According to new research, as both mice and humans grow older, immune signals change at the interface between blood and cerebrospinal fluid.
Perfectly healthy mitochondria can sicken neurons simply by being in the wrong place.
A man lacking ApoE appears to have no cognitive deficits, and his brain and CSF biomarker profiles appear normal. Some claim the findings support ApoE as a rational drug target for AD.
The first large-scale surveys of DNA methylation in Alzheimer’s brains turned up numerous altered regions that may point to new genes involved in pathology.
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.
Compounds that bind RNA temper toxicity related to ALS and FTD.
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.
Researchers are ramping up efforts to target tau for Alzheimer’s and other tauopathies.
Blocking the microglial receptor for pro-inflammatory prostaglandin D2 protects motor neurons from glial toxicity in ALS cell and mouse models.
In gritty and sometimes harrowing detail, activist Meryl Comer describes the reality of caring for a loved one with Alzheimer’s disease.
Not the RNA aggregates, but the repeat dipeptides made from expansions in the C9ORF72 gene are responsible for neurodegeneration, a study claims.
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.
Scientists have turned a yeast heat shock protein into a powerful disaggregase that attacks TDP-43, FUS, and α-synuclein mutants.
Researchers continue to screen blood for factors that signal neurodegenerative disease.
In a large observational study, high blood pressure in midlife correlated with faster cognitive decline over the next two decades.