An active immunotherapy is coming to the fore as researchers continue to try novel therapies.
Does a tau-based early diagnosis look more likely?
In a large observational study, high blood pressure in midlife correlated with faster cognitive decline over the next two decades.
Researchers continue to screen blood for factors that signal neurodegenerative disease.
Neurons derived from an octogenarian donor thrived in rat spinal cord lesions, extending thousands of axons along the length of the cord, even into the cortex.
Not the RNA aggregates, but the repeat dipeptides made from expansions in the C9ORF72 gene are responsible for neurodegeneration, a study claims.
Blocking the microglial receptor for pro-inflammatory prostaglandin D2 protects motor neurons from glial toxicity in ALS cell and mouse models.
Connections across neural networks break down as cognition declines in people with different forms of AD, suggesting the wiring problems may be a hallmark of disease progression.
Compounds that bind RNA temper toxicity related to ALS and FTD.
Researchers predict that a new BACE1 mouse recapitulates the early stages of sporadic Alzheimer’s, and can serve as a testing ground for BACE1 inhibitors.
According to new research, as both mice and humans grow older, immune signals change at the interface between blood and cerebrospinal fluid.
Restraining the activity of a calcium-activated phosphatase may take the edge off a-synuclein toxicity.
Aβ in mitochondria slows the maturation of proteins that enter the organelle from cytosol, according to a new study. The finding could help explain the wide range of mitochondrial deficits seen in Alzheimer’s disease.
In a reverse twist on the spread of pathology in Alzheimer’s, axonal proteins translated in the presence of Aβ migrate back to cell bodies, where they promote cell death.
Improved magnetic resonance imaging methods confirm damage in a subclass of motor neurons in ALS.