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.
A study of nearly 2 million people reports that obesity lowers dementia risk, while being underweight raises it.
At the AD/PD conference, researchers reported a protective gene variant that delays Alzheimer’s onset by 10 years, and parsed pathways to find out why particular neurons take the hit in specific diseases.
Peptides made from D-amino acids bind to Aβ oligomers and trigger their removal from the brain. Some appear poised to enter Phase 1.
The highs and lows of cerebrospinal fluid Aβ and PET amyloid imaging don't necessarily agree.
In the presynaptic terminals of the hippocampus, pathological aggregates of tau weakened calcium influx and plasticity. A little later, the synapses disappeared.
By dampening translation, these tiny RNAs keep protein levels from fluctuating wildly.
Qualification could follow, but only if trial sponsors fork over fresh data.
A screen in round worms identifies a novel mechanism for degradation of toxic proteins.
Two new open-access journals will cover specialized areas of Alzheimer’s research.
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