A plasma assay for Alzheimer’s could radically speed up screening for clinical trials; alas, competing assays don’t measure the same thing.
In mouse models of tauopathy, microglia populations are far from binary. Different activation stages emerge at different phases of disease, some marked by viral defense pathways.
New drug application is first for Alzheimer’s disease in the U.S. since 2003, and first based on amyloid hypothesis.
New synaptic profiling and imaging techniques are enabling scientists to zero in on synaptic proteins, including phospho-tau, that make the difference between clinical Alzheimer’s and resilience.
Two cohorts—IDEAS and WHIMS—show Aβ accumulation and brain shrinkage in cognitively normal and impaired elderly who were exposed to levels of air pollution even within current EPA limits.
At CTAD, intranasal insulin trial stumbles, pioglitazone gets a postmortem, a RAGE inhibitor tries to hang on.
Researchers found that bits of tau from the protein’s microtubule-binding region can be detected in the cerebrospinal fluid. These, not phospho-tau or total tau, reflect neurofibrillary tangles in the Alzheimer’s brain.
Confronting unprecedented challenges this past year, scientists found ways to tide their research over and keep clinical trials mostly on track.
Plaque-busting antibodies reset the time course of amyloid accumulation, but so far provide only hints of a clinical benefit in mild AD. Good news: once gone, plaque stays gone for a while.
Changes in the composition of the cerebrospinal fluid and synapses may reveal novel insights into AD pathology.
In cultured cells, lysosomal activity was necessary to enable tau seeds to break out of internalized exosomes and trigger the aggregation of tau in the cytosol.
In Barcelona, data ran the gamut from a few hopeful little hints on new treatments to mixed signals on familiar players, and failed drugs thrown on the scrap heap.
Parkinson's disease is one of the most common neurodegenerative diseases, affecting about one percent of all people over the age of 65. It is characterized by rigidity, bradykinesia and tremors, which are caused by the progressive degeneration of dopamine-containing neurons...
Topline results suggested that the anti-inflammatory treatment stabilized cognition and function over six months. The trial did not include biomarkers.
Progressive supranuclear palsy is a poorly understood movement disorder that has come to be of intense interest to age-related neurodegenerative disease researchers...