Articles tagged with Tau Proteins
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A recent study reveals that Down syndrome brains develop the same amyloid beta and tau prions as Alzheimer's disease, causing neurological dysfunction. With over 50% of people with Down syndrome developing Alzheimer's by age 40, this discovery offers new insights into the common underlying causes of these two diseases.
Researchers at Washington University School of Medicine studied 350 people to understand how Alzheimer's disease affects the brain. The study found that gene APOE is active in the areas most damaged by the disease, leading to symptoms like language and vision problems.
Researchers at Lund University have discovered that people with Alzheimer's disease can be identified before symptoms appear, using PET scans to visualize tau and amyloid proteins in the brain. Participants found to have these biomarkers were at a 20-40 times higher risk of developing cognitive decline in the next few years.
Researchers have identified a new biomarker, p-tau198, that could help diagnose Alzheimer's disease earlier than current tests. This biomarker shows promise in distinguishing AD from other neurodegenerative diseases and mild cognitive impairment.
Amanda Woerman's research aims to disrupt tau misfolding, a common thread in fatal neurodegenerative disorders PSP and CBD. The grant-funded study seeks to test a proof-of-concept gene therapy for these conditions, potentially leading to personalized medicine breakthroughs.
Researchers found lower serum TDP-43 levels in patients with C9orf72 repeat expansion or motoneuron disease, distinguishing them from other FTD subtypes. This study suggests TDP-43 as a potential biomarker for diagnosing specific FTD subtypes, enabling patient-specific interventions.
Scientists uncover mechanism controlling cellular levels of tau, a protein linked to devastating neurodegenerative diseases. Overexpression of specific form of numb protein Numb-72 decreases tau levels and slows neuron loss in animal models.
Researchers at Brigham and Women's Hospital identified ganglioside GM2 activator (GM2A) as a protein that may contribute to Alzheimer's disease progression. The protein reduces neuronal firing and induces loss of neurite integrity, suggesting its potential role in AD pathogenesis.
A mouse study found that female brains express higher levels of an X-linked enzyme called USP11, leading to greater accumulation of tau protein and increased vulnerability to Alzheimer's disease. The results suggest that excessive activity of USP11 drives this increased susceptibility in females.
The Keck School of Medicine of USC's Stevens INI has received a $149 million grant to study Alzheimer’s disease among diverse communities. The HABS-HD study aims to develop biomarkers that determine risk for developing the disease, addressing health disparities among Hispanic and African American populations.
Researchers used novel 3D imaging technology to study a human brainstem nucleus and found intriguing complexity and previously undescribed cellular forms of tau pathology. The study reveals dendritic atrophy as an early sign of tau-bearing neuron degeneration, potentially contributing to symptoms like sleep disturbances and anxiety.
Neurobiologists identified mechanisms underlying atypical protein tangles that kill neurons in neurodegenerative disorders. Engineering Drosophila adults with human Tau revealed a 'traffic jam' effect, where reduced retromer activity accelerates neurodegeneration. Inhibiting the shortened form of Tau could stall neuron loss.
New research reveals that tau protein can self-assemble to form an envelope around microtubules, compacting them and affecting how other proteins attach. This novel behavior may play a regulatory role in healthy brain tissue, bringing us closer to understanding its connection to disease.
A recent study has identified the tau protein's involvement in normal learning and memory processes in the healthy brain. The researchers used proximity labelling to map out all proteins that interact with tau and found that it interacts with enzymes controlling vesicles and cell surface receptors for neurotransmitters.
Researchers at UC San Diego have received a $1.3 million grant to study the role of misfolded tau proteins in causing neurodegenerative diseases like dementia. The team aims to develop new tools for understanding and treating these diseases, which affect nearly 6 million people worldwide.
Researchers have developed a new test that can detect even slightly elevated levels of tau protein in cerebrospinal fluid, potentially identifying Alzheimer’s disease at its earliest stages. The method uses optical sensors and 'lab-on-fiber' technology to achieve high sensitivity.
Researchers found reduced levels of Histone Deacetylase I (HDAC I) in the brains of patients with Alzheimer's disease, linked to deleterious effects of misfolded beta-amyloid and tau proteins. HDAC inhibitors, currently being tested against mild Alzheimer's disease, may be harming patients rather than helping them.
Research at Massachusetts General Hospital has identified plasma biomarkers Tau-PT217 and Tau-PT181 as predictors of postoperative delirium. High preoperative concentrations of these biomarkers are associated with increased risk, suggesting a potential early warning sign for patients.
A Flinders University study reveals how a protein called tau transforms into a disease state, providing hope for preventing this process and reducing toxic effects on brain cells. The researchers identified 'master sites' in tau that govern subsequent modifications, leading to a similar state seen in Alzheimer's patients.
