A new study shows that a combination of inflammation and hypoxia activates microglia in a way that persistently weakens the connection between neurons, contributing to brain damage in conditions such as stroke and Alzheimer's disease.
http://www.eurekalert.org/pub_releases/2014-03/uobc-scb031214.php
Brain scans of 10 persons with Down syndrome but no dementia, 10 persons with Down syndrome and dementia, and 10 healthy controls, have revealed a linear correlation between cognitive ability and compromised white matter connections in the frontal lobes among those with Down syndrome. Those with higher cognitive ability and motor skill coordination had healthier white matter integrity, and those with additional dementia showed the most deterioration.
Adults with Down Syndrome are known to be at high risk of developing Alzheimer’s after age 40.
A new function has been found for the amyloid precursor protein (APP), which may help explain how it goes awry in Alzheimer's disease. It appears that APP (which is involved in the creation of amyloid-beta), also helps control the growth and maturation of newborn brain cells, by regulating a specific microRNA (microRNA-574-5p) that normally promotes neurogenesis.
http://www.eurekalert.org/pub_releases/2014-04/s-nrd041814.php
New research helps explain the role of amyloid-beta plaques in the development of Alzheimer's, by finding that the prion protein known to bind strongly to small aggregates of amyloid-beta peptides, also attaches to large fibrillar clumps of amyloid-beta. However, it doesn’t break them down into smaller, more harmful pieces, as has been suggested. This suggests that prion-protein-based compounds might be a useful means of treatment, to stop these smaller pieces from forming.
Creating amyloid-beta requires the convergence of a protein called amyloid precursor protein (APP) and an enzyme that cleaves APP into smaller toxic fragments (beta-secretase or BACE). Both APP and BACE are common in the brain, so why don’t we all get Alzheimer’s?
A study involving 74 older adults (70+), of whom 3 had mild dementia, 33 were cognitively normal and 38 had mild cognitive impairment, has found that high levels of "good" cholesterol and low levels of "bad" cholesterol correlated with lower levels of the amyloid-beta plaques in the brain (a hallmark of Alzheimer's disease).
http://www.eurekalert.org/pub_releases/2013-12/uoc--hga122613.php
A new study adds to growing evidence of a link between sleep problems and Alzheimer’s. The interesting thing is that this association – between sleep apnea and Alzheimer’s biomarkers — wasn’t revealed until the data was separated out according to BMI.
Last year, a cancer drug, Bexarotene, was touted as a potential treatment for Alzheimer’s disease. However, four independent studies have now failed to replicate the most dramatic result of the original study: a claim that the drug could clear half the amyloid plaques in a mere 72 hours.
Still, two of the studies confirmed findings that the drug reduced levels of amyloid-beta, and one showed improved cognition in mice.
The inconsistencies suggest more research is needed. The drug is now being tested in humans.
I’ve been happily generous with cinnamon on my breakfast ever since the first hints came out that cinnamon might help protect against Alzheimer’s (it’s not like it’s an ordeal to add cinnamon!). Now a new study has revealed why. Two compounds found in cinnamon —cinnamaldehyde and epicatechin —appear to help prevent tau tangles (one of the characteristics of Alzheimer’s).
Late-life depression is associated with an increased risk for all-cause dementia, Alzheimer’s disease, and, most predominantly, vascular dementia, a new study shows.
A new meta-analysis extends previous research showing a link between depression and Alzheimer’s disease to late-life depression and dementia. The analysis of 23 studies concluded that those with late-life depression were significantly more likely to develop dementia (1.85 times more likely), and that the risk of developing vascular dementia was significantly greater than that of developing Alzheimer’s (2.52 vs 1.65).