:09 AM   #7
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A possible green tea-based supplement for Alzheimer's disease

Talking of supplements:

Another supplement might be developed, based on a compound found in green tea. Here's a BBC article about it.

Quote:
An ingredient of green tea may help to protect the brain against the ravages of Alzheimer's disease, research in the US suggests.

University of South Florida scientists found the component prevented Alzheimer's-like damage in the brains of mice bred to develop symptoms. ...

After treating Alzheimer's mice for several months with daily injections of pure EGCG, the researchers observed a dramatic decrease - as much as 54% - of brain-clogging Alzheimer's plaques. ...

Green tea contains many antioxidants, including those known as flavonoids, that can protect against damage to the brain caused by charged particles called free radicals.

However, the Florida team showed that other flavonoids in green tea actually block EGCG's ability to prevent the harmful build up of beta-amyloid.

Thus drinking green tea alone would not likely have a beneficial effect. ...

Humans would need a daily dose of 1,500 to 1,600 mg of EGCG to approximate the level that had a positive impact on mice.

That dosage has already been studied in healthy human volunteers and was found to be safe and well tolerated.

The Florida team now plans to study whether multiple oral doses of EGCG can reduce memory loss in Alzheimer's mice as well as reducing plaque formation. ...
It doesn't say how long they estimate it might be before a supplement is developed though, or whether they might realise it won't work in humans after all.
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Old 9th March 2009, 11:00 AM   #8
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http://mayoresearch.mayo.edu/mayo/re...n_lab/more.cfm

"Our lab focuses on the 13-amino-acid neuropeptide neurotensin, which was first discovered in the brain more than 30 years ago. Evidence suggests that brains affected by Alzheimer's disease have neurotensin deficits in areas involved with memory function. Neurotensin also may be involved in Parkinson's disease and schizophrenia. Our goal is to develop new drugs that stimulate brain receptors for neurotensin in an effort to reverse or stop the progression of these neuropsychiatric diseases."

http://mayoresearch.mayo.edu/mayo/re...b/overview.cfm

"We are currently evaluating the role of ECE and other reported A? degrading enzymes using transgenic and knockout approaches as well as further examining the role of these enzymes in AD. In addition, our group is using high throughput cell-based screens to identify compounds that are capable of influencing A? accumulation. These compounds can be used to investigate the factors contributing to A? accumulation and may provide novel leads for drug discovery. Using these approaches we have already identified several compounds capable of influencing A? accumulation, including one that selectively reduces A? ending at position A?42."

Linda
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Old 9th March 2009, 05:14 PM   #9
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While I await the cure, I take turmeric. I fill my own capsules because I don't cook often enough to get adequate curry in my diet.

Turmeric and Alzheimers
Quote:
...Previous studies have noted that elderly individuals living in Indian villages appear to have the lowest incidence of Alzheimer's disease in the world, with just 1% of those aged 65 and older contracting the degenerative brain condition. The reasons for this low incidence remain unclear, however.

Frautschy speculated that curcumin found in curry could provide a clue to this puzzle since the compound has ``a long history of dietary and herbal medicinal use'' and is also a powerful antioxidant and anti-inflammatory agent. In her study, Frautschy fed middle-aged (9 months old) and aged (22 months old) rats diets rich in curcumin. All of the rats had received brain injections of amyloid to mimic progressive Alzheimer's disease.

``Curcumin reduced the accumulation of beta-amyloid and the associated loss of proteins'' in the synapses, or gaps, between individual brain cells, Frautschy reported.

.... This type of memory preservation may have been reflected in the fact that rats fed curcumin also performed much better in memory-dependent maze tests compared with rats on normal diets, according to Frautschy. Curcumin also appeared to reduce Alzheimer's-related inflammation in neurologic tissue.

Because ``a combined anti-inflammatory and antioxidant approach will be useful for Alzheimer's prevention or treatment,'' Frautschy speculates that curcumin could be especially valuable in the fight against the disease, especially in combination with anti-inflammatory drugs like ibuprofen. Her team is hopeful they will soon receive funding for clinical trials to investigate curcumin-ibuprofen combination therapy.

