Alzheimer's disease (AD) is an irreversible, progressive brain disease that slowly destroys memory and thinking skills and, eventually, the ability to carry out the simplest tasks of daily living. In most people with AD, symptoms first appear after age 60. AD is the most common cause of dementia among older people, but it is not a normal part of aging. Dementia refers to a decline in cognitive function that interferes with daily life and activities. AD starts in a region of the brain that affects recent memory, then gradually spreads to other parts of the brain. Although treatment can slow the progression of AD and help manage its symptoms in some people, currently there is no cure for this devastating disease.
Researchers at the Case Western Reserve University School of Medicine have led a team that has discovered a novel therapeutic strategy for treating neurodegenerative illnesses, raising the prospect of better care for conditions like multiple sclerosis, Alzheimer's disease, Parkinson's disease, and Vanishing White Matter disease.
Researchers have discovered particular oxytocin neurons in the mouse brain that influence memory for object recognition.
The results of a recent study led by the Geisel School of Medicine and Thayer School of Engineering at Dartmouth, and published in Cell Reports Medicine, provide new information about the role that antibodies play in preventing herpes simplex virus (HSV) infections.
The largest genetic risk factor for late-onset Alzheimer's disease is apolipoprotein E (APOE), and researchers Sarah Cohen, PhD, and Ian Windham, a former PhD student from the Cohen group, have made a novel discovery about this protein.
Cell death is fundamental to life and, thus, healthy aging. In the realm of cellular biology, ferroptosis (a form of programmed cell death) has emerged not only as a focal point of research for its potential in eliminating cancer cells, but also its role in a plethora of other diseases, including neurodegenerative diseases such as Alzheimer's disease, eye diseases such as Retinitis pigmentosa and age-related macular degeneration, as well as ischemia, cardiovascular disease, liver disease, acute kidney injury and inflammation.
By tracking when distinct subsets of brain cells activate, researchers have understood the complex activity patterns found in both human and animal brains for many years. Knowing how long those neurons stay active and when they turn off again is crucial to understanding the brain and its associated disorders.
Scientists at St. Jude Children's Research Hospital revealed the complex structure of two Parkinson's disease-related proteins, both of which are implicated in late-onset cases.
Researchers have identified a mechanism that promotes the breakdown of harmful protein deposits. If it malfunctions, it can lead to Parkinson’s disease.
A group of researchers has introduced a set of free tools designed for analyzing extensive collections of brain dissection images from brain banks worldwide.
Some Covid-19 vaccines safely and effectively used lipid nanoparticles (LNPs) to deliver messenger RNA to cells.
Developing treatments for Alzheimer's disease (AD) is difficult because complex underlying mechanisms drive different types of cells that may contribute to the disorder.
Neurodegenerative diseases are characterized by the deposition of clumped proteins in the brain and progressive neuronal cell death.
Researchers at Gladstone Institutes have discovered that a rare genetic variant known as the "Christchurch mutation" can block detrimental effects of apolipoprotein E4, the best-established risk factor for the most common form of Alzheimer's disease.
Having healthy mitochondria, the organelles that produce energy in all our cells, usually portends a long healthy life whether in humans or in C. elegans, a tiny, short-lived nematode worm often used to study the aging process.
Mount Sinai researchers have shed valuable light on the mechanism of a key protein that regulates the plasticity and function of the hippocampus, a key brain region involved in memory and learning, and that decreases with age in mice.
If you've ever belly-flopped into a pool, then you know: water can be surprisingly hard if you hit it at the wrong angle. But many species of kingfishers dive headfirst into water to catch their fishy prey.
Alzheimer’s disease, a neurological disorder characterized by gradual cognitive decline, including memory loss, affects up to 5.8 million Americans today. Protein aggregates made up of beta-amyloid or other proteins occur in the brains of Alzheimer’s patients. These beta-amyloid plaques appear to be a major cause of the disease.
Cognitive decline associated with Alzheimer's disease (AD) develops when neurons begin to die, which can be caused by inappropriate immune responses and excessive inflammation in the brain triggered by amyloid beta deposits and tau tangles, two hallmarks of the disease.
In July, the first direct-to-consumer blood test designed to assess a user’s risk for developing Alzheimer’s disease hit the market. The test, which has not undergone Food and Drug Administration (FDA) review, measures the level of a protein called beta amyloid, a key component of plaques that form in the brains of Alzheimer’s disease patients, disrupting brain function.
Most of us who've reached middle age have noticed a slowing in memory and cognition, but scientists don't have a clear picture of the molecular changes that take place in the brain to cause it.