In a cell culture system, astrocytes from people with ALS kill motor neurons. The model could yield more discoveries about the fundamental biology of this disease.
It’s not just for tugging APP around the neuron: The SORLA receptor may also bind Aβ and hasten its demise.
Mutant FUS meddles with RNA splicing and DNA damage repair in transgenic mice that succumb to disease.
Already linked to Alzheimer’s and other neurodegenerative diseases, a TREM2 variant now shows up on the ALS radar, too.
The antidepressant citalopram reduces agitation in Alzheimer’s patients, but caused abnormal heart rhythms at the tested dose.
The FDA has stopped the personal genome sequencing company 23andMe from selling health assessments, saying its tests need validation. What do Alzheimer scientists think?
Researchers have identified the striatum as a site of neurogenesis in the adult brain, but not in people with Huntington’s disease.
Detecting oligomers in the cerebrospinal fluid is no easy feat. The latest test is among the most sensitive yet, but is it useful?
A new initiative in the U.K. will fund research into potential treatments for dementia and neurodegeneration.
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.
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?
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.
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.
The scientific spotlight often shines on excitatory neurons as the brain’s main Aβ factories. What about other cell types?
Scientists may have discovered another explanation for why DNA repeat sequences cause neurodegenerative diseases: A six-nucleotide expansion in the C9ORF72 gene forms stable structures that interfere with its transcription.
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