At AD/PD, researchers further tied TREM2 to phagocytosis and enumerated markers that may distinguish beneficial microglia from harmful ones.
The growth factor turns off microglia, major support cells for neurons.
Genetic and animal studies hint that B and T cells control amyloid accumulation, though the mechanisms remain unclear.
A mouse model that was previously thought to express a transgene predominantly in the entorhinal cortex may be much leakier than previously thought. This complicates interpretation of some previous studies reporting propagation of toxic tau aggregates.
Deep brain stimulation helps many people with Parkinson’s, but how it does so remains a mystery. A new study suggests it normalizes brain rhythms.
In a preliminary study, 15 percent of people with ALS had antibodies against an enzyme that processes the wheat protein gluten.
Four new studies call into question PLD3’s status as an AD risk factor. Larger studies may be needed to settle the debate.
The Centers for Medicare and Medicaid services has given the nod to an 18,000-patient study to see whether amyloid scans prove their worth. Researchers hope for coverage afterward.
Senataxin, a gene associated with early onset ALS, regulates how cells respond to viruses.
Researchers link the AD Risk gene BIN1 to tau and amyloid in different model systems, and propose a mechanism for how a PICALM variant might be protective.
Scientists have found that the nuclear receptor ERRγ ramps up mitochondrial energy production in neurons.
Researchers no longer debate whether misfolded proteins spread through the brain in neurodegenerative disease. Now they want to know how.
Blamed for neurodegeneration and memory problems, the transcription factor ATF4 may also be a gatekeeper for synaptic plasticity and memory formation.
The same or similar molecules might treat a variety of protein-misfolding conditions.
New data argue that multimers of α-synuclein may protect against pathological aggregation.