Getting Under Your Skin: Does Vitiligo Elevate Dementia Risk?
In a retrospective study, people with vitiligo had 12 times the risk of developing Alzheimer’s disease than did healthy controls. Why is that?
206 RESULTS
Sort By:
In a retrospective study, people with vitiligo had 12 times the risk of developing Alzheimer’s disease than did healthy controls. Why is that?
By pinpointing where tau pathology starts in a person’s brain, researchers better predicted future spread and determined small changes in tangle load.
Amyloids of AIMP2 found in Parkinson’s disease may seed α-synuclein aggregation.
Among a growing number of blood-based tauopathy markers, this new immunoassay may offer a way to catch preclinical disease just before symptoms show up.
In mice, forebrain neurons with hobbled retromers ooze fragments of tau and several BACE1 substrates into the CSF. Similar proteins are up in CSF from people with MCI and Alzheimer’s disease.
This astrocytic glycoprotein greases glial phagocytosis and reduces plaque burden in mice. The circadian clock protein Bmal1 suppresses it.
Breaking familiar gene-disease patterns, HTT trinucleotide expansions lead to huntingtin aggregates in prefrontal cortex. Noncoding caveolin 1 variants suppress its expression.
This pathway may transmogrify microglia during neurodegeneration, without the help of TREM2.
In people with Alzheimer’s biomarkers, the basal forebrain shrinks early, foreshadowing microglial neurotoxicity, atrophy in the medial temporal lobe, and cognitive decline.
Alector’s AL002c antibody mobilizes microglia, reduces neuronal dystrophy, and restores normal behavior—all in mice. The clinical version is in Phase 1.
The transcription factor NFATc2 mediates this response.
When observed over an eight-year period, people with the highest plasma concentrations were more likely to die than people with lower levels.
Aberrant protein-protein interactions centered on HSP90 may contribute to Alzheimer’s disease. Can an inhibitor set things right?
Frequent heading weakened verbal memory in amateur soccer players, and more so in ApoE4 carriers.
Poor lysosomal function in dopaminergic neurons derived from people with YOPD points to disease origin and potential therapies.