News reports of research into Alzheimer's disease July - December 2003

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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.

December

Low blood pressure risk factor for Alzheimer's

A long-term study of 488 adults over 75 (the Bronx Aging Study) found that 122 participants developed dementia (65 Alzheimer’s, 28 vascular dementia,29 other), and that the relative risk of dementia increased as a function of decreases in blood pressure (diastolic and mean arterial). Low diastolic BP significantly increased the risk of developing Alzheimer’s, but not vascular dementia. Those with mildly to moderately raised systolic BP had a reduced risk of developing Alzheimer’s. The risk of developing dementia was higher in those who had persistently low BP over 2 years.
The report appeared in the December 23 issue of Neurology. Full reference

Distress-prone people more likely to develop Alzheimer's disease

The Religious Orders Study has found that those who most often experience negative emotions like depression and anxiety were twice as likely to develop Alzheimer's disease as those who were least prone to experience negative emotions. A person’s tendency to experience psychological distress has been shown to be a stable personality trait throughout adulthood. Proneness to stress was specifically associated with a decline in episodic memory (measured by asking participants to recall a list of words or a story) — an area particularly problematic for those with Alzheimer's. Episodic memory ability declined 10 times faster in those high in proneness to distress than in those low in this response. This result was not altered when participants’ engagement in cognitively stimulating activities. Examination of the brains of those who have died during the long-term study appears to rule out the possibility that proneness to distress is an early sign of Alzheimer's disease rather than a risk factor, although more research is needed to confirm this.
The study was published in the December 9 issue of Neurology. Full reference
http://www.eurekalert.org/pub_releases/2003-12/aaon-pm120203.htm

Late-life Alzheimer's begins in midlife

A new model of human brain aging identifies midlife breakdown of myelin, a fatty insulation with very high cholesterol content that wraps tightly around axons (part of the neurons) and enables messages to pass along the “wiring” of the brain speedily, as a possible key to the onset of Alzheimer's disease later in life. Imaging studies and examination of brain tissue shows that the brain's wiring develops until middle age and then begins to decline as the breakdown of myelin triggers a destructive domino affect. It is suggested that genetic factors coupled with the brain's own developmental process of increasing cholesterol and iron levels in middle age help degrade the myelin. The complex connections that take the longest to develop and allow humans to think at their highest level are among the first to deteriorate as the brain's myelin breaks down in reverse order of development. The model suggests that the best time to address the inevitability of myelin breakdown is when it begins, in middle age. Possible preventive therapies include cholesterol- and iron-lowering medications, anti-inflammatory medications, diet and exercise programs and possibly hormone replacement therapy designed to prevent menopause rather than simply ease the symptoms. Education and cognitively stimulating activities may also stimulate the production of myelin.
The report was published in the January edition of Neurobiology of Aging. Full reference
http://www.eurekalert.org/pub_releases/2003-12/uoc--mbc122303.htm

Hippocampal damage seen in those with alcoholic memory disorder and those with Alzheimer's

A comparison between the brains of five men with alcoholic Korsakoff's syndrome and the brains of men with Alzheimer's disease as well as the brains of healthy men, found that the brains of all Korsakoff's patients and Alzheimer's patients were comparable in significant volume loss in the hippocampus. Greater hippocampal damage (for Korsakoff's patients) and smaller hippocampal size (for Alzheimer’s) was correlated with poorer memory performance. It is suggested that, although there are of course a number of differences between these disorders, the nature of the memory impairment may be the same. Awareness of the similarities may help detection of both disorders.
The study was published in the December 23 issue of Neurology. Full reference
http://www.eurekalert.org/pub_releases/2003-12/aaon-seu121503.htm

Clioquinol slowed progression of cognitive decline in Alzheimer's patients

A new clinical trial has found that the drug Clioquinol slowed the progression of cognitive decline in a group of 36 patients with moderate to severe Alzheimer’s, over a period of 24 weeks. PBT-1 (Clioquinol) is a chemical that binds zinc and copper, and has been shown to lower the levels of beta-amyloid and the associated toxicity in the brains of transgenic mice used as a model of Alzheimer's disease.
The trial was reported in the December 15 issue of the Archives of Neurology. Full reference
http://www.eurekalert.org/pub_releases/2003-12/aaft-cto121503.htm

