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News reports of research into Alzheimer's disease Jan - June 2006

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There's a glossary of terms used in Alzheimer's research.

Disclaimer:
This section began as an offshoot of my gathering of news items about memory. I am not a medical expert. My background is in psychology. The information I have gathered here should not be taken as providing any advice.

May

Good physical function linked to Alzheimer's delay

A study following 2,288 older adults for six years found that those whose physical function was higher at the start of the study were three times less likely to develop dementia than were those whose physical function was lower.
The report appeared in the May 22 issue of Archives of Internal Medicine. Full reference
http://www.eurekalert.org/pub_releases/2006-05/ghcc-gpf051806.htm

Collaborative care has better outcomes for both patients and caregivers

An 18-month study involving 153 older adults with Alzheimer's disease and their caregivers has found that restructuring the primary care practice environment to emphasize a team approach to care significantly improved the quality of care and behavioral and psychological symptoms of dementia. Caregivers were also less stressed and less depressed.
The study was published in the May 10 issue of the Journal of the American Medical Association. Full reference
http://www.eurekalert.org/pub_releases/2006-05/iu-lai050406.htm

Link between size of hippocampus and progression to Alzheimer's

A study of 20 older adults with mild cognitive impairment has found that the hippocampus was smaller in those who developed into Alzheimer's during the 3 year period.
The research appeared in the May issue of the Archives of Neurology. Full reference
http://www.eurekalert.org/pub_releases/2006-05/uoc--rml050406.htm

Potential new treatment strategy for Alzheimer's

A study has identified several new compounds that could play a role in preventing or treating Alzheimer's disease and other degenerative conditions of the nervous system. In culture, these compounds bind with a receptor called p75NTR; a receptor that in the body binds neurotrophins. There is some evidence that in Alzheimer's, some of the neurons that die express the p75NTR binding site, indicating they may be dying because neurotrophins are binding to them. Because the new compounds bind with p75NTR in place of neurotrophins, they may provide a means of preventing damage that neurotrophins would otherwise be causing. The compounds were also found to inhibit the death of oligodendrocytes.
The study appeared in the May 17 issue of the Journal of Neuroscience. Full reference
http://www.eurekalert.org/pub_releases/2006-05/uoc--pnt051706.htm

Post-mortem brain studies reveal features of mild cognitive impairment

Autopsies have revealed that the brains of patients with mild cognitive impairment display pathologic features that appear to place them at an intermediate stage between normal aging and Alzheimer's disease. For instance, the patients had begun developing neurofibrillary tangles, but the number of plaques was similar to that in healthy patients. All patients with mild cognitive impairment had abnormalities in their temporal lobes, which likely caused their cognitive difficulties, and many also had abnormalities in other areas that did not relate to the features of Alzheimer's disease. In a second study, of 34 patients with mild cognitive impairment who had progressed to clinical dementia before their deaths, 24 were diagnosed (post-mortem) with Alzheimer’s, and 10 with other types of dementia. As in the other study, all patients had abnormalities in their temporal lobes.
The two studies appeared in the May issue of Archives of Neurology. Full reference 2nd
http://www.eurekalert.org/pub_releases/2006-05/jaaj-pbs050406.htm

Neurons can produce apolipoprotein E

Apolipoprotein E has been known to be synthesized in the brain in support cells such as astrocytes, microglia, and ependymal layer cells. Controversial for the last decade has been the question of whether or not neurons can produce apoE. Using a unique mouse model, researchers have now demonstrated that neurons can produce apoE, but only in response to injury to the brain.
The study was published in the May 10 issue of the Journal of Neuroscience. Full reference
http://www.eurekalert.org/pub_releases/2006-05/gi-gsp051006.htm

April

Social networks protect against Alzheimer's

Previous studies have found that older people with more extensive social networks are less likely to suffer cognitive impairment. Now a new study provides evidence that social networks, like education, offers a 'protective reserve' capacity that spares them the clinical manifestations of Alzheimer's disease. 89 elderly people without known dementia participating in the Rush Memory and Aging Project underwent annual clinical evaluation and cognitive tests. To determine social network, participants were asked about the number of children they have and see monthly; about the number of relatives, excluding spouse and children, and friends to whom they feel close and with whom they felt at ease and could talk to about private matters and could call upon for help, and how many of these people they see monthly. Their social network was the number of these individuals seen at least once per month. Brain autopsy was done at the time of death. It was found that, as the size of the social network increased, the same amount of Alzheimer’s pathology in the brain (i.e., extent of plaques and tangles) had less effect on cognitive test scores. In other words, for persons without much pathology, social network size had little effect on cognition. However, as the amount of pathology increased, the apparent protective effect on cognition also increased.
The study will be published in the May issue of The Lancet Neurology. Full reference
http://www.eurekalert.org/pub_releases/2006-04/rumc-snp042106.htm

