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A CSF proteomics study in ADAD mutation carriers identified 137 potential markers. They span the AD continuum. For 12 of them, their concentrations change prior to those of classic AD biomarkers.
In a tau PET GWAS, a SNP linked to higher expression of the oxidizing enzyme was associated with more cortical tangles.
Plaques rev up neural oscillations, while tangles turn them down, ultimately leading to sluggish synapses. The slowdown foreshadows symptoms.
Transcriptomes of more than 400 postmortem brains reveal microglia and astrocyte subtypes that collaborate to precipitate pathologic changes.
XWAS from three research groups identified a dozen genetic loci that may help explain sex differences in AD.
Dynamic, lipid-rich inclusions of α-synuclein appear toxic, while stable, fibril-rich aggregates seem to protect neurons.
A new strategy, which marries nanobodies or misfolded tau to a ubiquitin ligase RING domain, tags tangles for disposal.
The consortium has cranked out dozens of mouse models of late-onset AD for the research community. Strains carry humanized Aβ and tau, and a growing list of risk variants.
A retrospective study finds that gut damage precedes Parkinson’s disease onset, independent of bacterial infection.
This super-sized isoform resists phosphorylation and aggregation, and occurs in cerebellum and brainstem, regions largely spared from tau pathology.
The indefatigable Colombian neurologist leaves behind a legacy of Alzheimer’s prevention research, which, at the time of his passing, stands on the cusp of success.
Kynurenine curbs lactate production in astrocytes, which then fail to nourish neurons. Shutting down kynurenine production rescued cognition in AD mouse models.
Pathways of autophagy, ubiquitination, endocytosis, and glycolysis changed in Alzheimer’s. Treatment with the drug atomoxetine normalized some of them.
The plasma concentration of some 300 proteins foretold dementia. Fewer than half of the proteins were connected to Alzheimer’s independently of ApoE.
How—or even if—a newly spotted AluYb8 element raises risk of neurodegenerative disease has become a question of intense interest. Centenarians, it seems, are spared.
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