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November 2003

Dietary supplement helps Alzheimer’s

A three-month study of 55 elderly patients with mild or moderate Alzheimer’s found that those given EV-1, a dietary supplement containing, among other things, the putative antioxidant ingredient of red wine, showed no deterioration during the trial. The supplement is designed to interfere with a defective mitochondrial cycle thought to contribute to the metabolic disturbances associated with late onset Alzheimer’s. The Krebs tricarboxylic acid cycle is fuelled by glucose and regulates levels of reactive oxygen species in the body. EV-1 contains glucose, a compound called malate that primes or maintains the Krebs cycle, and resveratrol - the antioxidant component of red wine that is thought to soak up reactive oxygen species. More studies are needed to confirm this result.
The findings were presented in November at the annual meeting of the Society for Neuroscience (SFN) in New Orleans.
http://gateways.bmn.com/news/story?day=031121&story=1

Program helps physical and behavioral well-being of Alzheimer's patients

A controlled trial of 153 community-dwelling patients diagnosed with Alzheimer’s examined the effectiveness of a home-based exercise program combined with caregiver training in behavioral management techniques in reducing functional dependence and delay institutionalization. The program resulted in improved physical health and less depression. Specifically, after three months, those receiving the training were more likely to exercise at least 60 minutes a week, to have fewer days of restricted activity, to have improved scores for physical role functioning, and improved Cornell Depression Scale for Depression in Dementia scores, and have less institutionalization due to behavioral disturbance.
The study was reported in the Journal of the American Medical Association. Full reference

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October 2003

Conflicting results about benefit of anti-inflammatory drugs

It’s long been known that patients regularly taking nonsteroidal anti-inflammatory drugs, such as ibuprofen and naproxen, seem to have less risk of developing Alzheimer's. It’s been suggested that this might mean that Alzheimer's is a product of inflammation in the brain, and that damage happens when the microglia, the brain's immune cells, become overactive and attack healthy neurons. A new study of autopsy brain tissue, and of in vitro rat cultures indicates that, on the contrary, what’s happening is that, as microglia age, they lose their ability to protect the brain. Moreover, the latest study into the effects of anti-inflammatory drugs found no benefit for those suffering from Alzheimer’s. Indeed, it is possible that such drugs might exacerbate the problem. It is speculated that microglia may have the potential to both protect and attack neurons. The key may lie in the way microglia interact with beta-amyloid protein.
http://www.sciam.com/article.cfm?chanID=sa004&articleID=00079718-699A-1F98-A99A83414B7F0103

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September 2003

Brief telephone questionnaire screens for early signs of dementia

Researchers have developed a brief telephonic questionnaire that helps distinguish between persons with early signs of dementia and persons with normal cognitive function. The questionnaire provides a way to reach out to persons with dementia whose impairment otherwise may go undetected until substantial cognitive deterioration has occurred. The questionnaire consists of a test of delayed recall and 2 questions that ask whether the person needs help with remembering to take medications or with planning a trip for errands. It is estimated that of 100 people who score positive on this test, 42 will actually have cognitive impairment. In other words, this does not provide a diagnosis of Alzheimer’s, but provides evidence that further evaluation is required. The rate of false positives compares favorably to other types of screening tests. A further study is underway to confirm the validity and reliability of the test.
The report was published in the August issue of the Journal of Clinical Outcomes Management. Full reference
http://www.eurekalert.org/pub_releases/2003-09/twc-btq091603.htm

Cancer drug may help against Alzheimer's too

The drug Gleevec, approved for treatment of chronic myelogenous leukemia (CML) over two years ago, has been found to reduce the level of beta-amyloid in immature rat neurons and cultured human cells. The drug also significantly reduced the levels of amyloid peptides in live guinea pigs (who have amyloid peptides comparable to those found in humans). While still preliminary, the work may indicate a new approach to treating Alzheimer’s.
The report was published in the Proceedings of the National Academy of Sciences. Full reference
http://www.sciam.com/article.cfm?chanID=sa003&articleID=00014A83-AC91-1F78-AC9183414B7F0000

