Archives for October 2011

New Findings Contradict Dominant Theory in Alzheimer’s Disease

For decades the amyloid hypothesis has dominated the research field in Alzheimer’s disease. The theory describes how an increase in secreted beta-amyloid peptides leads to the formation of plaques, toxic clusters of damaged proteins between cells, which eventually result in neurodegeneration. Scientists at Lund University, Sweden, have now presented a study that turns this premise on its head. The research group’s data offers an opposite hypothesis, suggesting that it is in fact the neurons’ inability to secrete beta-amyloid that is at the heart of pathogenesis in Alzheimer’s disease.

The study, published in the October issue of the Journal of Neuroscience, shows an increase in unwanted intracellular beta-amyloid occurring early on in Alzheimer’s disease. The accumulation of beta-amyloid inside the neuron is here shown to be caused by the loss of normal function to secrete beta-amyloid.

Contrary to the dominant theory, where aggregated extracellular beta-amyloid is considered the main culprit, the study instead demonstrates that reduced secretion of beta-amyloid signals the beginning of the disease.

The damage to the neuron, created by the aggregated toxic beta-amyloid inside the cell, is believed to be a prior step to the formation of plaques, the long-time hallmark biomarker of the disease.

Professor Gunnar Gouras, the senior researcher of the study, hopes that the surprising new findings can help push the research field in a new direction.

“The many investigators and pharmaceutical companies screening for compounds that reduce secreted beta-amyloid have it the wrong way around. The problem is rather the opposite, that it is not getting secreted. To find the root of the disease, we now need to focus on this critical intracellular pool of beta-amyloid.

“We are showing here that the increase of intracellular beta-amyloid is one of the earliest events occurring in Alzheimer’s disease, before the formation of plaques. Our experiments clearly show a decreased secretion of beta-amyloid in our primary neuron disease model. This is probably because the cell’s metabolism and secretion pathways are disrupted in some way, leading beta-amyloid to be accumulated inside the cell instead of being secreted naturally,” says Davide Tampellini, first author of the study.

The theory of early accumulation of beta-amyloid inside the cell offers an alternate explanation for the formation of plaques. When excess amounts of beta-amyloid start to build up inside the cell, it is also stored in synapses. When the synapses can no longer hold the increasing amounts of the toxic peptide the membrane breaks, releasing the waste into the extracellular space. The toxins released now create the seed for other amyloids to gather and start forming the plaques.


The above story is reprinted from materials provided by Lund University.

Lund University (2011, October 28). New findings contradict dominant theory in Alzheimer’s disease. ScienceDaily. Retrieved October 31, 2011, from­ /releases/2011/10/111028103219.htm

Journal Reference:

  1. D. Tampellini, N. Rahman, M. T. Lin, E. Capetillo-Zarate, G. K. Gouras. Impaired  -Amyloid Secretion in Alzheimer’s Disease Pathogenesis. Journal of Neuroscience, 2011; 31 (43): 15384 DOI: 10.1523/JNEUROSCI.2986-11.2011 

Accera identifies genetic profile of AD patients with heightened response to Axona

Accera, Inc., a biotech company specializing in cognitive health, announced today that it has identified the genetic profile of Alzheimer’s disease (AD) patients who have a high probability of responding to Axona® (AC-1202), a prescription medical food product available at pharmacies nationwide.

In this current study, variances in the DNA sequences associated with the genes responsible for producing insulin degrading enzyme (IDE) and the pro-inflammatory cytokine interleukin-1beta (IL1B) were shown to be highly predictive for improvement in cognition among patients receiving Axona.

Other studies have shown a correlation between an increased risk for AD among carriers of the apolipoprotein E4 allele (APOE4), and Accera has previously published its findings from a double-blind, placebo-controlled study showing that AD patients who were non-carriers of the APOE4 gene (APOE4(-)) experienced significant cognitive improvements in a 90-day trial of AC-1202.  This additional analysis has shown that specific genotype combinations of E4(-), IDE and IL1B produced additive improvements in cognitive performance.

