Neurodegeneration is the umbrella term for the progressive loss of structure or function of neurons, including death of neurons.
Alzheimer's Disease (AD) is a complex neurodegenerative illness with genetic and environmental origins.
The USask research team uncovered a pair of genes involved in removing cells of toxins that build in the body and cause aging while working with small nematode worms called C. elegans. The researchers discovered that inactivating genes named CCF-1 and PAL-1 caused nematodes to die 50% faster than usual.
In a study published in Nature Communications, a team led by Krembil Brain Institute Senior Scientists, Drs. Lorraine Kalia and Suneil Kalia, and University of Toronto (U of T) Professor, Dr. Philip M. Kim, identified a protein-protein interaction that contributes to Parkinson's disease.
The human brain has a sweet tooth, burning through nearly one quarter of the body's sugar energy, or glucose, each day.
Neurodegeneration, or the gradual loss of neuron function, is one of the key features of Alzheimer's disease.
MIT neuroscientists have found a way to reverse neurodegeneration and other symptoms of Alzheimer's disease by interfering with an enzyme that is typically overactive in the brains of Alzheimer's patients.
A study from the National Eye Institute (NEI) identified rare genetic variants that could point to one of the general mechanisms driving age-related macular degeneration (AMD), a common cause of vision loss in older adults.
A new study conducted at the National Eye Institute (NEI) has identified incredibly rare genetic variants that might uncover the mechanisms underlying the development of AMD.
A National Eye Institute-led team has identified a compound already approved by the U.S. Food and Drug Administration that keeps light-sensitive photoreceptors alive in three models of Leber congenital amaurosis type 10 (LCA 10), an inherited retinal ciliopathy disease that often results in severe visual impairment or blindness in early childhood.
Scientists from the Trinity Biomedical Sciences Institute (TBSI) have shed new light on aging processes in the brain.
Nearly two dozen experimental therapies targeting the immune system are in clinical trials for Alzheimer's disease, a reflection of the growing recognition that immune processes play a key role in driving the brain damage that leads to confusion, memory loss and other debilitating symptoms.
Scientists have found a novel way to block the transportation of mutant RNA and subsequent production of toxic repeat proteins which lead to the death of nerve cells in the most common subtypes of motor neurone disease (MND) and frontotemporal dementia (FTD).
According to Johns Hopkins University scientists, a “biocomputer” fueled by human brain cells could be created within this lifetime. Such technology is expected to tremendously enhance the capabilities of modern computing and develop novel fields of study.
Nearly 100% of cases of amyotrophic lateral sclerosis-the progressive, fatal neurodegenerative disease known as ALS or Lou Gherig's disease-involve the buildup of a protein called TDP-43.
Northwestern Medicine scientists have discovered two ways to preserve diseased upper motor neurons that would normally be destroyed in ALS, based on a study in mice. Upper motor neurons initiate movement, and they degenerate in ALS.
Of all the known genetic risk factors for late-onset Alzheimer's disease, the strongest is a gene for the protein called ApoE4.
Every year, 5,000 people in the United States are diagnosed with ALS, an incurable neurodegenerative disease that will destroy them within two to five years.
Stem cells show particular promise in treating diseases for which few other effective treatments exist.
Damaged protein clusters in the brain are a hallmark of many neurodegenerative diseases, including Parkinson’s, Alzheimer’s, and others. Although they have made significant efforts, scientists have only partially succeeded in finding treatments for these conditions by removing these toxic clusters.
AZoLifesciences speaks to Dr. Anneline Pinson and Prof. Dr. Wieland B. Huttner from The Max Planck Institute of Molecular Cell Biology and Genetics about their latest research which found a greater neuron production in the frontal lobe during brain development in modern humans than Neanderthals, due to the change of a single amino acid in the protein TKTL1.