Older people who complain of memory problems are more likely to become measurably impaired and to have Alzheimer’s pathology in the brain, especially if they smoke or carry an ApoE4 allele.
Protein oligomers may be to blame in TDP-43 proteinopathies, as in other neurodegenerative conditions.
Researchers have partnered with Google-funded Calico Life Sciences to develop a molecule that protects neurons in a variety of conditions.
Starved for a protein that regulates lipids, neurons suffer and Aβ production soars, according to a new study.
In narrower claim, the drug is said to promote ApoE lipidation only in brain regions with extensive amyloid in mice carrying human ApoE4.
Data suggest Aβ-dependent and –independent pathways combine forces to compromise cognition in otherwise healthy people.
Neural circuits in the hippocampus defy current views about its structure and function.
Brain extracts from AD patients, but not their cerebrospinal fluid, contain exceedingly potent Aβ seeds that survive formaldehyde treatment. The findings further implicate Aβ in prion-like pathology.
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.