Alzheimer’s patients who carried combinations of common variants in IDE, APOE and IL1B showed as much as a 7 point increase in cognitive function as measured by the Alzheimer’s Disease Assessment Scale-Cognitive subscale (ADAS-Cog), one of the most widely used scales for anti-dementia drugs in the US.  Changes in the ADAS-cog scores of more than 3-4 points are generally recognized as being clinically meaningful.  Since the specific variations in the genes for IDE and IL1B are commonly observed in the AD population, the number of patients who are likely to experience a heightened therapeutic benefit from Axona should be significant.

This result was particularly surprising because the majority of participants in the study were already taking one or more approved Alzheimer’s disease medications. “More than two dozen clinical trials have demonstrated that certain therapies offer clear genotype dependent clinical improvements,” commented Dr. Judes Poirier of McGill University.  Dr. Poirier is internationally renowned for his works on the role of apolipoprotein E in the normal and injured brain, and in the genetics of Alzheimer’s disease.  According to Dr. Poirier, “this study takes this notion to the next level, linking multiple genetic risk factors to significant therapeutic response in a state-of-the-art, randomized, double-blind, placebo controlled study in mild-to-moderate Alzheimer’s disease.”

Alzheimer’s disease is characterized by decreases in the brain’s ability to metabolize glucose, a well recognized condition known as hypometabolism.  Since glucose is the predominant fuel used by the brain, disruptions in glucose metabolism are associated with cognitive impairment.  Axona, a medical food product taken once daily, overcomes this deficiency by providing the brain with ketone bodies, an alternative fuel source that results in improved cognition.

Dr. Richard Isaacson, Associate Professor of Clinical Neurology at the University of Miami Miller School of Medicine and author of the book “Alzheimer’s Treatment / Alzheimer’s Prevention: A Patient and Family Guide” also finds these results encouraging.  Dr. Isaacson explains that “clinicians have been struggling to understand why certain patients with Alzheimer’s disease may preferentially respond to one therapy, while other patients will not respond.  This exploratory study is important in that it takes the first steps toward understanding how specific genes may influence the response to ketosis therapy, and improve our ability to address glucose hypometabolism in the brain.”


SOURCE Accera, Inc.

Health Care Reform Brings New Options for Alzheimer’s Care

Little noticed in the new health care reform bill signed into law by President Obama in March is a provision that may provide help to families affected by Alzheimer’s disease. The provision, known as the CLASS Act, for Community Living Assistance for Services and Supports Plan, creates a nationwide voluntary insurance program to provide long-term care services and support to families affected by long-term ailments, including Alzheimer’s.

The insurance program will help people with Alzheimer’s to live at home and remain independent longer by providing benefits that can be used to pay for home care aides, transportation and respite care. While Alzheimer’s care is often much more expensive, the extra funds can help to pay for a family member or other home aide, for example, to help with dressing or bathing. CLASS funds could also help install a grab-bar or ramp in the home so that an elderly person with Alzheimer’s can stay at home longer.

People can also use their CLASS benefits for assistive devices, adult day programs, assisted living or nursing homes.

All working adults 18 or older can participate in the program. People will pay small monthly premiums through their employers, deducted from their paychecks. After five years, they are then eligible for home care benefits.

If a participant becomes disabled, through Alzheimer’s or any illness or accident, he or she is eligible for cash benefits of $50 to $100 a day to help pay for care, provided he or she has been in the program for at least five years.

Currently, many people cannot get any long-term care insurance at all. And many cannot afford it. It is estimated that fewer than 10 percent of older adults have bought long-term care policies.

Many families mistakenly believe that existing government programs like Medicare will provide financial assistance for an ill loved one living at home. But even though such care is less expensive than hospital or nursing home care, Medicare does not contribute to home expenses, though Medicaid does pay for some of these expenses for people who have run out of money. In many instances, family members must volunteer their time and efforts to help a loved one with Alzheimer’s.

