Stress Relief: Anti-Stress Granule Therapy Saves ALS Models
New research suggests that TDP-43 attacks neurons by deactivating a translation initiation factor. Keeping the factor active holds toxicity at bay in flies.
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New research suggests that TDP-43 attacks neurons by deactivating a translation initiation factor. Keeping the factor active holds toxicity at bay in flies.
Researchers at BACE meeting explore how trafficking and degradation of the protease relate to amyloid pathology in AD.
By stopping familial amyloid polyneuropathy in its tracks, a repurposed anti-inflammatory medication supports the idea that artificial chaperones can prevent protein aggregation.
Alzforum’s summary of research highlights of 2013.
Vitamin E slows functional deterioration in people with mild to moderate Alzheimer's disease, according to a new study.
Evidence builds that amyotrophic lateral sclerosis and frontotemporal lobar degeneration sit on the same pathological spectrum, but scientists are unsure how the disease marker TDP-43 fits in.
A combination of high clusterin and low Aβ42 in cerebrospinal fluid associates with early Alzheimer’s neurodegeneration, hinting at a mechanistic interaction between the proteins.
Amyotrophic lateral sclerosis may be inherited more often than previously believed, prompting neurologists to rethink how they define familial versus sporadic disease.
People with previous head injuries may be more prone to amyloid deposition and have a higher risk for Alzheimer's.
New data questions whether LRRK2’s kinase activity contributes to Parkinson’s, finding instead that absolute levels of the protein matter more.
Scientists are trying to help the brain replace lost dopamine in people with Parkinson's. Will gene therapy or cell replacement work eventually?
The 2014 U.S. budget increases Alzheimer’s research funding by $80 million, offsetting some of the damage done by the 2013 sequestration.
Data from Phase 3 solanezumab and bapineuzumab trials are formally published. Both missed their primary endpoints, but researchers gleaned insights about Alzheimer’s diagnosis and biomarkers, as well as how to proceed with amyloid immunotherapy therapy.
Neuroligin, a synapse-building protein previously tied to autism, may play a part in Alzheimer’s disease through neuroinflammation and DNA transcription.
Unaffected members of families with a history of late-onset Alzheimer’s disease have an increased risk of progressing to the disease, a new study confirms.