From ApoE to Zzz’s—Does Sleep Quality Affect Dementia Risk?
Two studies strengthen the link between shut-eye and Alzheimer’s disease, and a mouse analysis of how the brain drains waste offers insight into the connection.
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Two studies strengthen the link between shut-eye and Alzheimer’s disease, and a mouse analysis of how the brain drains waste offers insight into the connection.
An astrocyte protein stymies toxic interplay between Aβ oligomers and prion proteins.
Among cognitively healthy older adults, the rate of change in cerebrospinal fluid biomarkers helps predict who will develop Alzheimer’s disease.
Silencing aberrant C9ORF72 mRNA helps normalize pathology in neurons, suggesting the transcripts are toxic to the cells.
The latest data on TREM2 confirm that a variant in the gene associates with AD, and link it to Parkinson’s, brain degeneration, and γ-secretase.
A cancer drug-turned-Alzheimer’s prospect now appears to have potential against a third disease, reportedly protecting animal models from Parkinson’s damage.
The receptor tyrosine kinase ErbB4 could be the latest gene for amyotrophic lateral sclerosis.
Functional neuroimaging scans can pick up stark neural abnormalities in football players with repeated head injuries before their cognition drops much in executive function tests.
As NIH researchers are preparing to return to their laboratories, Alzheimer's researchers warn about the greater consequences of cutting already limited resources.
Conventional wisdom says that excess excitation promotes degeneration of motor neurons in ALS, but a new study suggests excitability could be a good thing.
Clinical trials could prove the value of amyloid scans to health insurers.
An inhibitor of a cellular stress response prevents neurodegeneration in mice infected with prion protein, and might have potential in other neurodegenerative diseases.
A mouse study suggests it may be possible to co-opt the liver to boost expression of neurotrophins in the brain.
A new study proposes microtubule-chopping enzymes as the missing link in the cascade of pathology leading from Aβ to tau to neuronal death.
People who carry the Huntington’s gene develop progressively abnormal brain metabolism a decade or more before diagnosis.