The CLASS Act is a legacy of Senator Edward M. Kennedy, who died last year. The program is scheduled to take effect in Jan. 2011. Administrators are currently seeking to figure out how much premiums will cost, and how people might be able to participate if they are self-employed or if their employers decline to participate.

Among the unknowns is how many people will participate. The more younger and healthy people who do participate, the cheaper the program will be. Participation may be aided by the fact that all people who work for larger companies will automatically be enrolled in the program; individuals can opt out if they do not wish to participate.

Other features of the new health care law may also help certain families affected by Alzheimer’s.

People who have early-onset Alzheimer’s, a rare form of the disease that strikes before age 65, will now be able to purchase insurance. Insurers will no longer be able to deny coverage due to this pre-existing medical condition.

In addition, there will be new funds to study various pilot programs for delivering aid and care to Alzheimer’s patients in the coming years. Programs deemed successful for helping patients stay at home longer, for example, or for delivering care at lower costs can then be expanded.

By [1], The Alzheimer’s Information Site. Reviewed by William J. Netzer [2], Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.



Article printed from Fisher Center for Alzheimer’s Research Foundation:

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[2] William J. Netzer:

A Treatment Overview of Alzheimer’s Disease

Dementia is a condition of mental decline that causes progressive memory impairment and problems with learning, judgment, communication, and quality of life. Alzheimer’s disease, a progressive brain disorder, is the most common form of dementia. While there is no cure for Alzheimer’s disease and no treatment to reverse or halt its progression, there are medicines available that can help treat symptoms in some people with Alzheimer’s disease. If Alzheimer’s disease is diagnosed earlier, treatment may enable people to carry out their daily activities and independent living for a longer period of time and may prolong the time that patients can be managed at home. Health care providers may also use other medicines to help manage other troubling symptoms of Alzheimer’s disease, including depression, sleeplessness, and behavioral problems such as agitation and aggression.

Planning and medical/social management can help ease the burden on both patients and family members. Exercise, good nutrition, activities, and social interaction are important. A calm, structured environment also may help the person with Alzheimer’s disease to continue functioning as independently as possible.


How Is Alzheimer’s Disease Treated?

Your doctor will determine the best treatment for the Alzheimer’s patient based on various factors, including:

  • The patient’s age, overall health, and medical history
  • Extent of the disease
  • The patient’s tolerance for specific medicines and therapies
  • Expectations for the course of the disease
  • The patient and his or her caregiver’s opinions or preferences

What Drugs Are Used to Treat Alzheimer’s Disease?

  • Cholinesterase inhibitors (Aricept, Cognex, Exelon, Razadyne). Cholinesterase inhibitors curb the breakdown of acetylcholine, a chemical in the brain important for memory and learning. These types of medications help increase the levels of acetylcholine in the brain. These drugs may slow the progression of symptoms for about half of people taking them for a limited time, on average 6 to 12 months.
  • Aricept is the only treatment approved by the FDA for all stages of Alzheimer’s disease: mild, moderate, and severe. It is available as tablets to swallow or tablets to dissolve in the mouth. Cognex was the first of these drugs to be FDA approved, but it is used less commonly than the other medications.   Exelon is approved for use in mild to moderate Alzheimer’s dementia and is available as a skin patch, capsules, and liquid form. Razadyne (formerly Reminyl) is also approved for mild to moderate Alzheimer’s dementia and is available as an extended-release capsule, immediate-release tablet, and liquid forms. Common side effects are usually mild for these medications and include diarrhea, vomiting, nausea, fatigue, insomnia, loss of appetite, and weight loss. Cognex use may cause liver damage, so your doctor will need to perform tests to monitor liver function.
  • Namenda. Namenda is approved to treat moderate-to-severe Alzheimer’s disease. Namenda works by a different mechanism than other Alzheimer’s treatments; it is thought to play a protective role in the brain by regulating the activity of a different brain chemical called glutamate. Glutamate also plays a role in learning and memory. Brain cells in people with Alzheimer’s disease release too much glutamate. Namenda helps regulate glutamate activity. Namenda is the only drug for Alzheimer’s that works this way. It may improve mental function and performance of daily activities for some people. Namenda may have increased benefit when used with Aricept, Exelon, Razadyne, or Cognex. Side effects of Namenda include tiredness, dizziness, confusion, constipation, and headache.

