A new collection of articles explores mapping brain overexcitability that underpins the dysregulation of vigilance, sleep-wake cycles, and validating effective biomarkers for Alzheimer's disease.
Combining electrical stimulation with sounds that activate the somatosensory cortex could help bring relief to those suffering from chronic pain and other neurological conditions.
Terazosin, a drug commonly prescribed for the treatment of enlarged prostate and high blood pressure, shows promise as a treatment for ALS.
The levels of two protein biomarkers, GFAP and UCH-L1 found in blood samples taken 24 hours after a traumatic brain injury can help to predict which patients will die and which will obtain a severe disability.
Multiple sclerosis-associated retinal layer thinning predicts the severity of future relapses and the likelihood of disability.
Interferon betas, a class of drugs commonly prescribed to those with multiple sclerosis reduces the binding of zinc, C-peptide and albumin to red blood cells.
Older adults who spend their free time embarking on intellectually stimulating activities, such as reading, writing, or making crafts, have a 23% lower risk of developing dementia. Additionally, those who exercise and spend time socializing with family or friends also have a significantly decreased risk of dementia.
Researchers identified a pathway that begins in the gut and ends with a pro-inflammatory protein in the brain that appears to contribute to the development and progression of Alzheimer's disease.
Fatigue and headaches top the list of common lingering symptoms four months after COVID infection, with muscle aches, changes in sense of taste and smell, cough, and congestion following close behind.
The effects of COVID-19 infection on neurological health are becoming more apparent. A new study reveals COVID-19 can predispose people to irreversible neurological conditions, accelerate brain aging, and increase the risk of stroke and brain bleeds.
A newly developed novel fusion protein drug efficiently eliminates amyloid beta via an entirely different mechanism than amyloid-beta antibody-based immunotherapy.
Microglia that express the Alzheimer's associated APOE4 genetic variant are unable to effectively metabolize lipids. This causes lipids to build up, promoting inflammation and preventing effective neurotransmission.
