The Brain: Alzheimer's and dementia news and discussions

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Deterioration of brain cells in Parkinson's disease is slowed by blocking the Bach1 protein, preclinical study shows
https://medicalxpress.com/news/2021-10- ... sease.html
by Medical University of South Carolina
Parkinson's disease (PD) is the most common neurodegenerative movement disorder, afflicting more than 10 million people worldwide and more than one million Americans. While there is no cure for PD, current therapies focus on treating motor symptoms and fail to reverse, or even address, the underlying neurological damage. In a new study, researchers at the Medical University of South Carolina (MUSC) have identified a novel role for the regulatory protein Bach1 in PD. Their results, published on Oct. 25 in the Proceedings of the National Academy of Sciences, showed that levels of Bach1 were increased in postmortem PD-affected brains, and that cells without Bach1 were protected from the damages that accumulate in PD. In collaboration with vTv Therapeutics, they identified a potent inhibitor of Bach1, called HPPE, that protected cells from inflammation and the buildup of toxic oxidative stress when administered either before or after the onset of disease symptoms.

"This is the first evidence that Bach1 is dysregulated in Parkinson's disease," said Bobby Thomas, Ph.D., professor of Pediatrics in the College of Medicine and the SmartState COEE Endowed Chair in Pediatric Neurotherapeutics.

In PD, brain cells that produce the chemical messenger dopamine begin to die as the disease progresses, resulting in tremors and other disruptions to motor function. Additionally, as we age, neurons accumulate damage through inflammation and the buildup of toxic oxidative stress.
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A diet of essential amino acids could keep dementia at bay
https://medicalxpress.com/news/2021-10- ... entia.html
by The National Institutes for Quantum Science and Technology
Dementia—a condition involving the extreme loss of cognitive function—is caused by a variety of disorders, including Alzheimer's disease. According to World Health Organization estimates, approximately 10 million individuals worldwide develop dementia every year, indicating the high psychological and social impact of this condition. Dementia mainly affects older people, and so far, simple and effective strategies for preventing this condition have remained elusive.

In a recent study published in Science Advances, Japanese researchers showed that a low protein diet can accelerate brain degeneration in mouse models of Alzheimer's disease. More importantly, they found that Amino LP7—a supplement containing seven specific amino acids—can slow down brain degeneration and dementia development in these animals. Their work expands on previous studies, which have demonstrated the effectiveness of Amino LP7 in improving cognitive function.

Dr. Makoto Higuchi from the National Institutes for Quantum Sciences and Technology, one of the lead scientists on the study, explains, "In older individuals, low protein diets are linked to poor maintenance of brain function. Amino acids are the building blocks of proteins. So, we wanted to understand whether supplementation with essential amino acids can protect the brains of older people from dementia, and if yes, what mechanisms would contribute to this protective effect."

First, the researchers studied how a low protein diet affects the brain in mouse models of Alzheimer's disease, which generally demonstrate neurodegeneration and abnormal protein aggregates called "Tau" aggregates in the brain. They found that mice consuming a low protein diet not only showed accelerated brain degeneration but also had signs of poor neuronal connectivity. Interestingly, these effects were reversed after supplementation with Amino LP7, indicating that the combination of seven specific amino acids could inhibit brain damage.
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Scientists identify the cause of Alzheimer's progression in the brain
https://medicalxpress.com/news/2021-10- ... brain.html
by University of Cambridge
For the first time, researchers have used human data to quantify the speed of different processes that lead to Alzheimer's disease and found that it develops in a very different way than previously thought. Their results could have important implications for the development of potential treatments.

The international team, led by the University of Cambridge, found that instead of starting from a single point in the brain and initiating a chain reaction which leads to the death of brain cells, Alzheimer's disease reaches different regions of the brain early. How quickly the disease kills cells in these regions, through the production of toxic protein clusters, limits how quickly the disease progresses overall.

The researchers used post-mortem brain samples from Alzheimer's patients, as well as PET scans from living patients, who ranged from those with mild cognitive impairment to those with full-blown Alzheimer's disease, to track the aggregation of tau, one of two key proteins implicated in the condition.
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Researchers investigate role of gene associated with Alzheimer's disease in brain's immune cells
https://medicalxpress.com/news/2021-11- ... brain.html
by Indiana University School of Medicine
When immune cells move throughout the brain, they act as the first line of defense against viruses, toxic materials and damaged neurons, rushing over to clear out them.

