Mouse Models and Markers for Cerebral Amyloid Angiopathy, ARIA
Researchers at AD/PD showcased progress in modeling these conditions, detecting CAA, and potentially mitigating microhemorrhages.
Researchers at AD/PD showcased progress in modeling these conditions, detecting CAA, and potentially mitigating microhemorrhages.
One variant promotes expression of TMEM106b in a subset of excitatory neurons, reducing their numbers. Another boosts ApoE4 in microglia.
Cerebrospinal fluid rides the pulses of cerebral arteries to enter the brain and spread into cortical tissue. This supports the existence of a human glymphatic system.
O-GlcNAcase inhibitors and a vaccine head to Phase 2. New antibody strategies co-opt the proteasome to clear intracellular and extracellular tau in preclinical models.
Based on exploratory endpoints and post hoc analyses, TauRx claims HMTM benefits a subgroup of participants with MCI. Trialists are unconvinced.
In peripheral macrophages and microglia, the receptor disrupts glucose metabolism. TREM1-deficient amyloidosis mice also had healthier neurons, better memories.
In a multiple sclerosis model, activated microglia reverse electron transport (RET) in their mitochondria, creating oxidative stress. Blocking RET eased pathology.
In a small dose-finding study, Roche’s new brain-shuttle-based anti-amyloid antibody mopped up nearly all plaques in three months, without triggering edema.
The existence of a glymphatic system in mice explains how CSF moves into brain tissue through perivascular spaces along arteries and drains out along veins. New MRI data indicated CSF traverses the human brain in the same way. Serial scans tracked a tracer as it hugged cerebral arteries in the subarachnoid space, then travelled along those deep in the cortex. It took some minutes for the tracer to then seep into adjacent brain parenchyma, suggesting a semi-permeable membrane around vessels that restricts CSF movement
The port city of Lisbon, the launch point of many a voyage of exploration, seemed a fitting site to host the 18th International Conference on Alzheimer’s and Parkinson’s Diseases and related neurological disorders. Disease-modifying therapies for amyloid plaques now approved, researchers are searching for similar treatments for tau, synuclein, and other potential drivers of neurodegeneration. With more than 4,700 attendees navigating 600+ presentations during five days, often spread across six parallel sessions, the conference was bustling, yet imbued with a sense of discovery. Speakers discussed new small-molecule and antibody therapies, combination approaches, new plasma biomarkers for tau and TDP43, and a good smattering of basic biology, from cellular resilience to microglial diversity. Follow along with Alzforum’s conference coverage.
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