Dementia is not a specific disease. It is a descriptive term for a collection of symptoms that can be caused by a number of disorders that affect the brain. People with dementia have significantly impaired intellectual functioning that interferes with normal activities and relationships. They also lose their ability to solve problems and maintain emotional control, and they may experience personality changes and behavioral problems, such as agitation, delusions, and hallucinations.
Why do some people develop Alzheimer's disease while others don't? And, even more puzzlingly, why do many individuals whose brains are chock-full of toxic amyloid aggregates-;a telltale sign of Alzheimer's brain pathology-;never go on to develop Alzheimer's-associated dementias?
Neurons in a key area of the brain have different functions based on their exact genetic identity, and understanding this diversity could lead to better understanding of the brain's computational flexibility and memory capacity, potentially informing disease treatment options, Cornell researchers report in a new study.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder affecting tens of millions of people worldwide, and it is the most common cause of dementia.
University of Queensland researchers have used artificial intelligence to build a 3D map of key cell components to better understand dementia and infectious diseases including COVID-19.
New research has discovered that some patients with motor neuron disease (MND) and frontotemporal dementia (FTD) carry the same rare genetic defects that cause other neurodegenerative diseases.
An international research team, comprising scientists from DZNE, University Hospital Bonn, the Netherlands, and the US has been awarded a US$ 1.3 million grant by the "Human Frontier Science Program" to investigate brain immune cells and manipulate them via light irradiation.
Inhibiting a tiny RNA whose levels significantly increase with age, along with problems like weaker bones and sagging muscles, may be a way to keep our bodies more youthful and healthy, scientists say.
Dr Catherine Mummery, a consultant neurologist at UCL Queen Square Institute of Neurology & the National Hospital for Neurology and Neurosurgery, has led a trial. The trial signifies for the first time that a “gene silencing” method has been taken in Alzheimer’s and dementia disease.
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.
People with dementia have protein build-up in astrocytes that may trigger abnormal antiviral activity and memory loss, according to a preclinical study by a team of Weill Cornell Medicine investigators.
A recent study using mice has revealed a way to turn back the clock after heart attack. The researchers behind the work used RNAs to instruct cells in an injured heart to eliminate scar tissue and recreate cardiac muscle, allowing the heart to function like new again.
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.
Bacteria have thousands of genes and functions that we, the human host, do not have. For instance, bacteria can help us digest fiber, provide support to our immune systems, and absorb important nutrients. But reaping the benefits of "good bacteria" is easier said than done.
According to a new study led by Anya Topiwala of Oxford Population Health, a division of the University of Oxford in the United Kingdom, and published on March 22nd, 2023 in the open-access journal PLOS ONE, changes in the brain caused by Alzheimer’s disease are connected to telomeres shortening, the protective caps on the ends of chromosomes that shorten as cells age.
An international study led by the Molecular Physiology Laboratory at the UPF Department of Medicine and Life Sciences (MELIS) identifies new genes that modulate the toxicity of the protein β-amyloid, responsible for causing Alzheimer's disease.
A protein named TDP-43 has been lost from its normal location in the nucleus of the cell in virtually all persons having amyotrophic lateral sclerosis (ALS) and in up to half of all cases of frontotemporal dementia and Alzheimer’s disease (AD).
In virtually all persons with amyotrophic lateral sclerosis (ALS) and in up to half of all cases of Alzheimer's disease (AD) and frontotemporal dementia, a protein called TDP-43 is lost from its normal location in the nucleus of the cell.
A team of global experts has discovered new signals of natural selection in humans.
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).
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.