Curcumin may not be the only compound in the kitchen spice rack able to ward off Alzheimer's. In an interview with Reuters Health, Frautschy said that ``chemicals from rosemary (rosmarinic acid) and ginger (vanillin and zingerone, also high in Indian diets) have similar structure and should be tested.''
The abstract can be found at the link.
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Old 9th March 2009, 05:17 PM   #10
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Suppression of the nuclear factor-kappaB activation pathway by spice-derived phytochemicals: reasoning for seasoning.
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Review: The activation of nuclear transcription factor kappaB has now been linked with a variety of inflammatory diseases, including cancer, atherosclerosis, myocardial infarction, diabetes, allergy, asthma, arthritis, Crohn's disease, multiple sclerosis, Alzheimer's disease, osteoporosis, psoriasis, septic shock, and AIDS. Extensive research in the last few years has shown that the pathway that activates this transcription factor can be interrupted by phytochemicals derived from spices such as turmeric (curcumin), red pepper (capsaicin), cloves (eugenol), ginger (gingerol), cumin, anise, and fennel (anethol), basil and rosemary (ursolic acid), garlic (diallyl sulfide, S-allylmercaptocysteine, ajoene), and pomegranate (ellagic acid). For the first time, therefore, research provides "reasoning for seasoning."
NSAID and antioxidant prevention of Alzheimer's disease: lessons from in vitro and animal models.
Quote:
Both oxidative damage and inflammation are elevated in brains of Alzheimer's disease (AD) patients, but their pathogenic significance remains unclear. The reduced AD risk associated with high intake of both nonsteroidal anti-inflammatory drugs (NSAIDs) and antioxidants suggests causal roles, but clinical trials in AD patients have yielded only limited or negative results. To test the potential efficacy and mechanisms of candidate approaches, we have explored conventional and unconventional NSAIDs, antioxidants, and combined NSAID/antioxidants in cell culture and animal models for AD (including aging APPsw transgenic mice and soluble Abeta rodent infusion models). The conventional NSAID ibuprofen has the strongest epidemiological support. At sustainable doses designed to mimic protective consumption in the epidemiology, ibuprofen reduces amyloid accumulation but suppresses a surprisingly limited subset of inflammatory markers in APPsw transgenic mice. Both Ab production (APP, beta- and gamma-secretases) and post-production pathways (those affecting Abeta aggregation or clearance: e.g., IL-1 or alpha1ACT) are potentially involved in ibuprofen and other NSAID anti-AD activities. The post-production pathways are predictably shared with other seemingly protective NSAIDs, including naproxen that do not lower Abeta42 in vitro. Using clinically feasible dosing, brain levels of NSAIDs appear too low to implicate a number of pharmacological dose targets that have been demonstrated in vitro. Ibuprofen did not suppress microglial markers related to phagocytosis. The putative anti-inflammatory omega-3 fatty acid DHA had a profound impact on pathogenesis but did not lower inflammation, while vitamin E was surprisingly ineffective in reducing oxidative damage or amyloid in the aged APPsw mouse. In contrast, the unconventional NSAID/antioxidant curcumin was effective, lowering oxidative damage, cognitive deficits, synaptic marker loss, and amyloid deposition. Curcumin proved to be immunomodulatory, simultaneously inhibiting cytokine and microglial activation indices related to neurotoxicity, but increasing an index of phagocytosis. Curcumin directly targeted Abeta and was also effective in other models, warranting further preclinical and clinical exploration.
Related Articles
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Old 9th March 2009, 05:23 PM   #11
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Mod WarningDiscussion on vitamin supplements split to new thread.
Posted By:Gaspode

Last edited by Gaspode; 9th March 2009 at 05:24 PM.
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Old 19th May 2009, 05:33 AM   #12
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This could be exciting.

Drugs That Target HDAC2 Gene Reversed Alzheimer's In Mice

Quote:
Building on earlier research where mice with symptoms of Alzheimer's disease regained long-term memories and the ability to learn, US researchers have now pinpointed the exact gene involved and shown that drugs that target the gene reverse the effect of Alzheimer's and boost cognitive function in mice. ...

Tsai said they think the gene, HDAC2 and its associated protein look like promising targets for treating memory impairments. ...

For the study, Tsai and colleagues used mice bred to have Alzheimer's-like symptoms and treated them with histone deacetylase (HDAC) inhibitors, a class
of drug that targets HDACs, which are a group of 11 enzymes that behave like master controllers of gene expression.

Following Alzheimer's-like brain atrophy, the mice appeared to have forgotten tasks they had previously learned.

But after they took HDAC inhibitors, the mice regained their long-term memories and ability to learn new tasks. Also, mice that were genetically engineered to have no HDAC2 genes at all showed enhanced memory formation.

HDAC inhibitors as a treatment for neurodegenerative diseases are still only at the experimental stage, although they have been is use for some time in
psychiatry and neurology as mood stabilizers and anti-epilectics. ...

Tsai said that as far they know, HDAC inhibitors have not been used to treat Alzheimer's disease or dementia.