Dietary supplements offer new hope for Alzheimer's patients

A "cocktail" of dietary supplements (omega-3 fatty acids, uridine and choline) has been found to dramatically increase the amount of membranes that form brain cell synapses in gerbils. The treatment is now in human clinical trials. It is hoped that such treatment may significantly delay Alzheimer's disease. The treatment offers a different approach from the traditional tactic of targeting amyloid plaques and tangles. Choline can be found in meats, nuts and eggs, and omega-3 fatty acids are found in a variety of sources, including fish, eggs, flaxseed and meat from grass-fed animals. Uridine, which is found in RNA and produced by the liver and kidney, is not obtained from the diet, although it is found in human breast milk.
The study appears in the May 9 issue of Brain Research. Full reference
http://www.eurekalert.org/pub_releases/2006-04/miot-mro042706.htm

New genetic cause of Alzheimer's disease

Amyloid protein originates when it is cut by enzymes from a larger precursor protein. In very rare cases, mutations appear in the amyloid precursor protein, causing it to change shape and be cut differently. The amyloid protein that is formed now has different characteristics, causing it to begin to stick together and precipitate as amyloid plaques. A genetic study of Alzheimer's patients younger than 70 has found genetic variations in the promoter that increases the gene expression and thus the formation of the amyloid precursor protein. The higher the expression (up to 150% as in Down syndrome), the younger the patient (starting between 50 and 60 years of age). Thus, the amount of amyloid precursor protein is a genetic risk factor for Alzheimer's disease.
The findings will appear in the June issue of The American Journal of Human Genetics. Full reference
http://www.eurekalert.org/pub_releases/2006-04/vfii-rda041906.htm

March

Protein identified as cause of memory loss

Researchers have identified a substance in the brain that is proven to cause memory loss, giving drug developers a target for creating drugs to treat memory loss in people with dementia. The substance is a form of the amyloid-beta protein that is distinct from plaques and has been given the name Ab*56. Ab*56 impairs memory independently of plaques or neuronal loss, and may contribute to cognitive deficits associated with Alzheimer's disease.
The research was published in the March 16 issue of Nature. Full reference
http://www.eurekalert.org/pub_releases/2006-03/uom-uom_1031306.htm
http://www.jhu.edu/news_info/news/home06/mar06/memory.html

Reduced insulin in the brain triggers Alzheimer's degeneration

By depleting insulin and its related proteins in the brain, researchers have replicated the progression of Alzheimer's disease – including plaque deposits, neurofibrillary tangles, impaired cognitive functioning, cell loss and overall brain deterioration – in an experimental animal model. Brain deterioration was not related to the pancreas, raising the possibility that Alzheimer's is a neuroendocrine disorder, or a Type 3 diabetes.
The study was published in the Journal of Alzheimer's Disease. Full reference
http://www.eurekalert.org/pub_releases/2006-03/l-rii031606.htm

Pin1 enzyme key in preventing onset of Alzheimer's disease

An enzyme called Pin1, previously shown to prevent the formation of the tangles characteristic of Alzheimer's brains, has now been shown to also play a pivotal role in guarding against the development of the plaques that are also characteristic of Alzheimer's. These findings establish a direct link between amyloid plaques and tau tangles, and provide further evidence that Pin1 (prolyl isomerase) is essential to protect individuals from age-related neurodegeneration.
The study appeared in the March 23 issue of Nature. Full reference
http://www.eurekalert.org/pub_releases/2006-03/hms-nrs032006.htm

February

Alzheimer's has higher genetic risk than thought

In a study far larger than any undertaken before, results suggest the highest estimates of the genetic risk of developing Alzheimer’s are in fact correct. The study involved all participants in the Swedish Twin Registry aged 65 or older in 1998 (nearly 12,000 of them) and found 392 pairs with evidence of Alzheimer's in at least one twin. In the model that best fit the data, genetic influence accounted for 79% of Alzheimer's risk, with 95% probability of being within the range 67 to 88%. The other 21% of Alzheimer's risk was due to non- shared environmental causes. Risk from shared environments was statistically negligible. Genetic risk for Alzheimer's was the same for men and women after controlling for age. The study raises doubts about the widely held view that Alzheimer's has two forms: the "familial," with genetic roots, and the "sporadic," with environmental causes. This doesn’t mean, however, that environment is unimportant.
The study appeared in the February 2006 issue of Archives of General Psychiatry. Full reference
http://www.eurekalert.org/pub_releases/2006-02/uosc-aft020206.htm

