In ALS and FTD, Two Different Routes to TDP-43 Aggregation
A C9ORF72 polydipeptide repeat induces aggregation by direct interaction with TDP-43, while progranulin mutations that trigger microglial toxicity cause TDP-43 to accumulate via complement.
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Herpes Viruses and Alzheimer’s—The Debate Continues
New study finds no uptick in herpes viruses in AD. If herpes plays a role, it says, then probably it acts as an early trigger of pathology.
Scientists Discover a Common Distress Signal in the Blood-Brain Barrier
The same endothelial cell response is found in various models of brain disease.
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.
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.
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.
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.
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.
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.
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?
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.
“Runner Plasma” Jogs Neurogenesis, Quells Neuroinflammation in Mice
Sedentary mice infused with the plasma of active ones had more newborn neurons in the brain and less neuroinflammation. Exercising upped plasma clusterin in mice and in humans.
Frontal Metabolic Patterns Mark Behavioral Subtype of AD
Hypometabolism in the frontal cortex and in the anterior default mode network distinguish the behavioral variant of AD from typical AD.
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