"But now that we know that inhibiting HDAC2 has the potential to boost synaptic plasticity, synapse formation and memory formation, in the next step, we will develop new HDAC2-selective inhibitors and test their function for human diseases associated with memory impairment to treat neurodegenerative diseases," she said.
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Old 30th May 2009, 11:41 AM   #13
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Discovery Of Molecular Cause Of Alzheimer's Disease Could Bring Early Diagnosis, Treatment Closer

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... Paudel and his team have discovered that it is the addition of a single phosphate to the Ser202 amino acid within the tau brain protein that is the principal culprit responsible for Alzheimer's.

"The impact of this study is twofold," said Paudel, associate professor at McGill's Dept. of Neurology and Neurosurgery, and Project Director at the Bloomfield Centre for Research in Aging at the Lady Davis. "We can now do brain imaging at the earliest stages of the disease. We don't have to look for many different tau phosphates, just this single phosphate. The possibility of early diagnosis now exists.

"Second, the enzyme which puts this phosphate on the tau can be targeted by drugs, so therapies can be developed. This discovery gives us, for the first time, a clear direction towards the early diagnosis and treatment of Alzheimer's." ...
Let's hope it comes to something.
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Old 3rd July 2009, 12:30 PM   #14
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Statins Can Protect Against Alzheimer's Disease, According To New Study

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How nerve cells die in Alzheimer's disease is complex but we know that nerve cells eventually die because they are strongly overstimulated, a process called excitotoxicity. In animal experiments conducted in the laboratory of Professor Ulrich Eisel, Department of Molecular Neurobiology, University of Groningen, Dolga and colleagues overstimulated such nerve cells. They clearly demonstrated that treatment with a statin called Lovastatin could prevent the death
of nerve cells under these conditions. The statins not only prevented cells from dying but also prevented the loss of memory capacity that normally occurs after such cell death. In a previous study Dolga had showed that these statins stimulate the protective capacity of tumor necrosis factor, which is a key player in the brain's immune response.
There seems to be something a little wrong with that paragraph. If they stopped the cells dying, naturally they'd prevent memory loss that happens after they die. Or perhaps there's more to the story we're not told.
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Old 4th July 2009, 03:45 PM   #15
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I'm not sure what your question is, BabyNem.
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Old 4th July 2009, 11:53 PM   #16
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It wasn't a question; I was just pondering on the possibility that perhaps there were a few things the article didn't tell us, since it said statins prevented the cell death, and the memory loss that would have happened after the cells died, as if the observation about the memory not being lost was something else in statins' favour, rather than just a natural consequence of the cells not dying. So I wondered if perhaps the absence of memory loss could have been more than could have been expected from just those particular cells not dying, or whether the statins only prevented some from not dying, rather than all of them which was the suggested impression the article gave, so the stabilisation of memory loss was more than can have been expected from the number that did die. Or I wondered if there was just a bit of misleading wording in the article. It said,

"The statins not only prevented cells from dying but also prevented the loss of memory capacity that normally occurs after such cell death."

I suppose it could have meant that they knew nerve cells died because of Alzheimer's, but they hadn't connected their death with memory loss before, even though they knew memory loss happened after they died, so it came as a nice surprise when they found that preventing them dying prevented memory loss.
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Old 9th July 2009, 05:45 AM   #17
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Hey this is interesting: Caffeine Equal To 5 Cups Of Coffee A Day Reversed Alzheimer's Signs In Mice

Quote:
New research from the US and Japan showed that giving the caffeine equivalent of five cups of coffee a day to aged mice with symptoms of Alzheimer's reversed two signs of the disease: it reversed memory impairment and reduced the hallmark protein in the animals' blood and brains. ...

Both studies build on previous work by scientists at the Florida ADRC where they showed that giving caffeine to young adult mice genetically bred to have symptoms of Alzheimer's prevented them developing the symptoms of the disease when they got old.

Lead author of the first paper and co-author of the second, Dr Gary Arendash, a neuroscientist with the Florida ADRC, told the media that these new findings show that:

"Caffeine could be a viable 'treatment' for established Alzheimer's disease, and not simply a protective strategy." ...

The researchers were inspired to investigate caffeine's potential as a treatment for Alzheimer's when they spotted a Portuguese study that found people with Alzheimer's had consumed less coffee in the previous 20 years of their lives than people who did not have the brain destroying disease.
Researchers Find Possible Environmental Causes For Alzheimer's, Diabetes

Quote:
A new study by researchers at Rhode Island Hospital have found a substantial link between increased levels of nitrates in our environment and food, with increased deaths from diseases, including Alzheimer's,
diabetes, mellitus and Parkinson's. The study was published in the Journal of Alzheimer's Disease (Volume 17:3 July 2009). ...

