Growing up and experiencing stimulating environments throughout life help to keep the hippocampus "young", and can help to preserve mental fitness in old age.
Cardiovascular problems can alter gene activity in the hippocampus, increasing the risk for cognitive decline and memory deficits, a new study reports.
Free radicals help control cellular processes vital for neuroplasticity and neurogenesis in mice.
Young adults with the Alzheimer's associated ApoE gene had differences in brain activity when presented with memory tasks.
A newly designed synthetic compound could act as a prototype for a novel class of drugs to treat neurological damage.
People with subjectively felt memory deficits also exhibited measurable cognitive deficits that were associated with abnormalities in spinal fluid.
In mouse models of Alzheimer's disease, active neurons still encode memory, and a group of active neurons encodes novel environmental information. The signal of the novelty containing neurons causes a superimposition disturbing the signal of memory encoding neurons.
Stimulating activation of microglia may help eliminate Alzheimer's associated plaques, thus helping to prevent the progression of the neurodegenerative disease.
Study finds a link between blood supply to the hippocampus and cognitive performance.
The NLPR3 inflammasome and the inflammatory response it triggers play a critical role in the emergence of tau pathology.
Embryonic damage caused by autoantibodies is implicated in a range of behavioral and psychological disorders, including schizophrenia, autism, and ADHD.
Using a gene vector, researchers channeled the blueprint of the human tau protein into different aged mice. After a period of twelve weeks, the tau protein spread twice as fast in older mice than the younger cohort. Findings shed light on why Alzheimer's is predominantly an age-related neurodegenerative disease.
