Microglial Kinase Promotes DAM, Blocks Lysosomal Aβ Digestion
RIPK1 catapults microglia into an inflammatory frenzy, disrupting their lysosomal pathway and undermining Aβ clearance. A new drug target?
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ApoE4 Makes All Things Tau Worse, From Beginning to End
ApoE, especially E4, interacts directly and indirectly with tau. This worsens outcomes along the pathogenic process, from soluble tau to glial activation and brain atrophy. All without Aβ.
ApoE4 Traps Insulin Receptor Inside Neurons
In old and in diabetic mice, ApoE4 sequesters the insulin receptor in early endosomes of neurons, interrupting its signaling. This may help explain ApoE effects seen in intranasal insulin trials.
Tau Toxicity Blamed for Widespread Cell Death After Stroke
Young tau knockout mice maintain healthy brain tissue after ischemia, while older knockouts lose this stroke protection due to brain iron buildup.
Estimates of RNA Decay Hint at Destabilization in Alzheimer’s Brains
Using a new algorithm that measures mRNA decay rates more accurately than before, scientists claim that two RNA-binding proteins and four miRNAs determine the stability of mRNAs in the brain. Loss of RBFOX1 may destabilize synaptic protein mRNAs in Alzheimer’s disease.
PET Staging Charts Gradual Course of Amyloid Deposition in Alzheimer’s
The scheme catches earlier cases of Aβ accumulation than do global amyloid PET measures with binary positivity thresholds. And: the neuropathologists were right.
Inflammation in Midlife Portends Late-Life Brain Shrinkage
A 24-year prospective study links high levels of systemic inflammation markers in middle age to memory and loss of brain volume, including areas associated with Alzheimer’s disease.
Stress Granule Protein Stabilizes Tau Oligomers, Hastens Neurodegeneration
TIA1 bolsters tau toxicity, leading to synaptic malfunctions, cognitive impairment, and early death in transgenic animals.
BACE1 Conditional Knockouts Model Adult BACE Inhibition
Researchers claim that amyloid deposits completely vanish when BACE1 expression is gradually shut down in adult, plaque-ridden mice.
Aβ, Then Metabolism, Then Atrophy: In Familial AD, Cascade is Definitive
Longitudinal neuroimaging of DIAN participants reveals that in most regions of the brain affected by AD pathology, Aβ accumulates first, then metabolism slows, then the brain shrinks.
Wiping Out Microglia Prevents Neuritic Plaques
In transgenic mice, killing off microglia with the CSF1R inhibitor PLX3397 prevented accumulation of intraneuronal Aβ, neuritic plaques.
Does Daytime Drowsiness Foreshadow Aβ Accumulation?
Researchers report a link between sleepiness and accelerated Aβ buildup in the cingulate and precuneus of elderly adults without dementia.
CSF Markers of Neuronal Injury Drop When Dementia Arrives
What goes up can come down—rising tides of VILIP-1, neurogranin, and SNAP-25 ebb after onset of AD symptoms.
Does Amyloid Accumulate After a Single Sleepless Night?
Volunteers kept awake all night retained more florbetaben in their hippocampi and thalami in morning-after PET scan.
Stuck in the Past? Microglial Memories Dictate Response to Aβ
Systemic inflammation can alter the epigenome of microglia, dictating whether the cells clean up Aβ pathology, or exacerbate it.
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