Aβ Acts Through Pericytes to Throttle Brain Blood Flow
In response to the peptide, these little cells squeeze capillaries, constricting them. This may contribute to neuronal dysfunction.
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Cognitive Decline Trips Up API Trials of BACE Inhibitor
Co-sponsors Banner, Novartis, and Amgen announced that they will stop testing CNP520 in two Phase 2/3 studies in people at risk of AD. The drug worsened cognition.
New PET Staging Scheme for Amyloid?
Longitudinal data identifies four stages of amyloid plaque buildup, with the earliest deposits appearing in the precuneus and posterior cingulate.
Blood Pressure: How Low to Prevent Dementia—and When?
Hypertension in people as young as the mid-30s can predict late-life cerebrovascular disease and brain shrinkage. Intensive reduction of blood pressure can prevent the damage, but not when given in late life.
End of the BACE Inhibitors? Elenbecestat Trials Halted Amid Safety Concerns
Biogen and Eisai announced the discontinuation of the Phase 3 program. Elenbecestat was the only remaining BACE inhibitor being tested for AD.
Cell-Specific Enhancer Atlas Centers AD Risk in Microglia. Again.
Cataloguing enhancer-promoter interactions in the four major cell types of the brain, researchers found that Alzheimer’s risk variants predominantly appeared in microglial enhancers.
Single-Cell Expression Atlas Charts Changes in Alzheimer’s Entorhinal Cortex
Specific patterns of expression defined distinct subtypes of neurons, astrocytes, oligodendrocytes, and microglia in this early affected brain region.
To Monitor Neurons, Microglia Talk With the Boss, aka the Soma
Prior research has focused on microglia interacting with synapses. New data show they also deal directly with the neuronal cell body. Like little conference rooms, specialized junctions host this communication.
Picking Through the Rubble, Field Tries to Salvage BACE Inhibitors
At CTAD, researchers discussed possible paths forward. One option: exploring whether low doses prevent plaque accumulation while avoiding the cognitive side effects.
Does Tau Kill Neurons by Way of Necroptosis?
In Alzheimer’s brain, granulovacuolar bodies in neurons harbor activated necrosomes. They correlate with tau pathology and neuron loss, raising new questions about how neurons die in this disease.
Alzheimer’s Gene BIN1 Promotes Synaptic Transmission
In a conditional mouse knockout, lack of neuronal BIN1 slowed excitatory signaling, leading to spatial memory problems. Could this play a role in Alzheimer’s?
Mutations in Epigenetic Gene Linked to Neurodegeneration
Loss-of-function variants in the demethylase TET2 raise a person’s risk for early and late-onset Alzheimer’s, as well as FTD and ALS, suggesting a common mechanism.
GnomAD: Stunning Variation Seen in Largest Collection of Human Genomes
In seven papers, researchers presented a dazzling set of findings gleaned from 125,748 exomes and 15,708 genomes housed in a new database. Tidbits emerge on tau, LRRK2, and other proteins implicated in neurodegeneration.
Blood-Brain Barrier Surprise: Proteins Flood into Young Brain
As mice age, a busy receptor-mediated protein transport across the barrier wanes; inhibiting an alkaline phosphatase restores it. Meanwhile, the aging barrier becomes generally leaky to large molecules.
γ-Secretase Spotted Traveling Solo or in Pairs, Not in Big Groups
Behold single proteins on the move: Super-resolution microscopy of living cells suggests the infamous protease does not form complexes with other secretases in the plasma membrane—in mouse fibroblasts, that is.
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