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.
Working with tiny bacteria, Michigan State University researchers led by Lee Kroos have made a discovery that could have big implications for biology.
It is highly regulated what goes into the brain and what does not. The phagocytes that encapsulate the blood arteries in the brain and maintain the blood-brain barrier have been examined by researchers at the University of Freiburg’s Faculty of Medicine.
Mutant mice are providing scientists with a new neurobiological framework to understand the brain changes observed in distractible humans who carry a common gene variant whose frequency has been associated with Attention Deficit Hyperactivity Disorder (ADHD).
Research from the Babraham Institute has developed a method to 'time jump' human skin cells by 30 years, turning back the aging clock for cells without losing their specialized function.
Researchers from a USC-led consortium have discovered 15 "hotspots" in the genome that either speed up brain aging or slow it down -; a finding that could provide new drug targets to resist Alzheimer's disease and other degenerative brain disorders, as well as developmental delays.
Most of us remember enough biology to recall that mitochondria are known as "the powerhouse of the cell." Even that audacious term may downplay the importance of mitochondria and what happens when mitochondria go bad.
New research may help scientists locate immature cells in the central nervous system that could shed light on the causes of neurodegenerative diseases like multiple sclerosis-;and autoimmune disease that affects the brain and nervous system-;and allow for the development of better therapeutic treatments.
Astrocytes form large networks of interconnected cells in the central nervous system. When these cell-to-cell couplings are disrupted in the brain of adult mice, the animals are no longer able to store spatial information.
In a study led by Cedars-Sinai, researchers have discovered two types of brain cells that play a key role in dividing continuous human experience into distinct segments that can be recalled later.
Take a cell-deep tour of a brain afflicted with Alzheimer's disease, and you will find minuscule clumps of protein that seem suspicious. Ever since the 1980s, when neuroscientists began identifying these protein tangles, researchers have discovered that other brain diseases have their own tangled-protein signatures.
Scientists from two independent research teams have discovered how the mislocalization of a protein, known as TDP-43, alters the genetic instructions for UNC13A, providing a possible therapeutic target that could also have implications in treating amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and other forms of dementia.
While the word "mutation" may conjure up alarming notions, a mutation in brain immune cells serves a positive role in protecting people against Alzheimer's disease.
Could a new paradigm in digital health treat blinding disorders and possibly also be a conduit for treating other parts of the brain? A multi-disciplinary team of world-renowned researchers at USC are exploring this exciting possibility.
Multiple changes in brain cells during the first month of embryonic development may contribute to schizophrenia later in life, according to a new study by Weill Cornell Medicine investigators.
For the first time, scientists have identified a rare population of potentially toxic senescent cells in human brains that can serve as a target for a new Alzheimer's disease treatment.
Scientists have determined for the first time the structure of the molecule associated with amyotrophic lateral sclerosis (ALS) and multiple other neurodegenerative diseases.
New research from the University of Chicago points to microglia, key immune cells in the brain, as a key mediator in the relationship between the gut microbiome and b-amyloid deposits in male mice in a model of Alzheimer's disease.
Neuroinflammatory diseases, including Alzheimer's disease and traumatic brain injury, have been linked to deposits of a tough protein known as fibrin, derived from the blood clotting factor fibrinogen.
When immune cells move throughout the brain, they act as the first line of defense against viruses, toxic materials and damaged neurons, rushing over to clear out them.
Losing memory is a hallmark of Alzheimer's, a symptom of the disease that depletes a patient's quality of life. Improving memory and slowing cognitive changes caused by the disease is an ongoing challenge for researchers seeking to develop novel therapies.