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.
More than 90% of people with Down syndrome, the most common chromosomal disorder in humans and the most frequent genetic cause of intellectual disability, are diagnosed with Alzheimer's disease by ages 55-60.
Scientists at The Florey have developed an mRNA technology approach to target the toxic protein tau, which builds up in patients with Alzheimer's disease and other dementias.
Aging may be less about specific "aging genes" and more about how long a gene is. Many of the changes associated with aging could be occurring due to decreased expression of long genes, say researchers in an opinion piece publishing March 21 in the journal Trends in Genetics.
Identifying genetic variants and the role they play in predisposing people to Alzheimer's disease can help researchers better understand how to treat the neurodegenerative condition for which there is currently no cure.
The scientist of the Faculty of Medicine of the University of Malaga José Luis Royo has coordinated a study that summarizes eight years of research and brings together 100 multidisciplinary specialists, identifying a mutation that alters Alzheimer's disease progression.
A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 4, entitled, "Single-Cell RNA-seq reveals transcriptomic modulation of Alzheimer's disease by activated protein C."
Epigenetic processes allow different cell types to emerge from a single genome. Throughout development, cells differentiate and acquire distinct characteristics by expressing the same genome in different ways.
Protein buildup and cell degeneration in specific populations of brain cells are hallmarks of the early stages of neurodegenerative diseases.
Receptor molecules on the cell surface are essential for cellular communication. Periodically, these receptors must be absorbed and sorted for them to be broken down or recycled.
The brain is typically depicted as a complex web of neurons sending and receiving messages. But neurons only make up half of the human brain.
UC Santa Barbara researchers and collaborators in Colombia, Brazil and Germany are progressing toward an understanding of mechanisms that underlie Alzheimer's disease, in particular an early-onset, genetic form that has afflicted generations of an extended family in Colombia.
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.
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