Nitrites and nitrates belong to a class of chemical compounds that have been found to be harmful to humans and animals. More than 90 percent of these compounds that have been tested have been determined to be carcinogenic in various organs. They are found in many food products, including fried bacon, cured meats and cheese products as well as beer and water. Exposure also occurs through manufacturing and processing of rubber and latex products, as well as fertilizers, pesticides and cosmetics.

Nitrosamines are formed by a chemical reaction between nitrites or other proteins. Sodium nitrite is deliberately added to meat and fish to prevent toxin production; it is also used to preserve, color and flavor meats. Ground beef, cured meats and bacon in particular contain abundant amounts of amines due to their high protein content. Because of the significant levels of added nitrates and nitrites, nitrosamines are nearly always detectable in these foods. Nitrosamines are also easily generated under strong acid conditions, such as in the stomach, or at high temperatures associated with frying or flame broiling. ...

De la Monte states, "If this hypothesis is correct, potential solutions include eliminating the use of nitrites and nitrates in food processing, preservation and agriculture; taking steps to prevent the formation of nitrosamines and employing safe and effective measures to detoxify food and water before human consumption."
New Research Reveals Shocking Lack Of Dementia Awareness In UK

Quote:
The good news is anyone can reduce their risk by making simple lifestyle choices. Alzheimer's Society's top tips for reducing risk are: stay active; eat healthily; don't smoke; keep a healthy weight and get regular blood pressure & cholesterol checks.
Memory Decline In Mice Reversed By Blood Stem Cell Growth Factor

Quote:
A human growth factor that stimulates blood stem cells to proliferate in the bone marrow reverses memory impairment in mice genetically altered to develop Alzheimer's disease, researchers at the University
of South Florida and James A. Haley Hospital found. The granulocyte-colony stimulating factor (GCSF) significantly reduced levels of the brain-clogging protein beta amyloid deposited in excess in the brains of the Alzheimer's mice, increased the production of new neurons and promoted nerve cell connections. ...

"GCSF has been used and studied clinically for a long time, but we're the first group to apply it to Alzheimer's disease," said USF neuroscientist Juan Sanchez-Ramos, MD, PhD, the study's lead author. "This growth factor could potentially provide a powerful new therapy for Alzheimer's disease - one that may actually reverse disease, not just alleviate symptoms like currently available drugs."
Alzheimer's Gene Risk Higher For Those Widowed in Mid Life and Stay Without a Partner

Quote:
Researchers in Sweden found that people who have the APOE Alzheimer's gene and who live alone in middle age after being widowed or separated from a life partner, are at higher risk of developing dementia. ...

The authors concluded that:

"Living in a relationship with a partner might imply cognitive and social challenges that have a protective effect against cognitive impairment later in life, consistent with the brain reserve hypothesis."
(That's the theory that the reason for the finding that the more educated a person is the less risk they have of getting Alzheimer's is because they have more brain cells to kill, so the disease will take more time to get to the point where it would begin to have a major effect, and the person might have died of something else before it does and they realise they've got it.)
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Old 9th July 2009, 07:31 AM   #18
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I was going to post something really important, but I forgot what it was...


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Old 9th July 2009, 07:40 AM   #19
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Completely anecdotal, but I read an account by a seemingly rational guy who claimed that there were able to stop and reverse his father's decline with the use of coconut oil - eating it.
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Old 9th July 2009, 08:34 AM   #20
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There are some new imaging agents in clinical trials that could be able to more accurately diagnose and better determine the effectiveness of drugs to treat the disease.

http://www.drugs.com/clinical_trials...on-s-7510.html
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Old 9th July 2009, 08:58 AM   #21
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Originally Posted by billydkid View Post
Completely anecdotal, but I read an account by a seemingly rational guy who claimed that there were able to stop and reverse his father's decline with the use of coconut oil - eating it.
How much?

I once heard an anecdote about someone who had his mercury fillings taken out and he recovered from dementia. I don't know what really happened.

Terry Pratchett blames his Alzheimer's on mercury fillings.

Quote:
Dental amalgam fillings, which contain 50% mercury, are under renewed scrutiny, although there is no hard evidence to support his beliefs. More than three million were inserted last year in the UK. Sweden last month banned all mercury products, including fillings, and Norway and Denmark have done the same. ...

But the Department of Health said fillings containing mercury are not harmful, except for the small number of people who are allergic. However, it still recommends pregnant women to avoid having any inserted or removed.

Peter Ward of the British Dental Association said the safety of mercury fillings had been subjected to numerous reviews and none had found evidence that they increase the risk of developing serious illnesses.

