Gastrointestinal adverse events prompted the FDA to press the pause button on the α7 nicotinic acetylcholine receptor agonist.
Researchers using transcranial magnetic stimulation report that C9ORF72-based ALS, like other forms, leads to motor cortex hyperexcitability.
Paper Alert: Longitudinal Data Support CSF Neurogranin as an Early Synaptic Marker of Alzheimer’s Disease
Neurogranin could be a promising early CSF biomarker of Alzheimer’s disease.
TBK1 helps autophagy adaptors clutch damaged organelles.
Postmortem pathology confirms that some people who were diagnosed with AD during life had no appreciable amyloid in the brain, leaving researchers to puzzle over what caused their cognitive decline.
Scientists struggle to understand neurodegeneration in the SNAP syndrome.
Alzheimer’s Transmission Between People? Amyloid Plaques in Hormone Recipients Hint at Prion-like Spread
Decades after getting injections of human growth hormone from brain donors, some people developed amyloid pathology that researchers attribute to transmission of Aβ seeds hidden in the injections.
The protein FUS forms liquid organelles in healthy cells. Does it trigger neurodegeneration by switching to a solid state?
Appoptosin, a gene linked to progressive supranuclear palsy, triggers tauopathy by activating caspase-3, which cleaves tau to unleash its synaptotoxic potential.
For every unit increase in body mass index in midlife, the age at onset of AD dropped by more than half a year. Amyloid PET links the effect to AD pathology.
At AAIC, researchers reported that estrogen may decrease dementia risk if given to healthy women during early menopause.
Relieving systemic immune suppression facilitates the entry of immune cells into the brain and slows amyloid accumulation in a mouse model of aggressive Aβ pathology, scientists claim.
Scientists flesh out how PINK1 and parkin instigate mitophagy and what role the ALS genes optineuron and TBK1 play in the process.
A third trial continues in the United States
The fragment occurs naturally and rises after BACE inhibition, adding another layer of complexity to inhibitor therapy.