Alzheimer's progresses more rapidly in highly educated people

A study of 312 New Yorkers aged 65 and older, who were diagnosed with Alzheimer's disease and monitored for over 5 years, found that overall mental agility declined faster for each additional year of education, particularly in the speed of thought processes and memory, and was independent of age, mental ability at diagnosis, or other factors likely to affect brain function, such as depression and vascular disease. It’s suggested this may reflect the greater ability of brains with a higher cognitive reserve to tolerate damage, meaning the damage is greater by the time it becomes observable in behavior. The finding confirms earlier findings from some epidemiological studies.
The research appeared in the Journal of Neurology Neurosurgery and Psychiatry. Full reference
http://www.eurekalert.org/pub_releases/2006-02/bsj-adp021506.htm

Depression associated with changes in the brain in Alzheimer's

A lifetime history of depression is associated with increased plaques and tangles in the brains of those with Alzheimer's disease and more rapid cognitive decline, confirming previous indications that depression may be a risk factor for Alzheimer’s.
The study is published in the February issue of Archives of General Psychiatry. Full reference
http://www.eurekalert.org/pub_releases/2006-02/tmsh-ldb020306.htm

New drug reduces plaque and tangles in Alzheimer's mice

Alzheimer's mice that received a compound known as AF267B for eight weeks performed significantly better on a spatial memory test than untreated mice did. A different memory test that involved associating a place with a shock was not affected. The drug was found to reduce plaques and tangles in the hippocampus but not in the amygdala. AF267B seems to work in part by enhancing the activity of receptors for the neurotransmitter acetylcholine, and boosting the levels of an enzyme called alpha secretase, which blocks the production of beta-amyloid proteins. Suppressing the M1 receptors worsened the condition and performance of Alzheimer’s mice, confirming the important role of M1 receptors in modulating the plaques and tangles characteristic of Alzheimer’s.
The report appeared in the March 2 issue of Neuron. Full reference
http://www.sciam.com/article.cfm?chanID=sa003&articleID=000332CA-2F01-1405-AE5A83414B7F4945

Link between APOE and memory neurotransmitter

A new link in the complex chain of Alzheimer’s development has been found. It’s been found that receptors that bind apolipoprotein E (APOE) and those that bind glutamate are in fact connected, separated only by a small protein. It may be that inefficient or high levels of APOE are clogging these binding sites, preventing glutamate from activating the processes necessary to form memories. It may also be that the APOE4 variant — associated with Alzheimer's — is less efficient at removing lipid debris in the brain than is APOE2 or APOE3.
The study was published in the February 10 issue of the Journal of Biological Chemistry. Full reference
http://www.eurekalert.org/pub_releases/2006-02/gumc-nrr020906.htm

January

Use your brain, halve your risk of dementia

In the first comprehensive review of the research into 'cognitive reserve', which looks at the role of education, occupational complexity and mentally stimulating activities in preventing cognitive decline, researchers concluded that complex mental activity across people’s lives almost halves the risk of dementia. All the studies also agreed that it was never too late to build cognitive reserve. The review covered 29,000 individuals across 22 studies.
The paper was published online October 6 and will appear in a forthcoming issue of Psychological Medicine. Full reference
http://www.eurekalert.org/pub_releases/2006-01/uons-uyb012406.htm

Exercise protects against Alzheimer's

A study following 1,740 seniors (aged 65 and older) over a six-year period, found that those who exercised three or more times a week had a 30 — 40% lower risk for developing dementia compared with those who exercised fewer than three times per week. Even modest amounts, such as walking 15 minutes a day, appear beneficial, and the more frail the person was, the more they benefited from regular exercise.
The report appeared in the January 17 issue of Annals of Internal Medicine. Full reference
http://www.eurekalert.org/pub_releases/2006-01/ghcc-eil011006.htm

