Down Syndrome risk of Alzheimer’s connected to white matter integrity

Most of the (few) approved Alzheimer’s drugs are cholinesterase inhibitors — that is, they stop the breakdown of the neurotransmitter acetylcholine. A new study explains why they help. It appears they allow signals to enter the brain with more precision and less background noise.

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.

Because long-term cognitive decline can occur in some older adults after undergoing surgery, there has been some concern that exposure to anesthesia may be associated with increased dementia risk. It is therefore pleasing to report that data from the very large, long-running Mayo Clinic Study, the Rochester Epidemiology Project, has found that receiving general anesthesia for procedures after age 45 is not a risk factor for developing dementia.

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.

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).

We know that the E4 variant of the APOE gene greatly increases the risk of developing Alzheimer’s disease, but the reason is a little more mysterious. It has been thought that it makes it easier for amyloid plaques to form because it produces a protein that binds to amyloid beta. However, a new study shows that APOE and amyloid beta don’t bind together in cerebrospinal fluid and in fluids present outside cells grown in dishes, making it unlikely that they are binding together in the brain.

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).

Analysis of data from 418 older adults (70+) has found that carriers of the ‘Alzheimer’s gene’, APOEe4, were 58% more likely to develop mild cognitive impairment compared to non-carriers. However, ε4 carriers with MCI developed Alzheimer’s at the same rate as non-carriers. The finding turns prevailing thinking on its head: rather than the gene increasing the risk of developing Alzheimer’s, it appears that it increases the risk of MCI — and people with MCI are the main source of new Alzheimer’s diagnoses.

A study involving nearly 6,000 African American older adults has found those with a specific gene variant have almost double the risk of developing late-onset Alzheimer’s disease compared with African Americans who lack the variant. The size of the effect is comparable to that of the ‘Alzheimer’s gene’, APOE-e4.

The gene (ABCA7) is involved in the production of cholesterol and lipids. It also affects the transport of several important proteins, including amyloid precursor protein, which is involved in the production of amyloid-beta.

New findings support a mathematical model predicting that the slow, steady firing of neurons in the dorsolateral prefrontal cortex that maintains visual representations in working memory relies on a class of NMDA receptors known as NR2B receptors. Blocking these receptors abolished persistent firing among pyramidal Delay cells.