The research focused on the biomarkers involved in the buildup
of brain plaques in the caudate and hippocampus.
The overabundance of this protein leads to the formation
of the brain plaques associated with Alzheimer's, the researchers believe.
«Structure
of brain plaques in Huntington's disease described.»
After three months of feeding, the mice had reductions in Aβ plaques of up to 70 percent in the hippocampus and up to 40 percent in the cortex, whereas mice fed capsules that contained lettuce leaves without CTB - MBP added and mice that were not fed any capsules did not have any reduction in evidence
of brain plaques.
In addition to speeding up the development
of brain plaques associated with Alzheimer's, a gene variant known as APOE4 also makes tau tangles — another signature of the disease — worse, researchers report online September 20 in Nature.
The «amyloid hypothesis» figures that a buildup
of brain plaque is what leads to the cognitive decline that Alzheimer's patients experience.
Not exact matches
For one, it would give them three specific biological markers to hone in on: The buildup
of beta amyloid and tau proteins, which cause
brain plaques associated with Alzheimer's, and
brain nerve cell death.
Mice that were given the drug showed reduced
plaque buildup in the
brain (a sign
of Alzheimer's) and overall improved memory.
After the night with disrupted sleep, the researchers found people had higher levels
of beta - amyloid proteins, the proteins that clump together and form the
plaque found in Alzheimer's - afflicted
brains, in the volunteers» spinal fluid.
A polyphenol called punicalagin is the anti-inflammatory agent in the fruit that vanquishes traces
of plaque that accumulates in the
brain cells.
It offers cardio protection, it helps lower bad cholesterol, it may help prevent the progression
of multiple sclerosis, it has the ability to regenerate
brain cells after a stroke, it has the ability to cross the blood -
brain barrier to potentially ward off Alzheimer's disease, apparently it's good at wiping amyloid
plaque from the
brain (which studies haves linked to Alzheimer's), it may help to prevent certain types
of cancer, and studies have shown that it inhibits cancer cell growth and metastases (meaning it keeps cancer from spreading).
Recent studies even show that
plaque that builds up in the
brain from unhealthy levels
of cholesterol may be one
of the most common reasons for Alzheimer's disease.
IN BRIEF Scientists have new evidence that suggests that THC inhibits the formation
of amyloid
plaques by blocking the enzyme in the
brain that produces them.
An essential factor for preventing the buildup
of this
plaque will be ensuring the
brain health throughout a person's life.
The actual process
of vascular aging may predispose a person's
brain to the increased amount
of amyloid
plaque buildup.
Studies at autopsy
of people who had dementia have detected many
of these so - called microvascular infarcts either by themselves or along with the
plaques and tangles more typical
of Alzheimer's in the
brains of people with dementia.
Ongoing studies at Uppsala University in Sweden have shown that the chemical agent dubbed Pittsburgh Compound - B, or PIB, is a highly accurate marker
of plaque buildup and that its abundance in the
brain can predict whether patients with mild cognitive impairment will develop Alzheimer's — and when that decline will likely start.
LACK
of sleep could accelerate the onset
of Alzheimer's disease by encouraging toxic
plaques to develop in the
brain.
«Amyloid is one
of many substances that builds up in
plaques as a result
of dying cells and atrophy in the
brain,» he says.
«
Brain cells from mice fed diets enriched with extra-virgin olive oil had higher levels
of autophagy and reduced levels
of amyloid
plaques and phosphorylated tau,» Dr. Praticò said.
Rats with
brain plaques develop further symptoms
of Alzheimer's when given nicotine.
In addition, compared to mice on a regular diet,
brain cells from animals in the olive oil group showed a dramatic increase in nerve cell autophagy activation, which was ultimately responsible for the reduction in levels
of amyloid
plaques and phosphorylated tau.
A composite biomarker score, created by combining two different ratios, predicted the presence or absence
of A-beta
plaques in the
brain with about 90 percent accuracy in both groups
of patients, the researchers found.
When Deter died five years later, an autopsy revealed that her
brain was riddled with strange tangles and
plaques of a fibrous material containing the remnants
of dead
brain cells.
