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.
When exposed to stressful conditions, several proteins tend to misfold and form aggregates inside or outside cells.
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.
A new publication in the May issue of Nature Aging by researchers from Integrated Biosciences, a biotechnology company combining synthetic biology and machine learning to target aging, demonstrates the power of artificial intelligence (AI) to discover novel senolytic compounds, a class of small molecules under intense study for their ability to suppress age-related processes such as fibrosis, inflammation and cancer.
Adding long-chain fatty acids can thicken cell membranes and alter the activity of a key enzyme, as LMU scientists have demonstrated in cell cultures.
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.
Neurodegeneration, or the gradual loss of neuron function, is one of the key features of Alzheimer's disease.
Physical activity is often quoted as a method of increasing mental and physical health. Scientists at the Beckman Institute for Advanced Science and Technology have proved that it might also enhance brain health more directly.
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 brimming inbox on Monday morning sets your head spinning. You take a moment to breathe and your mind clears enough to survey the emails one by one.
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.
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.
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.
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.
A team of global experts has discovered new signals of natural selection in humans.
Certain diseases, including Alzheimer's, are currently considered "undruggable" because traditional small molecule drugs can't interfere with the proteins responsible for the illnesses.
The Lieber Institute for Brain Development has received a $1 million, two-year grant from the Chan Zuckerberg Initiative to support the work of the African Ancestry Neuroscience Research Initiative (AANRI) to promote racial equity throughout the field of neuroscience.
A research group at Uppsala University has developed a simple and effective artificial blood-brain barrier model that can be used to determine how well antibody-based therapies can enter the brain.
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.
Mount Sinai researchers have published a study in Alzheimer's & Dementia: The Journal of the Alzheimer's Association that sheds new light on the role of DNA methylation in Alzheimer's disease (AD).