Atypical brain development begins at the very earliest stages of brain organization, at the level of individual neurons.
Human-on-a-chip technology could provide a more valuable clinical-based model for ALS.
Study finds allele-specific open chromatin variants are likely to be linked to several neuropsychiatric traits and illnesses, including schizophrenia and bipolar disorder.
Study points to a common gene expression profile, regardless of DNA mutations, applicable to any person on the autism spectrum. The dysregulation occurs in neural progenitor cells. While the genetic cause of ASD may be different between individuals, the behavior of the genes is similar in people with autism, and differ from those who are not on the autism spectrum.
10% of patients diagnosed with Parkinson's disease are between the ages of 21 and 50. For those with young-onset Parkinson's disease, researchers report the foundations for the disease may have been apparent before they were born. The study also points to a drug, currently approved to treat precancerous skin growths, that has the potential to reduce elevated levels of alpha-synuclein.
Using induced pluripotent stem cells derived from patients with neurodegenerative disorders, researcher recreated the blood-brain barrier inside Organ-Chips.
Researchers have developed a new technique to study the development of human neurons compared to the neurons of nonhuman primates. The findings shed new light on the evolution of the human brain.
Using CRISPR gene editing technology, researchers discover increased activity in neurons deficient in the CNTN5 or EHMT2 genes may cause ASD related characteristics in humans.
Tasquinimod, a new cancer drug, appears to control genes associated with Parkinson's disease, a new study reports.
A new study reports disrupted transportation routes in nerve cells are a significant cause of Parkinson's disease.
A new method reveals some ALS affected neurons display hypo-excitability. Researchers say these changes most likely represent early steps in the disease progression.
In Parkinson's disease, alpha synuclein clumps move to and damage mitochondrial proteins, making them less efficient and causing the mitochondrial to burst, leaking out chemicals that tell the cells to die, researchers say.
