Researchers highlight some of the current strategies being pursued to help restore lost function and regenerate brain areas affected by Parkinson's disease.
Drugs that increase signaling of Sonic Hedgehog (Shh) can help suppress the involuntary movements associated with dopamine replacement therapy for those with Parkinson's disease.
Microglia immune cells can join together to form networks when needed, a new study reports. However, certain mutations associated with Parkinson's disease can impair this process.
Researchers discovered people with a specific variant of the oxytocin receptor gene OXTR follow more people on Instagram. However, there no evidence was found to suggest gene-environment interactions influence online sociability.
The olfactory system works in combination with the brain's reward and aversion systems in both learning and memory formation.
Cellular reprogramming of glioma cells into neural cells may be a promising treatment for glioblastoma brain cancer.
A new algorithm uses neuroimaging data of amyloid levels in the brain and takes into account a person's age to determine when a person with genetic Alzheimer's risk factors, and with no signs of cognitive decline, will develop the disease.
H3 acetylation of basal neural precursor cells may have been an important factor in the evolution of the human neocortex.
A newly identified gene therapy pathway has the potential to protect us against dementia and cancer, researchers report.
Stem cell study reveals astrocytes carrying the Alzheimer's associated APOE4 gene release more cholesterol than those carrying the APOE3 gene. Findings shed light on how different versions of the APOE gene in astrocytes influence amyloid-beta production and how the oversupply of cholesterol associated with APOE4 astrocytes may promote amyloid-beta formation in Alzheimer's patients.
Study reveals the molecular mechanisms implicated in the regulation of toxic proteins in neurodegenerative diseases like Alzheimer's and Parkinson's disease.
Researchers discovered mutations of the OPTN gene resulted in increased herpesvirus 1 growth in the brains of mice, leading to the death of local neurons. This resulted in accelerated neurodegeneration. OPTN deficiency was also associated with impairments in immune response. While these findings are specific to the HSV-1 virus, researchers believe the findings may apply to up to eight herpesvirus infections.