Last edited by Baby Nemesis; 9th July 2009 at 09:00 AM.
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Old 31st August 2009, 10:10 AM   #22
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Here's an interesting article: Alzheimer's Gene Slows Brain's Ability To Export Toxic Protein

Quote:
The only known genetic risk factor for Alzheimer's disease slows down the brain's ability to export a toxic protein known as amyloid-beta that is central to the damage the disease causes, scientists have found.

The research, published by the Journal of Clinical Investigation, provides new clues into the workings of a protein known as apolipoprotein E4, or ApoE4. People who carry two copies of the gene have roughly eight to 10 times the risk of getting Alzheimer's disease than people who do not.

The new results mark a step toward resolving a longstanding question that scientists have had about exactly how ApoE4 increases a person's risk for the disease. The findings point to differences in the way that amyloid-beta is removed from the brain depending on which ApoE protein is involved.

Scientists found that when ApoE4 is present, the brain is less efficient at ridding itself of the toxic material, because a molecule that is much slower at removing the substance becomes much more involved.
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Old 17th September 2009, 03:27 PM   #23
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Alzheimer's Society Research Finds Link Between Infection And Memory Loss

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People with Alzheimer's disease who develop an infection need to be treated as soon as possible to prevent it worsening their dementia, according to research conducted by Alzheimer's Society
The research found a link between common infections, such as a cold, stomach bug or urine infection and an increase in inflammation like reactions in the brain which led to an increased rate of cognitive decline.

Researchers at the University of Southampton investigated how inflammatory proteins released during an infection might affect the brain. Results showed that people who got an infection had twice the rate of cognitive decline as people without infections.

Dr Susanne Sorensen, Head of Research, Alzheimer's Society says,

'This study is an important step towards understanding the processes that occur during the onset of Alzheimer's disease. We know there might be a link between inflammatory processes and Alzheimer's but this is not yet fully understood. These findings are helping us to understand more about possible reasons for this link. More research is now needed to further this line of investigation.
Dementia Mysteries Unveiled By Largest Ever Alzheimer's Gene Study

Quote:
Previously only one gene, APOE4, had been associated with Alzheimer's disease. This study reveals two further genes, CLU and PICALM, are related to the disease. This is expected to provide scientists with a much clearer route to developing new treatments.

The paper's lead-author, Prof Julie Williams, Chief Scientific Adviser to the Alzheimer's Research Trust, said: "Both CLU and PICALM highlight new pathways that lead to Alzheimer's disease. The CLU gene produces clusterin which normally acts to protect the brain in a variety of ways. Variation in this gene could remove this protection and contribute to Alzheimer's development. PICALM is important at synapses - connections between brain cells - and is involved in the transport of molecules into and inside of nerve cells, helping form memories and other brain functions. We know that the health of synapses is closely related to memory performance in Alzheimer's disease, thus changes in genes which affect synapses are likely to have a direct effect on disease development."

"This research is changing our understanding of what causes the common form of Alzheimer's disease and provides valuable new leads in the race to find treatments and possibly cures."
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Old 17th September 2009, 05:48 PM   #24
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I seem to do better taking Curry than the extract Curcumin.

I 'discovered' Curry as an adjunct to gluten free diet for my angina. If If I ate some hidden gluten, I would get chest pains and shortness of breath. Curry made it go away the next day. Nitro helps immediately.

Seems the Curcumin/Curry/ Turmeric acts as a mast cell inhibitor. In the 2-3 months time that I have been taking the curry, my chronic rash on my calves (mastosytosis? ) has improved about 50%. The degenerative disc in my neck isn't causing neck spasms either.

I seem to have lots of inflammatory problems. Two back disc procedures, two carpal tunnels, five trigger fingers, calf skin. I'm really thinking Mast Cells over action are a possible 'epidemic'.

And I have been using Coconut Oil for cooking the last couple years. Seems it is chock-full of short chain oils, so a body does not have to break them down as much to use them. While totally saturated, no study has linked coconut oil to CAD.

The cheapest source of food grade coconut oil is the home made soap supplies sources. $11/gallon instead of $16/ pint at the health food stores.
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Old 18th September 2009, 01:17 AM   #25
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Turmeric itself doesn't taste like curry, so people could buy the spice on its own and put it in any cooking they wanted if they didn't like curry. It isn't a hot spice. I don't think it tastes all that nice; but it's quite mild, so a bit here and there probably wouldn't make much difference to the flavour, at least with some things. It might be worth anyone who thinks it might be good for them to experiment a bit with it.
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Old 18th September 2009, 01:25 AM   #26
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... and down the road there will be another set of articles explaining how all these diets, potions and pills impact negatively on another disease. For example the reccomended diets for heart disease and Parkinson's are contradictory so if you have both (quite common) you're stuffed. Ditto if you have protate problems then caffeine and curry ingredients are on your avoid list.

