An expanded set of CSF biomarkers exposed tight connections between p-tau, synaptic dysfunction, and neuroinflammation in people with brain amyloid.
This past year, therapeutic antibodies massively reduced brain amyloid, blood tests came into their own, and systems-based approaches transformed the study of gene expression, glial cells, and selective vulnerability.
Positive allosteric modulators improve learning and memory in mouse models of AD and epilepsy.
In early Alzheimer’s disease, the pattern of tau deposition also strongly predicts areas destined for subsequent degeneration.
New potential immunotherapies and insight into single-cell responses were highlights of a small meeting in Denmark.
These oily microglia resemble the foamy macrophages seen in atherosclerotic plaques. They correlate with aging, inflammation, and neurodegenerative disease.
Aberrant protein-protein interactions centered on HSP90 may contribute to Alzheimer’s disease. Can an inhibitor set things right?
Frequent heading weakened verbal memory in amateur soccer players, and more so in ApoE4 carriers.
Poor lysosomal function in dopaminergic neurons derived from people with YOPD points to disease origin and potential therapies.
Data from different next-generation tracers look similar. It shows spreading plaques kick off tangles by Braak region; memory starts slipping later.
ApoE2 homozygotes have a dramatically lower risk of AD than even the previously known low-risk E2/3 heterozygotes. More study of this protective allele could reveal roots of resilience.
The DIAN Trials Unit is nearing the end of its first two secondary prevention trials. It has begun a cognitive run-in period for its next trial, of a tau-based drug, and for a primary prevention study in people as young as 18.
Synapse loss and mitochondrial stress, as seen by separate PET tracers, go hand-in-hand in Alzheimer’s, Parkinson’s, and frontotemporal dementia.
FDA approves adding safety and efficacy data from an Alzheimer’s trial to the drug’s label.
The creation of long-term memories requires a continual supply of myelin provided by newly formed oligodendrocytes. Alas, the generation of fresh oligodendrocytes diminishes with age, along with memory.