Researchers at Indiana University School of Medicine have been investigating how these immune cells in the brain—microglia—relate to a gene mutation recently found in Alzheimer's disease patients. They published their findings today in Science Advances.

The study, led by Hande Karahan, Ph.D., postdoctoral fellow in medical and molecular genetics, and Jungsu Kim, Ph.D., the P. Michael Conneally Professor of Medical and Molecular Genetics, found that deleting the gene—called ABI3—significantly increased amyloid-beta plaque accumulation in the brain and decreased the amount of microglia around the plaques.

"This study can provide further insight into understanding the key functions of microglia contributing to the disease and help identify new therapeutic targets," Karahan said.Karahan based her research on a human genetics study of more than 85,000 people—fewer than half were Alzheimer's patients—that identified the mutation in the ABI3 gene. Researchers concluded this mutation increased the risk of late-onset Alzheimer's.
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Vascular defects appear to underlie the progression of Parkinson's disease
https://medicalxpress.com/news/2021-11- ... sease.html
by Georgetown University Medical Center

In an unexpected discovery, Georgetown University Medical Center researchers have identified what appears to be a significant vascular defect in patients with moderately severe Parkinson's disease. The finding could help explain an earlier outcome of the same study, in which the drug nilotinib was able to halt motor and non-motor (cognition and quality of life) decline in the long term.

The researchers say their finding, detailed in a study published November 12, 2021, in Neurology Genetics, suggests that blood vessel walls called the blood brain barrier, which normally act as a crucial filter to protect the brain against toxins as well as allow passage of nutrients to nourish it, doesn't work correctly in some Parkinson's patients: It prohibits toxins from leaving the brain and inhibits nutrients such as glucose from entering. Perhaps even more damaging, the dysfunctional barrier allows inflammatory cells and molecules from the body to enter and damage the brain.

The research, the first longitudinal study to use such advanced genomics, now provides investigators with a new target for therapeutic intervention in Parkinson's disease, says the study's senior author, Charbel Moussa, MBBS, Ph.D., director of the Medical Center's Translational Neurotherapeutics Program.
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Huntington's disease: The ultrastructure of huntingtin inclusions revealed
https://medicalxpress.com/news/2021-11- ... sions.html
by Ecole Polytechnique Federale de Lausanne
Huntington's disease is a progressively debilitating brain disease that causes uncontrolled movements, psychological problems, and loss of cognition. Huntington's is caused by a mutation in the gene that encodes huntingtin, a protein that normally plays important roles in keeping brain cells healthy and active. But the mutation gives huntingtin an abnormally long tail of glutamine amino acids, which cause huntingtin to aggregate inside neurons and eventually kill them.

These aggregates, or inclusion bodies, of huntingtin have been the subject of a lot of research efforts in the attempt to find a way to understand and treat Huntington's. What has been missing, though, is a deep analysis of the inclusions' ultrastructure—a term that describes the level of structure that lies beyond the capacity of a conventional microscope to observe.
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Researchers identify new biomarker of Alzheimer's disease
https://medicalxpress.com/news/2021-11- ... sease.html
by University of Texas at Dallas
A study of large-scale functional brain network organization and educational history, led by researchers at the Center for Vital Longevity (CVL), has identified a new biomarker of Alzheimer's disease. The findings, published online this week in Nature Aging, describe how declines in a measure of brain network organization precede cognitive impairment in older adults. Researchers also found that brain network declines are greater among individuals without a college education, suggesting that there are aspects of an individual's environment that may accelerate brain aging.

