Memory Maker or Neuron Killer? For Transcription Factor, It May Depend on Mood
Blamed for neurodegeneration and memory problems, the transcription factor ATF4 may also be a gatekeeper for synaptic plasticity and memory formation.
6538 RESULTS
Sort By:
Blamed for neurodegeneration and memory problems, the transcription factor ATF4 may also be a gatekeeper for synaptic plasticity and memory formation.
Researchers no longer debate whether misfolded proteins spread through the brain in neurodegenerative disease. Now they want to know how.
Scientists have found that the nuclear receptor ERRγ ramps up mitochondrial energy production in neurons.
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.
Senataxin, a gene associated with early onset ALS, regulates how cells respond to viruses.
Four new studies call into question PLD3’s status as an AD risk factor. Larger studies may be needed to settle the debate.
In a preliminary study, 15 percent of people with ALS had antibodies against an enzyme that processes the wheat protein gluten.
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.
The growth factor turns off microglia, major support cells for neurons.
At AD/PD, researchers further tied TREM2 to phagocytosis and enumerated markers that may distinguish beneficial microglia from harmful ones.
A new study suggests that tau oligomers as small as trimers enter neurons and corrupt native tau proteins inside.
In a Solomonic move, a prestigious prize for research in neurodegenerative disease goes to a veteran tauist and a self-professed inhabitant of “amyloid land.”
A protein instigates axon degeneration by promoting destruction of the essential enzyme cofactor, NAD+.
As DIAN Plans Trial Number Two, the Goal Is to Go Big DIAN-TU Pharma Consortium NexGen Trial Meeting
Researchers identify N-terminally extended Aβ peptides that are toxic to synapses and rise after BACE1 inhibition, though whether they occur in human disease remains unclear.
No filters selected