Amyloid fibrils in those with frontotemporal lobar degeneration (FTLD) contain a little-known protein called TMEM106B. Researchers speculate TMEM106B could be found to be the cause of FTLD.
Researchers discover the role the p62 protein plays in the accumulation of amyloid beta in the brain.
Researchers create neurons from the skin cells of ALS patients in order to "treat" a gene defect in a dish.
While evidence suggests pathological proteins linked to the onset and progression of neurodegenerative disorders are capable of spreading from cell-to-cell within the brains of affected individuals, new research shows no evidence to support concerns that these abnormal disease proteins are “infectious” or transmitted from animals to humans or from one person to another.