Cognex, Exelon, and Razadyne seem to help only those with mild or moderate symptoms of Alzheimer’s disease. Aricept is approved by the FDA to treat all stages of Alzheimer’s disease: mild, moderate, and severe. Namenda is prescribed for patients who have moderate-to-severe Alzheimer’s. In addition to these medicines, the American Academy of Neurology has stated that vitamin E (alpha-tocopherol) and selegiline (a drug used for Parkinson’s disease) may help with some Alzheimer’s symptoms. Studies looking at the role of supplements such as coenzyme Q10, coral calcium, gingko biloba, and huperzine A have not shown a benefit in their use for Alzheimer’s disease. Study findings from omega-3 fatty acids have been mixed, and research is ongoing.

It is important to know that new research findings are giving reason for hope, and several drugs are being studied in clinical trials to determine if they can slow the progress of the disease or improve memory or other symptoms for a period of time. Scientists also continue to look for methods to diagnose Alzheimer’s earlier, before symptoms appear, which can allow for earlier pursuit of treatment.

A number of other therapeutic approaches such as an Alzheimer’s vaccine are being actively investigated.


Alzheimer’s Association: “Standard Treatments,” “FDA-Approved Treatments for Alzheimer’s,” “Alternative Treatments.”

American Academy of Neurology Guideline Summary for Patients and their Families: “Alzheimer’s Disease.”

Alzheimer’s Disease Education & Referral Center: “Treatment.”

Reviewed by Brunilda Nazario, MD on October 10, 2011
© 2011 WebMD, LLC. All rights reserved.

Study Shows Alzheimer’s Disease–Related Peptides Form Toxic Calcium Channels in the Plasma Membrane

Alzheimer’s disease is triggered by the inappropriate processing of amyloid precursor protein to generate excess amounts of short peptide fragments called A-beta. For many years, the neurodegeneration associated with Alzheimer’s disease was thought to be caused by the buildup of A-beta in insoluble, fibrous plaques. However, increasing suspicion now falls on smaller, soluble A-beta complexes as the toxic form of the protein, partly through their ability to induce excess calcium influx into cells, which disrupts synaptic signaling and stimulates cell death. A new study in The Journal of Cell Biology ( uses high-resolution imaging to reveal that A-beta oligomers elevate calcium by forming calcium-permeable pores in the plasma membrane.

A-beta oligomers could induce calcium influx by physically disrupting the cell’s outer membrane or by activating endogenous calcium channels. But studies have also shown that A-beta peptides can form calcium-permeable pores themselves in both artificial and cell membranes. A limitation of experimental techniques used to date, says Angelo Demuro, from the University of California, Irvine, is that they only monitor the activity of one or two channels at a time. In addition, different groups have obtained disparate results regarding the properties of A-beta channels using this approach.

To overcome these problems, Demuro and colleagues developed an alternative method to measure the activity of calcium channels in living cells. “We can simultaneously record the behavior of thousands of channels using an imaging technique we call optical patch-clamping,” Demuro explains. In this approach, frog eggs are filled with a calcium-sensitive dye, and the researchers observe the part of the cell nearest to the cell’s outer membrane. When membrane channels open to let calcium into the cell, small fluorescent flashes indicate the duration and extent of calcium influx at each individual pore.

Demuro et al. found that, just twenty minutes after A-beta oligomers were added to the eggs, they displayed flickering spots of fluorescence signifying calcium influx through single membrane channels. This influx was unlikely to be through endogenous channels activated by A-beta because frog eggs barely express calcium channels of their own. Moreover, A-beta aggregates weren’t simply disrupting the eggs’ membrane, as the influx was inhibited by zinc ions, which block calcium-permeable pores.