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August 2003

New toxic protein found

New research has found up to 70 times more small, soluble aggregated proteins called "amyloid b-derived diffusible ligands" (ADDLs) in the brain tissue of individuals with Alzheimer's disease compared to that of normal individuals. This supports a recent theory in which ADDLs accumulate at the beginning of Alzheimer's disease and block memory function by a process predicted to be reversible. ADDLs have the ability to attack the memory-building activity of synapses, points of communication where neurons exchange information, without killing neurons. While both are a form of amyloid beta, ADDLs differ significantly from the amyloid fibrils (plaques) that are diagnostic of Alzheimer's. ADDLs are much, much smaller than fibrils. Unlike fibrils, ADDLs are soluble and diffuse between brain cells until they find vulnerable synapses. The discovery of ADDLs may help explain the poor correlation between plaques and neurological deficits.
The findings were published online by the Proceedings of the National Academy of Sciences during the week of August 18. Full reference
http://www.eurekalert.org/pub_releases/2003-08/nu-tpc081803.htm

Anti-inflammatories lower Alzheimer disease–related protein levels in mice

Following earlier research showing three commonly used nonsteroidal anti-inflammatory drugs (NSAIDs) were capable of selectively lowering the levels of Abeta42 (an isoform of the amyloid beta protein) in mice, investigation of 20 commonly used NSAIDs found 8 FDA-approved drugs successfully lowered Abeta42 levels in mice at doses achievable in humans.
The report was published in the August 1 issue of the Journal of Clinical Investigation. Full reference
http://www.eurekalert.org/pub_releases/2003-08/joci-fds072503.htm

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July 2003

Higher education or larger brain size may protect against dementia

More findings from the Nun Study, a longitudinal study of aging and Alzheimer's disease. It was found that nuns who completed 16 or more years of formal education or whose head circumference was in the upper two-thirds were four times less likely to be demented than those with both smaller head circumferences and lower education. (Head circumference is a good indicator of the volume or size of the brain.) It was not that these nuns were less likely to have the brain abnormalities characteristic of Alzheimer's disease, but that the larger brain size and more education provided extra reserve, allowing them to function normally in the presence of such brain abnormalities.
The study was published in the June issue of the Journal of Clinical and Experimental Neuropsychology. Full reference
http://www.eurekalert.org/pub_releases/2003-07/uosf-heo071003.htm

Anti-inflammatories offer some protection against developing Alzheimer's

A review of 9 observational studies that examined the role of NSAID use in preventing Alzheimer's disease found the pooled relative risk of Alzheimer's disease among users of NSAIDs was 0.72. Therisk was 0.95 among short term users (< 1 month), 0.83 among intermediate term (mostly < 24 months) and 0.27 for long term (mostly> 24 months) users. The pooled relative risk in 8 studies of aspirin use was 0.87. It was concluded that NSAIDs offer some protection against the development of Alzheimer's disease.
The report appeared in the July 19 issue of the British Medical Journal. Full reference

Imaging techniques help distinguish between Alzheimer's and vascular dementia

A combination of magnetic resonance imaging (MRI) and MR spectroscopy has enabled researchers to differentiate between Alzheimer’s and dementia caused by poor blood flow (vascular dementia). Comparison of the brains of those with Alzheimer’s, those who had suffered subcortical ischemic vascular dementia (SIVD), and those belonging to cognitively normal older adults, also found significant differences in the chemical signature of various brain regions, leading researchers to suggest that in patients with SIVD, there may only be neuronal dysfunction rather than neuronal loss, offering hope for recovery of neuronal function in these areas. More research is needed to confirm these results.
The study appeared in the August 12 issue of Neurology. Full reference

High cholesterol risk factor for the development of Alzheimer-related amyloid deposits

A review of autopsy cases of patients over 40 years old found that high blood cholesterol levels were correlated with the presence of amyloid deposits in the brain in the youngest subjects (aged 40-55).
The report appeared in the July 22 issue of Neurology. Full reference

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