Be well

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Old 18th September 2009, 02:01 AM   #27
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Originally Posted by oggiesnr View Post
... and down the road there will be another set of articles explaining how all these diets, potions and pills impact negatively on another disease. For example the reccomended diets for heart disease and Parkinson's are contradictory so if you have both (quite common) you're stuffed. Ditto if you have protate problems then caffeine and curry ingredients are on your avoid list.

Be well

Steve
Quite possibly. It's probably best not to go overboard with eating anything, and for people to do a bit of research on any food they're planning to increase in their diet for health purposes, especially if they've got some kind of health problem already.

But do you mean prostate problems? If you do, it seems scientists think turmeric can help get rid of prostate cancer as well as helping with Alzheimer's. From ScienceDaily: Curry And Cauliflower Could Halt Prostate Cancer

Quote:
ScienceDaily (Jan. 15, 2006) — Rutgers researchers have found that the curry spice turmeric holds real potential for the treatment and prevention of prostate
cancer, particularly when combined with certain vegetables. ...

The scientists tested turmeric, also known as curcumin, along with phenethyl isothiocyanate (PEITC), a naturally occurring substance particularly abundant in a group of vegetables that includes watercress, cabbage, winter cress, broccoli, Brussels sprouts, kale, cauliflower, kohlrabi and turnips. "The bottom line is that PEITC and curcumin, alone or in combination, demonstrate significant cancer-preventive qualities in laboratory mice, and the combination of PEITC and curcumin could be effective in treating established prostate cancers," said Ah-Ng Tony Kong, a professor of pharmaceutics at Rutgers, The State University of New Jersey. ...
I'm dubious of your claim that the diets recommended for people with heart disease and Parkinson's conflict with each other healthwise, apart from in that Parkinson's sufferers apparently need to be careful they don't lose too much weight. But the recommended diets for both seem to be much the same - a balanced diet containing a lot of fruit and vegetables. From an article called Foods to Eat on a Parkinson's Diet

Quote:
... Parkinson's patients need to stay away from a high-fat diet. Italian scientists have discovered that people who stay with a strict Mediterranean diet are at less risk of developing Parkinson's disease, as well as other disorders, such as Alzheimer's, heart disease and cancer. This type of low-fat diet relies on fruits and vegetables, olive oil, grains and fish. It is low in red meat and dairy products. Weight loss is a concern for Parkinson's patients, and a low-fat diet can contribute to weight loss. If this happens, patients can get extra calories from complex carbohydrates and the good fats, such as olive oil.
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Old 30th September 2009, 09:50 AM   #28
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Hey this could be good, if the source is credible and it works:

Researchers Identify Protein That Repairs Alzheimer's Brain Damage

Quote:
In explaining the findings, Nagele likened neurons to a tree with long strands called dendrites branching off from the main part of the cell. The dendrite
branches are covered with 10,000 tiny "leaves" called synapses that allow neurons to communicate with each other. Vimentin is an essential protein for
building the dendrite branches that support the synapses.

"A hallmark of Alzheimer's is the accumulation of amyloid deposits that gradually destroy the synapses and cause the collapse of dendrite branches," he
said. "When the dendrites and synapses degenerate, the neuron releases vimentin in an attempt to re-grow the dendrite tree branches and synapses. It's
a rerun of the embryonic program that allowed the brain to develop in the early years of life."

The researchers also reported some initial findings that indicated a similar damage response mechanism takes place following traumatic brain injury, suggesting
the possibility that similar therapeutic agents could be developed to enhance repair both for sudden brain trauma and for progressive neurodegenerative
diseases.
And then there's this:

Historic Gene Therapy Trial To Treat Alzheimer's Disease Underway At Georgetown

Quote:
The phase II study examines the safety and possible benefits of CERE-110. CERE-110 contains a gene and is injected during surgery into a part of the brain
affected by Alzheimer's disease. The gene will instruct brain cells to produce more of a protein, called Nerve Growth Factor or NGF, which helps nerve
cells survive and function properly. The transfer of this gene into the brain is a medical technique called gene therapy.
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Old 3rd December 2009, 02:19 PM   #29
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Possible Vaccine for Alzheimer's on the Horizon
http://www.medicalnewstoday.com:80/articles/171614.php

Quote:
AFFiRiS AG will focus its Alzheimer's vaccine program on one product candidate at an unexpectedly early stage of development: the vaccine candidate AD02 is planned to enter into Phase II clinical trial early in 2010. ...