A-beta oligomers therefore form calcium-permeable channels of their own in the membrane. Demuro and colleagues characterized the properties of these pores by simultaneously imaging the activity of thousands of channels in a single membrane region. “They are all different,” says Demuro. “[The pores] show a wide variety of behaviors.” Most pores opened infrequently and only let in small amounts of calcium, but some opened more often and channeled large amounts of calcium into the cell. Though few in number, Demuro et al.’s measurements suggest that this latter type of pore may be largely responsible for the toxic increase in cytoplasmic calcium levels.

Differences in the properties of individual pores may be caused by differences in the number of A-beta peptides assembled into each channel, with higher-order oligomers forming the more active species of pore. “It would be nice to visualize how many A-beta peptides each pore has and whether this is related to the activity of the channel,” Demuro says. If pore activity is affected by the oligomerization state of A-beta, it appears that A-beta peptides continue to assemble after their insertion into membranes, as the pores became more active as eggs were exposed to A-beta oligomers for longer periods. This increase in calcium influx over time may be related to the gradual progression of Alzheimer’s symptoms.

Beyond Alzheimer’s disease, Demuro et al.’s approach may help explain the pathogenesis of other neurodegenerative disorders like Parkinson’s and Huntington’s disease, in which misfolded and aggregated proteins have also been reported to form calcium-permeable channels.

About The Journal of Cell Biology

Founded in 1955, The Journal of Cell Biology (JCB) is published by The Rockefeller University Press. All editorial decisions on manuscripts submitted are made by active scientists in conjunction with our in-house scientific editors. JCB content is posted to PubMed Central, where it is available to the public for free six months after publication. Authors retain copyright of their published works and third parties may reuse the content for non-commercial purposes under a creative commons license. For more information, please visit


Released: 10/19/2011 11:25 AM EDT
Embargo expired: 10/24/2011 12:00 PM EDT
Source: Rockefeller University Press

Demuro, A., et al. 2011. J. Cell Biol. doi:10.1083/jcb.201104133

Family History Affects Biomarkers, Science Tracks Their Course

The profile of cerebrospinal fluid (CSF) amyloid-β (Aβ), tau, and other biomarkers associated with Alzheimer’s disease depends in part on a family history of AD, and the markers’ trajectory over time depends on the stage of disease. As laid out in two papers in the October Archives of Neurology, the findings strengthen the case for using biomarkers to determine who is at risk for AD before symptoms develop (see ARF related news story on Schott et al., 2010). “This type of research is so important. Everyone believes that Alzheimer’s starts early and we need ways to detect it,” said Henrik Zetterberg at the Sahlgrenska University Hospital in Sweden, who was not involved in the work.

First author Chengjie Xiong and colleagues took a snapshot of the biomarker profiles of more than 260 cognitively normal middle-aged to older people participating in the Adult Children Study (ACS) at Washington University. They found that a family history of the disease influences their levels. “If people have a family history of Alzheimer’s, their biomarker profiles look a bit more like those of people with the disease,” said Zetterberg. In the second paper, Raymond Lo in the laboratory of William Jagust at the University of California, Berkeley, and colleagues describe the changes in biomarkers that occur over the course of two to three years in more than 800 people participating in the Alzheimer’s Disease Neuroimaging Initiative (ADNI). They found that CSF molecules and brain volume not only change over time, but do so at different rates in people who are cognitively normal versus those with mild cognitive impairment (MCI) or AD.

Because some of these changes happen before any noticeable cognitive symptoms, they could be used to identify people in the preclinical stage of AD. The idea of treating patients at this stage has gained momentum in recent years. “It is incumbent on the AD research community to educate our colleagues, the public, and regulatory agencies to accept that it is necessary to treat AD before it is symptomatic,” wrote Archives editor Roger Rosenberg in an accompanying editorial.