Blackcurrants may protect against Alzheimer's

A cultured cell study has found that compounds in blackcurrants strongly protect neuronal cells against the types of stress caused by dopamine and amyloid-b, a peptide associated with Alzheimer's disease. Blackcurrants and boysenberries contain anthocyanins. Those that are darker (like British blackcurrants) have more anthocyanins and are likely to be more potent. Compounds from these berries are already known to act as antioxidants, but a role in neuroprotection has not been demonstrated previously.
The paper was published online 23 January and will appear in a forthcoming issue of the Journal of the Science of Food and Agriculture. Full reference
http://www.eurekalert.org/pub_releases/2006-01/jws-bbb011906.htm

New compound stops brain cell degeneration in Alzheimer's disease

A new orally administered compound specifically targeted to suppress brain cell inflammation and neuron loss associated with Alzheimer's disease has been developed. The compound, MW01-5-188WH, is rapidly absorbed by the brain and is non-toxic. It selectively inhibits production of pro-inflammatory proteins called cytokines by glia, giving it relevance for several neurodegenerative disorders. The compound suppressed brain inflammation and neuron dysfunction in the hippocampus and protected against cognitive decline in genetically engineered mice. The compound also restored normal levels of markers of synaptic dysfunction in the hippocampus and attenuated Alzheimer's-like behavioral deficits. The compound represents a new approach to Alzheimer’s therapy.
The report appeared in the January 11 issue of the Journal of Neuroscience. Full reference
http://www.eurekalert.org/pub_releases/2006-01/nu-ncs011906.htm

Two pathways lead to Alzheimer's disease

Mild cognitive impairment (MCI), a transitional stage between normal cognition and Alzheimer's disease, has been categorized into two sub-types on the basis of differing symptoms. Those with the amnesic subtype (MCI-A) have memory impairments only, while those with the multiple cognitive domain subtype (MCI-MCD) have other types of mild impairments, such as in judgment or language, and mild or no memory loss. Both sub-types progress to Alzheimer's disease at the same rate. A new imaging technique has now revealed that these types do in fact have different pathologies. The hippocampus of patients with MCI-A was not significantly different from that of Alzheimer's patients (who show substantial shrinkage), but the hippocampus of those with MCI-MCD was not significantly different from that of the healthy controls.
The report appeared in the January issue of Archives of Neurology. Full reference
http://www.eurekalert.org/pub_releases/2006-01/uopm-tpf010606.htm

Key genetic risk for Alzheimer's linked to myelin breakdown

Myelin, the fatty insulation coating the brain's internal wiring, builds up in childhood, and breaks down as we age. Myelin is critical for speedy communication between neurons. A new study supports a growing body of evidence that myelin breakdown is a key contributor to the onset of Alzheimer disease later in life. Moreover, it has also revealed that the severity and rate of myelin breakdown in healthy older individuals is associated with ApoE status. Thus both age, the most important risk factor for Alzheimer disease, and ApoE status, the second-most important risk factor, seem to act through the process of myelin breakdown.
The findings are detailed in the January edition of Archives of General Psychiatry. Full reference
http://www.eurekalert.org/pub_releases/2006-01/uoc--isl122805.htm

Study links Alzheimer's and Down’s syndrome

New research suggests the cognitive problems observed in Alzheimer’s are related to defects in the machinery controlling neuronal connections — PAK enzyme signaling pathways. PAK (p21-activated kinase) enzymes form a family that includes two members (PAK1 and PAK3) that play critical roles in learning and memory. Humans with genetic loss of PAK3 have severe mental retardation. The study reveals that both PAK1 and PAK3 are abnormally distributed and reduced in Alzheimer patients, and that beta-amyloid was directly involved in PAK signaling deficits. The finding suggests therapies designed to address the PAK defect could treat cognitive problems in both patient populations.
The paper was published online January 15 in Nature Neuroscience. Full reference
http://www.eurekalert.org/pub_releases/2006-01/uoc--sid012506.htm

Study links Alzheimer's disease to abnormal cell division

Neurons affected by Alzheimer’s and many other neurodegenerative diseases often start to divide before they die. A new mouse study shows that this abnormal cell division starts long before amyloid plaques or other markers of the disease appear, suggesting a new approach to therapy for Alzheimer's. The findings also shed new light on the theory that the accumulation of amyloid beta in the brain causes the neuron death in Alzheimer’s, indicating that micro-molecular aggregates (tiny clumps made up of several amyloid beta molecules) rather than amyloid plaques may trigger the disease.
The report appeared in the January 18 issue of the Journal of Neuroscience. Full reference
http://www.eurekalert.org/pub_releases/2006-01/nion-sla011206.htm

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