The vaccine development program of AFFiRiS is based on the company's AFFITOME(R) technology, which also delivered the vaccines tested so far. Also based on this technology are six other vaccination programs being developed by AFFiRiS AG, which target, among other indications, Parkinson's disease and atherosclerosis.
A touch of distortion/media sensationalism here? Or could it be true?:

TAU Finds That A Destructive Protein Is Also Essential For Normal Brain Function

Quote:
Alzheimer's disease is caused by the build-up of a brain peptide called amyloid-beta. That's why eliminating the protein has been the focus of almost all drug research pursuing a cure for the devastating neurodegenerative condition.

But that may be counterproductive, says Dr. Inna Slutsky of Tel Aviv University's Department of Physiology and Pharmacology, Sackler Faculty of Medicine. Her recent research demonstrates that amyloid-beta is also necessary to maintain proper brain functioning.

These findings may shake the foundations of Alzheimer's research. ...
Time to get exercising, it would seem:

Fat Around The Middle Increases The Risk Of Dementia

Quote:
Women who store fat on their waist in middle age are more than twice as likely to develop dementia when they get older, reveals a new study from the Sahlgrenska Academy.
This sounds interesting: Cancer Drug May Improve Memory In Alzheimer's Patients

Quote:
The reason why the drug improves memory lies in the way the brain records new memories. To create new memories, the neurons in the brain must manufacture new proteins. The first step is to open up and read the DNA, which contains instructions for making the proteins.

To read the DNA, the neuron attaches a chemical reactive group to the spool around which DNA is tightly wound. "These groups, called acetyls, unwind the DNA to make it more accessible," says co-author Yitshak Francis, Ph.D., a postdoctoral research scientist at Columbia. "It's like unwinding knitting wool from its spool."

This unwrapping step, the researchers found, is impaired in mice with a form of Alzheimer's disease. The mice with Alzheimer's attached about half as many acetyls to DNA as normal mice and had poorer memory.

The researchers then discovered that they could improve memory in the Alzheimer's-afflicted mice with a cancer drug from a family of compounds, called HDAC inhibitors, which increase the DNA's spool acetylation and gene transcription. The drug improved memory performance to the level found in normal mice.
Mouse genes to be put in human brains?

Mouse Gene Suppresses Alzheimer's Plaques And Tangles

Quote:
Investigators at Burnham Institute for Medical Research (Burnham) and colleagues have identified a novel mouse gene (Rps23r1) that reduces the accumulation of two toxic proteins that are major players in Alzheimer's disease: amyloid beta and tau. The amyloid and tau lowering functions of this gene were demonstrated in both human and mouse cells. Amyloid beta is responsible for the plaques found in the brains of Alzheimer's patients. Tau causes the tangles found within patients' brain cells. The study was published in the journal Neuron on November 12. These findings could lead to new treatments for Alzheimer's disease. ...
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Old 17th January 2010, 08:02 AM   #30
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Here's an interesting one: Cell Phone Exposure May Protect Against And Reverse Alzheimer's Disease

Quote:
"It surprised us to find that cell phone exposure, begun in early adulthood, protects the memory of mice otherwise destined to develop Alzheimer's symptoms," said lead author Gary Arendash, PhD, USF Research Professor at the Florida ADRC. "It was even more astonishing that the electromagnetic waves generated by cell phones actually reversed memory impairment in old Alzheimer's mice."

The researchers showed that exposing old Alzheimer's mice to electromagnetic waves generated by cell phones erased brain deposits of the harmful protein beta-amyloid, in addition to preventing the protein's build-up in younger Alzheimer's mice. The sticky brain plaques formed by the abnormal accumulation of beta amyloid are a hallmark of Alzheimer's disease. Most treatments against Alzheimer's try to target beta-amyloid. ...

Months of cell phone exposure even boosted the memories of normal mice to above-normal levels. The memory benefits of cell phone exposure took months to show up, suggesting that a similar effect in humans would take years if cell phone-level electromagnetic exposure was provided. ...
New Approach To Fighting Alzheimer's Shows Potential In Clinical Trial

Quote:
In the early stages of Alzheimer's disease, patients typically suffer a major loss of the brain connections necessary for memory and information processing. Now, a combination of nutrients that was developed at MIT has shown the potential to improve memory in Alzheimer's patients by stimulating growth of new brain connections.

In a clinical trial of 225 Alzheimer's patients, researchers found that a cocktail of three naturally occurring nutrients believed to promote growth of those connections, known as synapses, plus other ingredients (B vitamins, phosopholipids and antioxidants), improved verbal memory in patients with mild Alzheimer's.
University Hospitals Case Medical Center Testing Gene Therapy For Alzheimer's Disease

Quote:
University Hospitals Case Medical Center is one of 12 sites conducting the first Phase 2 clinical trial of a gene therapy for Alzheimer's disease (AD). The study uses a viral-based gene transfer system called CERE-110, which is designed to deliver nerve growth factor (NGF) into the brain. ...