When Xiong and colleagues analyzed CSF amyloid-β42 (Aβ42), in the ACS cohort, they found that the amounts were lower in older than in younger people, and this difference was more pronounced for those with a family history of AD. The presence of the ApoE4 allele, the major genetic risk factor for sporadic AD, did not change this relationship. Rather, people with the E4 allele have lower levels of CSF Aβ42 (see Tosun et al., 2010) than those without it, and family history of AD exacerbated this difference. The scientists also found differences in other disease indicators, such as CSF tau levels, and in the amount of brain amyloid detected by positron emission tomography using Pittsburgh compound B, depending on whether people had a family history of AD or not.

The study supports growing evidence that genetic factors beyond ApoE influence biomarker variations (see ARF related news story on Sheline et al., 2010; Kauwe et al., 2010). Genomewide association studies also implicate several genes that predispose to AD (see ARF related news story on Naj et al., 2011 and Hollingworth et al., 2011 and AlzGene GWAS summary). However, people who have a family history share not only genes with their affected forebears. “It is possible that environmental factors and diet may also play a role in these biomarker changes,” said Morris. “It does not negate the role of genetics but raises some additional areas of research.” Xiong cautioned that this cross-sectional study did not determine whether the measured changes predict disease.

Toward that goal, Lo and other ADNI investigators analyzed CSF samples collected from participants 55 to 90 years of age over the course of three years. Surprisingly, perhaps, the scientists found no significant changes in CSF tau measurements in either group. They did find that levels of CSF Aβ42 fell over time, dropping faster in people with normal cognition than in those with MCI or AD. Glucose metabolism and brain hippocampal volume also dropped over time, but did so more slowly in cognitively normal people than in people with MCI and AD. These results suggest that amyloid deposition occurs before hypometabolism or hippocampal atrophy. “Amyloid changes most likely occur before anything else, early in the disease process,” said Zetterberg. The ADNI group had previously reported biomarker changes in the first year of follow-up of participants (Beckett et al., 2010); this study extends the results to up to 36 months.

The findings are largely consistent with the model of biomarker trajectories proposed by Clifford Jack, Mayo Clinic, Rochester, Minnesota, and colleagues (Jack et al., 2010), suggesting that different biomarkers reflect different pathologies at different stages of the disease. Studies are now starting to provide actual numbers for those projections by measuring the slope by which each marker changes at each stage. “It is a good start, but we are still far away from realizing the curvilinear trajectories since we do not have sufficient data to draw a good curve,” wrote Lo. “Jack’s model used logistic curves to describe various biomarker trajectories, which were biologically plausible but hard to prove. The model is still mostly valid, except for tau, which did not significantly change over time during the follow-up period.” Lo noted the study was limited by the length of observation.

The researchers found that all biomarker changes correlated with declines in cognitive function in people with MCI and AD but not in cognitively normal people (see ARF related news story on Fjell et al., 2010 and Stomrud et al., 2010). Why this association does not apply to healthy people is not clear. “One possibility is that our assessment tools are designed to measure overt cognitive impairment, but are not sensitive enough to capture the decline in cognitively normal people,” wrote Lo. Research does predict that normal people in the ADNI cohort do begin to lose cognitive function if they test positive for brain amyloid at baseline (see ARF related news story and ARF news story.—Laura Bonetta.

Lo RY, Hubbard AE, Shaw LM, Trojanowski JQ, Petersen RC, Aisen PS, Weiner MW, Jagust WJ; for the Alzheimer’s Disease Neuroimaging Initiative. Longitudinal Change of Biomarkers in Cognitive Decline. Arch Neurol. 2011 Oct;68(10):1257-1266. Abstract

Xiong C, Roe CM, Buckles V, Fagan A, Holtzman D, Balota D, Duchek J, Storandt M, Mintun M, Grant E, Snyder AZ, Head D, Benzinger TL, Mettenburg J, Csernansky J, Morris JC. Role of Family History for Alzheimer Biomarker Abnormalities in the Adult Children Study. Arch Neurol. 2011 Oct;68(10):1313-9. Abstract

Rosenberg RN. Treat Alzheimer disease before it is symptomatic. Arch Neurol. 2011 Oct;68(10):1237-8. Abstract          



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21 October 2011

Effect of Aging On the Brain

Research by biologists at the University of York and Hull York Medical School has revealed important new information about the way the brain is affected by age. Working with scientists at the Peninsula College of Medicine and Dentistry in Plymouth, they have studied responses to stress in synapses — neuronal connections.