"What's exciting about this study is that we've identified a measure of brain function that seems to be sensitive to an individual's past and present environmental exposures during adulthood. That brain network organization is also uniquely related to the prognosis of dementia, which opens up the possibility of incorporating the measure with other markers of Alzheimer's disease risk and pathology in a clinical setting," says Dr. Gagan Wig, director of the Wig Neuroimaging Lab at the CVL and associate professor at The University of Texas at Dallas.
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Targeting the brain's immune cells may help prevent or treat Alzheimer's disease
https://medicalxpress.com/news/2021-12- ... sease.html
by Weill Cornell Medical College
A gene mutation linked to Alzheimer's disease alters a signaling pathway in certain immune cells of individuals with the disease, according to a new study by scientists at Weill Cornell Medicine. The team also found that blocking the pathway—with a drug that's currently being tested in cancer clinical trials—protects against many features of the condition in a preclinical model. The results could lead to new strategies to block the development of Alzheimer's disease or slow its progression.

The study, published Dec. 1 in Science Translational Medicine, focused on microglia, immune cells of the central nervous system that are the first to respond when something goes wrong in the brain. Studies have identified many genetic variants linked to Alzheimer's disease that are highly expressed in microglia, providing compelling evidence that alterations within these cells may play a role in the disease's onset and progression.

"Microglia are guardians of the brain under healthy conditions, but can turn detrimental in disease conditions. Our goal is to identify how they become toxic and contribute to Alzheimer's disease pathogenesis and whether we can identify immune modulators to reverse the toxicity without diminishing their normal protective function," said senior author Dr. Li Gan, director of the Helen and Robert Appel Alzheimer's Disease Research Institute and the Burton P. and Judith B. Resnick Distinguished Professor in Neurodegenerative Diseases in the Feil Family Brain and Mind Research Institute at Weill Cornell Medicine.
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Compound shows promise for minimizing erratic movements in Parkinson's patients
https://medicalxpress.com/news/2021-12- ... inson.html
by Texas Biomedical Research Institute
A new study from Texas Biomedical Research Institute (Texas Biomed) and collaborators has identified a promising drug candidate to minimize uncontrolled, erratic muscle movements, called dyskinesia, associated with Parkinson's disease.

The small molecule, called PD13R, reduced dyskinesia by more than 85% in the marmoset animal model of Parkinson's disease. Additionally, the animals got much better sleep taking this compound compared to another drug often prescribed for dyskinesia. The results were published in the journal Experimental Neurology.

Dyskinesia is a common side effect in patients with Parkinson's disease. It is not a symptom of the disease itself, but typically emerges about five years into taking levodopa, the leading medication used to restore balance, reduce shaking and manage other motor control issues patients experience.

"Levodopa is amazing, it works like magic, but it has side effects. If we can eliminate these side effects, it could change the life of patients with Parkinson's," says Marcel Daadi, Ph.D., an associate professor at Texas Biomed and lead paper author.
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Three-dimensional X-ray image spotlights neurodegenerative disease
https://medicalxpress.com/news/2021-12- ... ative.html
by Göttingen University
What changes occur in parts of the brain affected by neurodegenerative disease? How does the structure of the neurons change? Some pathological changes in the tissue are easy to identify using standard microscopy. For example, the protein deposits known as "plaques," which occur in Alzheimer's disease, can be seen with staining techniques. However, pathological changes can also be of a more subtle nature and easily missed unless there is a complete digitilisation and analysis of the three-dimensional structure. Researchers at the University of Göttingen and University Medical Center Göttingen have now found a new technique to measure and quantify neuronal tissue architecture in three dimensions and at high resolution, which enabled them to identify changes in neurons in Alzheimer's. The results were published in the Proceedings of the National Academy of Sciences (PNAS).

The team developed a special X-ray imaging method that enabled them to detect a previously unknown transition in neuronal cell nuclei in tissue samples from the hippocampus of Alzheimer's patients. The changes indicate altered activity of neurons. The scientists examined neuronal tissue from the hippocampus, a brain region where memories are transferred from short-term to long-term memory. Chemically fixed tissue samples just a few millimeters wide were first X-rayed using phase-contrast tomography. The researchers used a special phase-contrast tomograph, which the team, led by Professor Tim Salditt from the Institute of X-ray Physics at the University of Göttingen, has set up at the PETRA III storage ring at the German Electron Synchrotron (DESY). The tomograph can be used to image tissue that only weakly absorbs X-rays, or not at all. This meant that large volumes of tissue could be recorded in their entirety, without damaging the samples and without time-consuming preparation.
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