Queen Sylvia of Sweden traveled to Gothenburg to welcome scientists to AD/PD. At the conference, the buzz was on about approaches to double levels of the lysosomal protein in FTD.
Biogen/IONIS’s tau ASO BIIB080 dropped participants’ tau PET signal below baseline in six months of treatment, according to data from a Phase 1 study presented at AD/PD.
Inclusions in tau seed sensor cells are made of amyloid fibrils, say scientists at AD/PD 2023. In those cells, and in human neurons, a dis-aggregase shreds them.
Perivascular macrophages both produce and react to the apolipoprotein, releasing toxic reactive oxygen species that constrict blood vessels.
Envelope proteins from endogenous retroviruses help shuttle tau seeds between cells. Could HERVs fuel tauopathies?
Clearance triggers improvement in downstream markers of inflammation and neurodegeneration—but not in those who started with high tangle burden. (Clue: women.)
At AD/PD, scientists showed 3- and 4-year amyloid immunotherapy data hinting at sustained cognitive benefits. The number of remaining participants is tiny.
At AD/PD, scientists placed more AD genes into microglial pathways, homed in on how TREM2 gets cleaved, debuted TREM2 agonists, and unearthed potential biomarkers.
Clusterin latches onto dimers of CD33 on the microglial cell surface, setting off inhibitory signaling that squelched phagocytosis.
The microglial receptor activates an antiviral signaling cascade. The virus downregulates TREM2 expression after infecting microglia.
Analysis of cerebrospinal fluid from the Parkinson’s Progression Markers Initiative identifies PD with high sensitivity and specificity.
Lilly’s Phase 3 antibody remternetug resembles donanemab, but without pesky antidrug antibodies; Prothena’s Phase 1 PRX012 may need fewer injections.
At AD/PD, scientists zeroed in on endolysosomal mechanisms in microglia that may contribute to neurodegenerative disease. Blending omics with cellular studies leads them from genes and function.
Scientists showed how pooling microglia from different donors, then putting them through cutting-edge analyses, can link genetic variation to functional change.
cGAS and STING initiate a type I interferon response, which weakens neurons’ resilience to tau pathology.
In Alzheimer’s, Parkinson’s, and Lewy body dementia, phospholipid and cholesterol homeostasis are disrupted early on. Scientists are bringing new methods to bear on the problem.
Data from TRIAD cohort cast activated microglia, egged on by ApoE4, as harbingers of tau pathology and neurodegeneration. Data from BioFinder hint that other microglia restrain these processes.
Scientists devised fresh approaches for curbing tau tangles that might better reach the protein inside cells, or target several pathologies at once.
While memory problems plague some people with lingering COVID symptoms, researchers do not yet understand what is going wrong in their brains.