Aggregates of TDP-43 in Muscle—Potential ALS Marker?
TDP-43 inclusions in intramuscular nerve bundles, paired with clinical criteria, may enable diagnoses at early stages of ALS.
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TDP-43 inclusions in intramuscular nerve bundles, paired with clinical criteria, may enable diagnoses at early stages of ALS.
A provocative new study suggests that unlike in mice, TSPO in people does not rise with microglial activation; instead, a higher PET signal reflects more microglia.
The first FDA approval of a CSF test, and increased options for plasma testing, will give patients easier access to these diagnostic aids. Will physicians interpret them properly?
Using a sensitive tau-PET tracer, researchers tied neuroimaging, CSF biomarkers, and cognitive symptoms to the progression of tau pathology in AD.
The guidance may help sponsors increase racial diversity in clinical trials. Studies in U.S. veterans and other cohorts show differences in incidence, and in blood levels of tau by race.
Low levels of Aβ37, 38, 40 reflect low processive activity of γ-secretase. They track with age at onset in people with autosomal-dominant mutations, and may track with cognitive decline in sporadic AD.
At AD/PD, some speakers sought to bolster the argument that amyloid removal slows cognitive decline, while others identified what type of patient is most likely to benefit.
At AD/PD, researchers presented pharmacologic analyses that could help predict antibody effects and select the right dosage to keep plaques at bay.
In familial AD, the faster sTREM2 rises in a person's cerebrospinal fluid, the slower his or her amyloid grows, cortex thins, and cognition fades.
In some people who had weathered COVID at home, olfactory regions in the brain shrank and executive function slowed. Will these changes resolve or persist?
CSF Aβ and tau are abnormal in older people with psychiatric problems. Are these symptoms an effect of AD pathogenesis, or risk factors for it?
A person's burden and spatial distribution of plaques, as measured by PiB-PET, varied greatly depending on his or her mutation. Their CSF Aβ42 or cognitive decline did not.
APP or presenilin mutation carriers who also carried the Met66 allele had more p-tau217 at presymptomatic stages, and more p-tau205 at symptomatic stages, than did Val carriers.
Among 39 sets of identical twins, tau tangles accumulated in a strikingly similar pattern within each pair. A pair's discordance was due to Aβ and factors such as exercise.
Alzforum editors review the highlights of last year’s clinical and research developments.