Not exact matches
In an interview, the Glasgow - based neurologist described how he had examined sections of
brain tissue in a retired rugby player and found
abnormal proteins associated with head injuries and dementia.
Mad cow is the common name for bovine spongiform encephalopathy (BSE), a fatal disease caused by
abnormal proteins (prions) in the
brain and nervous system.
All these diseases share a common feature:
abnormal buildup of a
protein called tau in the
brains of patients.
The researchers have now provided further evidence for this new theory by showing that the
abnormal protein coded for this genetic disorder can be transmitted to normal animals by the injection of diseased cells into their
brain.
The disease is caused by a genetic mutation that leads to
abnormal clumps of
protein in the
brain, eventually resulting in the atrophy and death of nerve cells.
LM22A - 4 treatment reduced the accumulation of
abnormal proteins in the striatum and cortex —
brain regions affected in Huntington's disease.
According to the proposal, called the amyloid hypothesis, Alzheimer's disease, estimated to affect more than 5 million people in the United States alone, is caused by
abnormal buildup of A-beta
protein in the
brain.
Most people associate prion diseases with the
brain, although scientists have found
abnormal infectious prion
protein in other organs, including the spleen, kidney, lungs and liver.
Prion diseases originate when normally harmless prion
protein molecules become
abnormal and gather in clusters and filaments in the human body and
brain.
Arising from the
abnormal buildup of a
protein known as alpha - synuclein in the
brain, such conditions damage the nerves that control blood pressure and heart rate.
These can then trigger normal
proteins to also misfold, producing a chain reaction that clogs the
brain with
abnormal proteins and so causing diseases such as vCJD.
Several factors have been implicated in Alzheimer's, including the build - up of an
abnormal protein called beta amyloid, fibrous tangles in the
brain involving
abnormal forms of a
protein called tau, and — most recently — an association between the disease and a gene called ApoE.
This turned out to be a normal
protein in the cells of organisms throughout the animal kingdom — but in
brains infected with scrapie and related diseases it turns up in both a normal, soluble form and an
abnormal, insoluble form which accumulates in deposits that eventually kill the cells.
In Alzheimer's disease, an
abnormal protein called amyloid beta begin s to appear on the neurons, forming plaques and compromising
brain activity.
Amyloid — an
abnormal protein whose accumulation in the
brain is a hallmark of Alzheimer's disease — starts accumulating inside neurons of people as young as 20, a much younger age than scientists ever imagined, reports a surprising new Northwestern Medicine study.
Amyloid — an
abnormal protein whose accumulation in the
brain is a hallmark of Alzheimer's disease — starts accumulating inside neurons of people as young as 20, a much younger age than scientists ever imagined.
The mice had symptoms such as
abnormal brain function, impaired memory and high levels of either amyloid - beta or tau
proteins in the
brain.
What these illnesses have in common is that they're caused by
abnormal proteins that accumulate in or between
brain cells to form plaques, producing damage that causes mental decline and early death.
In theory, these neurons should contain much higher levels of
abnormal prion
protein tangles than does CSF because they are directly connected to the
brain, Caughey notes.
Studies in mice specially bred to have features of the disease found that DHA reduces beta - amyloid plaques,
abnormal protein deposits in the
brain that are a hallmark of Alzheimer's, although a clinical trial of DHA showed no impact on people with mild to moderate Alzheimer's disease.
For nearly 30 years, researchers have gathered evidence that a group of bizarre, fatal
brain diseases — including mad cow and its human equivalent, Creutzfeldt - Jakob disease — are caused not by a virus or bacterium but by an
abnormal form of a
protein, called a prion.
The group» finding that the impaired intracellular
protein trafficking leads to neuropsychiatric disorders - related
abnormal higher
brain functions has high impact on the fields of psychiatry, basic medical sciences, and pharmaceutical sciences.
In most cases, CTE is thought to be caused by repeated blows to the head, which damage
brain tissue and lead to a buildup of an
abnormal protein called tau, according to the CTE Center.
Both types of dementia (memory and language) can be caused by an accumulation of beta - amyloid, an
abnormal toxic
protein in the
brain.
The gene variant creates an
abnormal protein that forms clumps in the
brain, eventually causing disease.
The disease is largely attributed to an
abnormal buildup of
proteins, which can form amyloid beta plaques and tangles in the
brain that trigger inflammation and result in the loss of
brain connections called synapses, the effect most strongly associated with cognitive decline.
