More than half of dementia patients near the end of life receive medications that may not help them, according to an analysis of U.S. nursing home data.
Scientists report a case of identical twins with the C9ORF72 DNA expansion—only one has ALS.
Controlling diabetes and hypertension and stopping smoking can slash dementia risk.
Overzealous neural responses may protect some amyloid-bearers from slipping into cognitive decline, a study suggests.
Prescribed to treat anxiety and insomnia, benzodiazepines may do more than put the mind at ease. A new study links their prolonged use to increased Alzheimer’s risk.
Expansions in ataxin 2 predispose people to the ALS end of the ALS-FTD spectrum, and never cause pure FTD, according to a new French study.
When strict quality control standards are followed, low Aβ in cerebrospinal fluid accurately predicts amyloid plaques in people with cognitive impairment in clinical practice.
A new drug combination is better than standard therapy for congestive heart failure. It includes an inhibitor of neprilysin, a protease that digests Aβ in the brain.
Don’t miss out on the 12th International Conference on Alzheimer’s and Parkinson’s diseases and related disorders, to be held next March 18–22 in Nice, France. Abstracts for the biennial meeting must be received by Wednesday, October 1. Find further details and instructions for submitting abstracts at the conference website.
Nursing home patients in the latest stages of dementia typically take between five and 15 medications daily, which can lead to uncomfortable side effects. Are all those pills really necessary? A new analysis suggests not. It reports that more than half of these patients take at least one medication listed as having questionable benefit. The finding has stirred some controversy among clinicians, who object to the inclusion of the AD drugs memantine and donepezil on that list.
Identical twins carrying the same genetic risk factor for amyotrophic lateral sclerosis present an interesting case for scientists. One has ALS, while the other may be showing early signs of frontotemporal dementia. These twins emphasize the effect that environmental influences may have on genetic disease.
Why do some people with amyloid plaques descend into dementia, whereas others remain sharp? According to a new study, cognitively normal people with brain amyloid may keep their mind functioning by ramping up neural activation in task-driven regions of the brain. That neural feat is well documented, but researchers were uncertain if it helps, hurts, or does nothing. Now, researchers report that, at least in the short run, this hyperactivation helps people form richer, more detailed memories. Whether it harms the brain in the long run is an open question.
- Gunnar Gouras on Differential Release of β-Amyloid from Dendrite- Versus Axon-Targeted APP.
- Bengt Winblad on Benzodiazepine use and risk of Alzheimer's disease: case-control study.
- Rebecca Gottesman on Angiotensin-neprilysin inhibition versus enalapril in heart failure.
- Nikolaos K. Robakis on Evidence for lymphatic Aβ clearance in Alzheimer's transgenic mice.
- Thomas Wisniewski on Evidence for lymphatic Aβ clearance in Alzheimer's transgenic mice.
- Xinglong Wang on Mislocalized Mitochondria Sufficient for Motor Neuron Malaise
- Carlos Cruchaga on Genetic variability in the regulation of gene expression in ten regions of the human brain.