In a study published online June 21 in the Annals
of Clinical and Translational Neurology, the researchers show that the consumption
of extra-virgin olive oil protects memory and learning ability and reduces the formation
of amyloid - beta
plaques and neurofibrillary tangles in the
brain — classic markers
of Alzheimer's disease.
But the
brains of 10 - month - old Alzheimer's mice that had a severely reduced amount
of an enzyme called BACE1 were essentially clear
of new and old
plaques.
A mouse engineered to have Alzheimer's disease and a gradual reduction in levels
of the
brain enzyme BACE1 stopped forming
plaques (arrows in the first panel) as it aged.
If a clump
of this tissue, called
plaque, breaks free, it can travel into the
brain and block a smaller blood vessel, causing a stroke.
The
brains of mice engineered to develop Alzheimer's disease were riddled with these
plaques, clumps
of amyloid - beta protein fragments, by the time the animals were 10 months old.
Alzheimer's mice with normal BACE1 levels experienced a steady increase in
plaques, clearly seen in samples
of their
brains.
Specifically, rodents genetically modified to express human amyloid precursor protein (hAPP), which can lead to the debilitating
plaques that form in the
brains of Alzheimer's patients, seem to struggle to find the hidden platform relative to their healthy peers.
IRON overload may accelerate Alzheimer's disease, according to research that also reveals the role
of beta - amyloid precursor protein (APP), which forms
plaques in affected
brains.
The HSP70 - boosted mice were much better than the others at finding their way around mazes, and post-mortems showed their
brains to be free
of the characteristic beta - amyloid
plaques that clog the
brains of people with Alzheimer's.
Subsequent analyses
of the
brains of these animals revealed that the drug reduced the
plaques and tangles in the hippocampus, which is known to play a key role in learning the water maze, but not in the amygdala, which figures importantly in the dark chamber test.
Previously, researchers have focused on the role
of protein deposits called amyloid
plaques that lodge in the
brain of Alzheimer's affected people.
Accumulations
of plaques and tangles in the
brains of patients with Alzheimer's disease were first observed more than a century ago.
The normal mice's
brain plaques seemed to be built from human A-beta protein, and the only source
of that was the blood
of the mutated partner mouse.
But these
plaques were also inside the
brains of the normal mice in the joined pairs.
Until recently, the only way to look at human
plaques was by analyzing the
brains of people who died from the disease — a challenge one scientist compared to looking at a car wreck and trying to puzzle out the accident's cause.
This aberrant
brain circuitry — the amyloid
plaques and tau tangles — became the twin hallmarks
of the disease that bears his name.
«Two individuals may harbor similar amounts
of amyloid
plaques and tau tangles in their
brains, but one may be completely healthy while the other may have severe memory loss and dementia,» he says.
Recent research also has illuminated how the deadly cascade that leads to
brain atrophy is set in motion: The buildup
of amyloid
plaques, working in tandem with certain gene mutations, sparks the formation
of the renegade tau proteins.
The pathological form is a misfolded version
of this molecule and known to initiate the formation
of toxic
plaques in the
brain.
To treat humans, researchers must still find a way to deliver the protein fragments past the blood -
brain barrier, which prevents circulating proteins from entering the
brain, and to the site
of the
plaques.
The UCLA researchers, led by David Eisenberg, director
of the UCLA - Department
of Energy Institute
of Genomics and Proteomics and a Howard Hughes Medical Institute investigator, report the first application
of this technique in the search for molecular compounds that bind to and inhibit the activity
of the amyloid - beta protein responsible for forming dangerous
plaques in the
brain of patients with Alzheimer's and other degenerative diseases.
In Alzheimer's disease,
plaques of amyloid beta protein accumulate in the
brain, damaging connections between neurons.
Because the protein is normally found outside
of blood vessels in the human
brain, this suggests that
plaques may form in a different way in chimps.
But Holtzman and other researchers previously demonstrated that
plaques of amyloid - beta protein build up faster in the
brains of APOE4 carriers (SN: 7/30/11, p. 9).
Rats with Alzheimer's
brain plaques go on to develop additional signs
of the disease when they are given nicotine
«Although previous research has shown that some head injury patients have these amyloid
plaques shortly after the incident, these findings suggest these
plaques are still present in the
brains of patients over 10 years later.