The researchers discovered that under stressful conditions, such as neuro-degeneration, resulting high energy forms of damaging oxygen cause synapses to grow excessively, potentially contributing to dysfunction.

Such stresses occur during neurodegenerative disease such as Alzheimer’s and Parkinson’s Disease.

The research, which was funded by the Medical Research Council and the Biotechnology and Biological Sciences Research Council, is published in the latest issue of the Proceedings of the National Academy of Sciences (PNAS).

Laboratory modelling was carried out using Drosophila, but similar pathways are present in humans. The scientists studied the responses using a model of lysosomal storage disease, an inherited incurable childhood neurodegeneration where enlarged synapses have been observed, but the role that growth has in disease progression and brain function is not yet clear.

Co-author Dr Sean Sweeney, of the Department of Biology at the University of York, said: “The findings have strong implications for neuronal function as brains age, and will add significantly to our understanding of neurodegenerative disease such as Alzheimer’s and Parkinson’s disease.”

Co-author Dr Iain Robinson, of the Peninsula College of Medicine and Dentistry, added: “Neuronal contacts in the brain are constantly changing. These changes in the brain enable us to form short term memories such as where we parked the car, or longer term memories, such as what is our pin number for the cash point machine. Our work sheds light on how our brain becomes less able to make these changes in neuronal contacts as we age and helps explain the loss of neuronal contacts seen in several neurodegenerative diseases.”



The above story is reprinted from materials provided by University of York.


1. Valerie J. Milton, Helen E. Jarrett, Kate Gowers, Salma Chalak, Laura Briggs, Iain M. Robinson, and Sean T. Sweeney. Oxidative stress induces overgrowth of the Drosophila neuromuscular junction. Proceedings of the National Academy of Sciences, October 10, 2011 DOI: 10.1073/pnas.1014511108


University of York (2011, October 10). Effect of aging on the brain. ScienceDaily. Retrieved October 24, 2011, from­ /releases/2011/10/111010173025.htm

Behind the Science: Want to Read the Latest Alzheimer’s Disease Hypotheses?


AlzSWAN is a community-driven knowledge base of Alzheimer disease that enables researchers to submit and annotate scientific hypotheses, claims, data, and information, putting these the context of testable hypotheses and treatment discovery. The system is powered by SWAN (Semantic Web Application in Neuromedicine), which uses Semantic Web technology, to tie together statements made in scientific publications or on the Web to scientific evidence, biological terminologies, and knowledge bases, and to claims and counterclaims made by other researchers.

Please view this tutorial [.pdf] to learn about the functions and features of AlzSWAN.

We welcome your feedback. Seedling hypotheses and observations that are not yet fleshed out scientifically are posted on the Hypothesis Factory page.



This is a collection of virtual seminars, online journal club discussions, recorded talks and other presentations on the Alzforum website that describe a variety of scientific hypotheses about the pathogenesis of Alzheimer disease. Readers are invited to submit commentaries on the posted hypotheses and contribute ideas about how these diverse hypotheses and data could be integrated into a more complete picture of the disease. A more extensive collection of hypotheses is being annotated for the SWAN Alzheimer Knowledge Base (see above). The ability to comment on SWAN claims will be available soon.



Our Hypothesis Factory is devoted to the presentation and exchange of ideas regarding novel hypotheses, hunches, theories-in-progress, and wild
speculation. It provides a forum where people can publicly present and discuss unconventional ideas, medical anecdotes, and other informal types of information that may nonetheless provide useful insights.


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