Reverse Electron Flow in Microglia Linked to Neuroinflammation
In a multiple sclerosis model, activated microglia reverse electron transport (RET) in their mitochondria, creating oxidative stress. Blocking RET eased pathology.
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In a multiple sclerosis model, activated microglia reverse electron transport (RET) in their mitochondria, creating oxidative stress. Blocking RET eased pathology.
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.
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.
One variant promotes expression of TMEM106b in a subset of excitatory neurons, reducing their numbers. Another boosts ApoE4 in microglia.
Researchers at AD/PD showcased progress in modeling these conditions, detecting CAA, and potentially mitigating microhemorrhages.
In peripheral macrophages and microglia, the receptor disrupts glucose metabolism. TREM1-deficient amyloidosis mice also had healthier neurons, better memories.
At AD/PD, scientists presented small molecules that break up fibrils and antibodies that target pathogenic forms of α-synuclein or hinder spread in iPSCs and mice.
New findings shed light on the intracellular processes that dictate tau seeding inside and between cells, and which forms are toxic to neurons.
An antibody against the inhibitory receptor LILRB4 prevented its binding to ApoE. The upshot? Microglia engulfed more Aβ fibrils and plaque load fell.
Reactive astrocytes spell trouble for synapses, while microglial transform from protective to destructive as disease progresses.
The addition of SUMO2 to tau prevents its phosphorylation and aggregation, preserving synapses and memory in tauopathy mouse models.
Two antibodies—one against the phosphoprotein, the other to tau’s N-terminus—restored proteostasis in the brain.
In a small sample set, phosphorylated α-synuclein was detected in the dermis of four such disorders.
Based on exploratory endpoints and post hoc analyses, TauRx claims HMTM benefits a subgroup of participants with MCI. Trialists are unconvinced.