DIAN Longitudinal Data Surprises With Late Drop in Tau
The first longitudinal data from DIAN conflict with some cross-sectional findings, revealing a small drop in CSF injury markers after the first appearance of symptoms of disease.
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The first longitudinal data from DIAN conflict with some cross-sectional findings, revealing a small drop in CSF injury markers after the first appearance of symptoms of disease.
AstraZeneca’s BACE inhibitor AZD3293 moves forward to a Phase 2/3 trial, joining Merck’s MK-8931 as the most advanced current compounds in this class.
Superficial siderosis, a leakage of blood matter onto the outer surface of the cerebral cortex, may be linked to AD and other dementias.
In Fragile X syndrome, mRNA from the mutant FMR1 gene binds to its own DNA to suppress protein expression. Could the same thing happen in other repeat expansion diseases?
Neurons in mice spit out monomeric tau when electrically stimulated, hinting that neural activity may help drive the spread of pathological forms of tau in the brain.
A new initiative in the U.K. will fund research into potential treatments for dementia and neurodegeneration.
Detecting oligomers in the cerebrospinal fluid is no easy feat. The latest test is among the most sensitive yet, but is it useful?
Researchers have identified the striatum as a site of neurogenesis in the adult brain, but not in people with Huntington’s disease.
The FDA has stopped the personal genome sequencing company 23andMe from selling health assessments, saying its tests need validation. What do Alzheimer scientists think?
The antidepressant citalopram reduces agitation in Alzheimer’s patients, but caused abnormal heart rhythms at the tested dose.
A Phase 2 trial suggests that the drug PBT2 is generally safe for Huntington’s patients. The drug's sponsor says it may have improved cognition, though experts remain unconvinced.
Already linked to Alzheimer’s and other neurodegenerative diseases, a TREM2 variant now shows up on the ALS radar, too.
Mutant FUS meddles with RNA splicing and DNA damage repair in transgenic mice that succumb to disease.
It’s not just for tugging APP around the neuron: The SORLA receptor may also bind Aβ and hasten its demise.
Government, industry, and advocacy together will provide nearly $130 million for the identification of surrogate markers and targets.