NGF is a naturally occurring protein that may prevent nerve cells in the brain from dying and may help these cells function better. During the study, CERE-110 will be injected by a neurosurgeon into the nucleus basalis of Meynert, an area of the brain where nerve cells die in patients with AD. ...

"Should the clinical development of this therapy be successful, CERE-110 could offer the possibility of delaying the course of Alzheimer's disease, a real improvement over existing therapies," said Dr. Lerner. "This would not be a cure for AD, but a way of slowing it down."
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Old 21st January 2010, 07:47 AM   #31
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Here are some more things that hopefully could be promising:

'Longevity Gene' Helps Prevent Memory Decline And Dementia

Quote:
Scientists at Albert Einstein College of Medicine of Yeshiva University have found that a "longevity gene" helps to slow age-related decline in brain function in older adults. Drugs that mimic the gene's effect are now under development, the researchers note, and could help protect against Alzheimer's disease. ...

At the beginning of the study, the 523 participants - all of them 70 or over - were cognitively healthy, and their blood samples were analyzed to determine which CETP gene variant they carried. They were then followed for an average of four years and tested annually to assess their rates of cognitive decline, the incidence of Alzheimer's disease and other changes.

"We found that people with two copies of the longevity variant of CETP had slower memory decline and a lower risk for developing dementia and Alzheimer's disease," says Amy E. Sanders, M.D., assistant professor in the Saul R. Korey Department of Neurology at Einstein and lead author of the paper. "More specifically, those participants who carried two copies of the favorable CETP variant had a 70 percent reduction in their risk for developing
Alzheimer's disease compared with participants who carried no copies of this gene variant."
I'm not sure how confident they really ought to be about their findings after only four years! Still, the project might yield some exciting results one day.

Eye Test Could Aid Alzheimer's Detection

Quote:
A simple and inexpensive eye test could aid detection and diagnosis of major neurological diseases such as Alzheimer's at an earlier stage than is currently possible, according to new research by UCL scientists. ...

Professor Cordeiro, UCL Institute of Ophthalmology, said: "The death of nerve cells is the key event in all neurodegenerative disorders - but until now it has not been possible to study cell death in real time. This technique means we should be able to directly observe retinal nerve cell death in patients, which has a number of advantages in terms of effective diagnosis. This could be critically important since identification of the early stages could lead to successful reversal of the disease progression with treatment.
Blood Pressure And Heart Disease Drugs May Help Fend Off Dementia, Including Alzheimer's Disease

Quote:
Professor Benjamin Wolozin from Boston University School of Medicine led the team of researchers. They investigated the incidence of dementia in over 800,000 individuals in the US from 2002 to 2006. They were mostly (98 percent) male subjects. The participants had cardiovascular disease and were 65 years of age or older.

The research subjects were divided in three groups: one using angiotensin receptor blockers, another the blood pressure lowering drug lisinopril and the third using other comparative drugs used for heart disease.

The findings indicate that the group on angiotensin receptor blockers was significantly less likely to develop Alzheimer's disease or dementia. In addition, they reveal that angiotensin receptor blockers have an additive effect when used in combination with another type of high blood pressure drug (ACE inhibitors). In fact, individuals with existing Alzheimer's disease or dementia who took both medicines were less likely to die early or be admitted to nursing homes.
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Old 22nd February 2010, 03:05 AM   #32
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Could people be routinely screened for evidence of Alzheimer's one day?

Study findings are thought to show that the earlier people are given drugs to treat it, the more chance there is that they'll actually work:

Neuroimaging Study May Pave Way For Effective Alzheimer's Treatments

Quote:
... The results of the survey, reported in a recent special issue of the journal Behavioral Neurology (vol. 21, Issues 1-2, 2009), may explain why patients with Alzheimer's disease have not responded to promising experimental drugs that target amyloid, and suggest that these drugs may be effective if administered earlier.

"Amyloid deposits appear to reach a plateau early in the disease course, when patients experience very mild symptoms or no symptoms at all," says Rabinovici, a recipient of new investigator awards from the Alzheimer's Association and the National Institute on Aging. "By the time patients have developed the symptoms of Alzheimer's disease, clinical decline and brain changes are occurring independently of further amyloid accumulation. This suggests that we have been starting treatment too late, and that amyloid-based therapies are most likely to work very early in the disease process." ...
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