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By tracing the transcriptomes of neurons that wither early and late in the course of Alzheimer’s disease, researchers peg subpopulations of excitatory neurons in entorhinal cortex as selectively vulnerable to tau. Reactive astrocytes aid and abet.
The blood-based marker may be far more scalable and cost-effective for tracking the disease than PET imaging and CSF biomarkers.
In cultured cells, lysosomal activity was necessary to enable tau seeds to break out of internalized exosomes and trigger the aggregation of tau in the cytosol.
High amyloid burden and neuroinflammation, neuronal excitability, and tangles and oligodendrocyte loss distinguish the disease types.
Among people with early AD, the monoclonal antibody wiped out Aβ plaques and slowed cognitive and functional decline by a third, relative to placebo.
Overexpressing the endosomal activator in neurons not only caused those organelles to swell, but also bungled synaptic transmission, goaded hyperphosphorylation of tau, and destroyed cholinergic neurons.
This pathway may transmogrify microglia during neurodegeneration, without the help of TREM2.
Confronting unprecedented challenges this past year, scientists found ways to tide their research over and keep clinical trials mostly on track.
In both mice and (wo)men, the sex difference comes down to an Aβ-glutamate receptor-prion protein troika.
Researchers identified genetic variants that may explain why some ApoE4 carriers remain free of Alzheimer’s, while some ApoE2 carriers do not.
Breaking familiar gene-disease patterns, HTT trinucleotide expansions lead to huntingtin aggregates in prefrontal cortex. Noncoding caveolin 1 variants suppress its expression.
This astrocytic glycoprotein greases glial phagocytosis and reduces plaque burden in mice. The circadian clock protein Bmal1 suppresses it.
Neurons take up extracellular vesicles containing tau oligomers more readily than they do free tau. Some gift: This speeds the march of tauopathy through mouse brain.
Topline results suggested that the anti-inflammatory treatment stabilized cognition and function over six months. The trial did not include biomarkers.
The brain shrinkage due to verubecestat emerged quickly but did not worsen or cause neurodegeneration. Curiously, both verubecestat and lanabecestat dulled episodic memory and boosted verbal fluency.
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