Researchers at National Institutes for Quantum Science and Technology found that p62 selectively degrades toxic tau species, preventing neurodegenerative disorders. The study demonstrates the pivotal role of p62 in suppressing abnormal protein aggregates using mouse models of dementia.
A recent study published in eLife has revealed that high levels of soluble tau protein impair signaling between neurons, leading to cognitive decline. The research suggests that targeting the binding site of dynamin, a protein that binds to microtubules, may rescue synaptic transmission and prevent memory impairment.
Scientists at UC Santa Barbara have discovered a novel membraneless organelle called BAG2 condensate that can sweep up faulty proteins, including tau protein associated with Alzheimer's disease. The discovery could lead to new treatments for neurodegenerative conditions by targeting misfolded proteins before they cause damage.
Scientists at Gladstone Institutes have discovered that reducing protein tau levels soon after birth can prevent autism and epilepsy in an experimental model. The study pinpointed the crucial brain cells where tau levels must be reduced to avoid these problems, and showed that lowering tau is still effective when initiated after birth.
Research suggests that EMFs can cause Alzheimer's disease by building up calcium levels in brain cells. This increase leads to changes in the brain, which develop conditions for Alzheimer's. The study highlights the importance of reducing EMF exposure to prevent or delay the onset of Alzheimer's.
Researchers at UT Health San Antonio have identified a novel mechanism by which tau protein causes neurons to die, which can be altered pharmacologically. This discovery provides a new framework for studying vertebrate models of tauopathy and eventually clinical trials.
Researchers found that high levels of both amyloid and tau proteins impair memory functions, but only when amyloid burden is also high. The study suggests that anti-amyloid therapies may be beneficial in reducing memory impairment in the early stages of Alzheimer's disease.
Researchers at Lewis Katz School of Medicine identify reduced efficiency of protein transport system as key factor in Alzheimer-like changes. The study suggests that targeting the retromer complex could lead to new treatments for Down syndrome-related dementia.
Researchers have discovered a common thread between multiple neurodegenerative diseases, including Alzheimer's, dementia with Lewy bodies, and frontotemporal lobar degeneration. A protein called TMEM106B forms fibrils in diseased brain tissue, potentially hobbling cells.
Scientists have identified hundreds of proteins constantly transported throughout healthy brain cells, offering a new understanding of neurological diseases like Alzheimer's and autism. The discovery reveals how protein transport goes awry in these conditions, paving the way for future research into intercellular communication.
Researchers found that non-mutated Apolipoprotein E was strongly enriched in dementia patients' brains, correlating with dementia diagnosis. Even those without the disease-driving APOE ε4 allele showed significant levels of ApoE peptides.
A team of Weill Cornell Medicine investigators created a comprehensive atlas, called Tau interactome, that maps all the Tau protein's interactions with other proteins in human neurons. They found that mutations diminish Tau-mitochondrial protein interaction may hamper energy production and lead to cognitive decline.
Scientists have mapped the tau interactome, showing that mutant tau impacts mitochondria function in human neurons. The study also reveals a mechanism for tau release from neurons and its binding to mitochondrial proteins, which may inform future studies on preventing diseased tau spread.
Researchers at University of Wisconsin-Madison discovered that increasing Nrf2 gene expression in astrocytes protects neurons from Alzheimer's disease progression. Boosting Nrf2 slowed cognitive and physical decline, reduced beta-amyloid accumulation, and reversed genetic changes in mouse models.
A study published in the journal Brain found that boosting levels of the neurotransmitter norepinephrine with atomoxetine reduced markers of neuroinflammation and stabilized protein Tau, which forms neurofibrillary tangles in the brain. The treatment showed promising results in people with mild cognitive impairment.
An experimental drug called NAP has been found effective in treating a broad spectrum of symptoms related to autism, intellectual disability, and Alzheimer's disease. Researchers discovered that NAP normalizes brain function in mice modeling ADNP syndrome, a rare disorder linked to these conditions.
Researchers at Tel-Aviv University have shed light on the Sigma-1 receptor's topology and function in neurodegenerative diseases. The study reveals that the receptor is retained in the endoplasmic reticulum and its amino end faces the cytoplasm, providing a crucial mechanism for therapeutic approaches to alleviate suffering from ALS.
Researchers found that people with brain buildup but no dementia had normal tau protein, while those who developed plaques or tangles also had a different-handed form of tau. This suggests that a slowdown in autophagy, the process of clearing spent proteins, may be underlying cause of Alzheimer's disease.
