Brain imaging distinguishes ALS patients with C9ORF72 expansions from those with other forms of the disease.
By looking for structural DNA variations in Alzheimer’s families, researchers identified 18 new genes that may play a role in AD pathology.
Researchers identify the Aβ-binding scavenger receptor CD36 as a key regulator of macrophage inflammasome responses...
Mouse studies point to a new pathway that mediates motor neuron disease caused by mutations in superoxide dismutase 1.
Removing a key component of the innate immune system worsens amyloid deposition but improves memory in mice that model Alzheimer's pathology.
Mass spectrometry data show how γ-secretase modulators skew APP processing toward Aβ40 rather than Aβ42, without upsetting cleavage of other substrates.
Motor and cortical neurons are particularly vulnerable to FUSopathy. A new paper suggests they fail because they depend strongly on FUS to regulate transcription.
Expansions in ataxin-2 can lead to either ALS or spinocerebellar ataxia—even in the same family, according to a new pedigree from New York.
A stem cell-derived structure mimics crucial features of human brain development and could aid studies in schizophrenia, autism, maybe neurodegeneration.
Functional genomics and mouse analyses blame waning levels of histone-binding protein for memory loss in aging.
In sporadic and familial Parkinson's, faulty parkin may damage dopamine neurons by letting a deadly protein linger.
Fueling (or rekindling) controversy over anti-aging benefits of sirtuins, researchers report that Sirt1 lengthens lifespan in mice.
As heat shock protein and co-chaperone team up to shield tau from degradation, they create toxic oligomers.
Older people improved memory and attention after playing a challenging video game, supporting the idea that multitasking could have benefits for cognition.
A deletion in chromosome 22 points to new genetic risk factors for Parkinson's disease.