Mouse study reveals chronic stress affects neurogenesis in the dentate gyrus.
Amyloid-beta proteins created in the liver are carried in the blood by lipoproteins to the brain. This results in neurodegeneration, brain atrophy, and inflammation, which are common features of Alzheimer's disease.
Sleep-deprived mice had increased activity in hippocampal inhibitory neurons, disrupting the processing and storage of new memories.
A specialized area of the mouse brain called the SuM specializes in detecting novel experiences. Within this brain area, responses to social novelty, or experiences related to unknown individuals, were segregated from those related to unfamiliar places, before being sent to areas of the brain associated with memory.
Neurons created as a result of adult neurogenesis mature for longer and grow larger than those created during infancy. Findings suggest adult-born neurons may have a more powerful function than those created during infancy and may play a critical role in neuroplasticity.
Suppressing TLR4 activity following a traumatic brain injury, such as concussion, reduces excitability, and improves working memory performance up-to a month later.
Reducing neuroinflammation in the brain before cognitive impairment becomes apparent can help slow the progression of Alzheimer's disease.
Vimentin, a cellular filament, helps neural stem cells to clear damaged and clumped proteins, assisting in neurogenesis.
Increased potassium currents were responsible for hyperactivity of CA3 neurons. When exposed to potassium channel blockers, the hyperactivity disappeared. However, when exposed to lithium, the drug not only reversed hyperactivity but reduced potassium currents at the same time. The findings strengthen the case that potassium currents play a role in bipolar disorder.