Abnormal levels of the
proteins may be useful biomarkers that could help us study early treatments to limit or reverse the damage to
brain cells and even prevent the development of the full - blown disease,» said study author Edward Goetzl, MD, a Professor of Medicine with the University of California, San Francisco, a researcher at the National Institute on Aging, and a scientist of NanoSomiX, Inc., a California - based biotechnology company that provided a grant for method development for the study.
Intriguingly,
brain cells (neurons) with decreased complex I levels are significantly less likely to contain Lewy bodies, the
abnormal protein - aggregates that characterize Parkinson's disease,» says researcher Charalampos Tzoulis at Department of Clinical Science, UiB.
What these illnesses have in common is that they're caused by
abnormal proteins that accummulate in or between
brain cells to form plaques, producing damage that causes mental decline and early death.
«Our results indicate that exercise may slow the progression of Parkinson's disease by turning on the protective gene DJ - 1 and thereby preventing
abnormal protein accumulation in
brain,» Freed said.
A new study by Columbia University Medical Center (CUMC) researchers strongly supports the latter, demonstrating that
abnormal tau
protein, a key feature of the neurofibrillary tangles seen in the
brains of those with Alzheimer's, propagates along linked
brain circuits, «jumping» from neuron to neuron.
«We still do not understand fully how these
abnormal amyloid and tau
protein depositions affect
brain functions and cause dementia,» stated Satoshi Minoshima, MD, PhD, chair of the SNMMI Scientific Program Committee.
Abnormal clumps of certain
proteins in the
brain are a prominent feature of Parkinson's and other neurodegenerative diseases, but the role those same
proteins might play in the normal
brain has been unknown.
Lewy bodies (accumulation of
abnormal alpha - synuclein A
protein in the human
brain that is associated with the development of Parkinson's.
The
brains of the mice were analyzed at different time points over 22 months to map the spread of
abnormal tau
protein.
Alzheimer's disease, the most common form of dementia, is characterized by the accumulation of plaques (composed of amyloid - beta
protein) and fibrous tangles (composed of
abnormal tau) in
brain cells called neurons.
For example, Gladstone scientists are researching how autophagy — a process by which cells eliminate
abnormal proteins — can help to prevent the destruction of
brain cells.
There were also heightened levels of two
abnormal proteins in the subjects»
brains.
• Keeping
abnormal proteins from building up and potentially shutting down major organs (heart, liver and nervous system, to name a few) • Protecting the
brain's functions of learning and memory against neurotransmitter toxicity • Activating or increasing the activity of
proteins that promote the initial growth, maintenance and survival of
brain neurons • Enhancing the movement of
proteins, lipids and other cell parts through the cytoplasm of cell bodies.
Abnormal proteins found in Alzheimer's, Parkinson's, and Huntington's disease all share a similar ability to cause damage when they invade
brain cells
They're caused by normally harmless
proteins that become
abnormal and form clumps in the
brain.
Deep inside the
brains of people with dementia and Lou Gehrig's disease, globs of
abnormal protein gum up the inner workings of
brain cells — dooming them to an early death.
But this is the first study to show how lifestyle factors directly influence levels of
abnormal protein deposits in the
brain that have been long tied to Alzheimer's disease.
The new study reinforces the idea that habits that are good for the body are also good for the
brain, says Merrill — and that they seem to have an impact on
abnormal protein buildup «for years, if not decades, prior to the diagnosis of Alzheimer's disease.»
Scientists have identified a basic pathologic process underlying Alzheimer's development that involves the formation of
abnormal protein deposits in the
brain known as beta - amyloid plaques, but they still aren't entirely sure what causes this to happen.
These findings clearly show that when taken orally as a supplement in moderate doses (1,000 mg and 4,000 mg / day is what was used in the study), curcumin has the ability to effectively pass into the
brain, bind to
abnormal proteins, and assist the body in their breakdown and excretion.
Parkinson's is due to degeneration of the
brain's dopamine area; parkinsonism is caused primarily by
abnormal clumping of
proteins called alpha - synuclein.
Alzheimer's Disease involves the accumulation of
abnormal protein — either amyloid beta or Tau
protein which gums up the
brain system.
As a result the mutated and damaged genes start making
abnormal proteins which trigger formation of destructive plagues in the
brain and symptoms of AD.
Although there is still a lot to learn about pathogenesis (the mechanism by which a disease is caused) of Alzheimer's yet we know that during Alzheimer's two
abnormal proteins are made by mutated genes of the
brain cells.