A study published in Brain Pathology found elevated levels of tau protein in the brains of people with ALS who carry a mutation in the C9orf72 gene. The researchers also identified new genetic mutations in the tau gene and discovered that the ratio of different forms of tau protein may be an indicator of disease progression.
Researchers at Massachusetts General Hospital discovered that reducing abnormal tau can reverse mitochondrial dysfunction and oxidative stress in ALS. By targeting tau with a specific degrader, the study suggests a promising new treatment strategy for this degenerative disease.
Researchers are modifying an arm of a worldwide clinical trial to evaluate a combination of drugs targeting two brain proteins: amyloid and tau. The Tau NexGen Trial aims to test the effectiveness of these treatments in slowing disease progression by targeting both Alzheimer's disease pathologies.
Researchers found that glatiramer acetate improved cognitive behavior and reduced amyloid plaques in a mouse model of Alzheimer's disease. This study suggests therapies targeting the immune system could be effective in treating the disease.
Researchers found that Alzheimer's disease develops by replicating aggregates in individual brain regions, rather than spreading them. The study used human data and PET scans to track the aggregation of tau protein, a key player in the disease.
Scientists at Gladstone Institutes discovered that non-convulsive epileptic activity drives chronic brain inflammation in Alzheimer's models, which can be reversed by eliminating protein tau or using the anti-epileptic drug levetiracetam. This link between brain networks and immune cells may hold promising treatments for Alzheimer's di...
Researchers at Gladstone Institutes found that reducing tau levels impacts both excitatory and inhibitory cells, leading to a reduction in excitation-inhibition ratios. This effect counteracts diseases that cause abnormal increases in this ratio, potentially improving the brain's ability to perform its functions.
Michel Goedert's research focuses on protein aggregates in Alzheimer's and Parkinson's, providing deep insights into disease development. His work is essential for finding new treatments, as evidenced by his discovery of gene mutations leading to dementia.
Researchers have developed a novel mouse model that accurately replicates the pathological propagation of tau protein isoforms in Alzheimer's disease, corticobasal degeneration, and Pick's disease. The model shows endogenous expression of both 3R and 4R tau, which accumulates in brain regions characteristic of each disease.
Researchers found that early accumulation of tau proteins in the brain, measured by PET scanner, is more effective at predicting memory impairment than other biomarkers. The study suggests that tau PET should be recommended for clinical prognostic assessment of cognitive decline in Alzheimer's patients.
Researchers have developed a potential blood test to diagnose Alzheimer's disease using atomic force microscopy technology. The test analyzes protein fibers made up of beta-amyloid peptides and tau proteins, which accumulate in patients' blood cells, indicating the stage of the disease.
Scientists have found that misfolded tau protein accumulates RNA tags called N6-Methyladenosine (m6A) in nerve cells, leading to neurodegeneration. Inhibiting this RNA-tagging pathway shows promise as a potential approach to treat Alzheimer's disease.
Georgia State University researcher Vince Calhoun has received a $3.5 million grant to develop new methods for capturing dynamic connectivity in the brain and identifying biomarkers for early detection of Alzheimer's disease. The researchers aim to analyze real-time connectivity patterns to predict future cognitive decline.
A study found a significant association between higher tau concentrations and lower physical activity with increased cognitive decline rates in individuals with Alzheimer's disease. The research suggests that increasing physical activity may help slow cognitive decline.
Researchers discover that a slightly acidic environment is conducive to the formation of Alzheimer's disease-causing toxic protein aggregates, known as Aβ oligomers. The study also reveals that endosomes and lysosomes play a crucial role in their development.
Researchers at Tokyo Metropolitan University have discovered that disulfide bonds on certain amino acids stabilize tau protein, leading to its accumulation and triggering neurodegenerative diseases like Alzheimer's. The study suggests that targeting these chemical groups may lead to novel treatments to reduce or prevent tau accumulation.
A new international study has identified a drug that can halt the progression of chronic traumatic encephalopathy (CTE) in sportspeople who sustain repeated head injuries. The treatment was successfully tested in animal models and shows promise for preventing neurological problems associated with CTE, which affects cognition and behavior.
Understanding how tau protein is regulated in brain cells could lead to better treatments for Parkinson's and other neurological conditions. Researchers discovered that similar lncRNAs control the production of tau and other key proteins involved in brain function.
Researchers identify 'antisense long non-coding RNA' regulating tau protein production, a crucial mechanism for brain cell function. The discovery may lead to new treatments for dementia-related diseases, including Parkinson's and Alzheimer's.
Researchers discovered a correlation between decreased Rbbp7 levels and increased tau protein tangle formation in Alzheimer's brains. Restoring Rbbp7 levels reversed tangle formation and cell loss, offering a new avenue for effective treatments.
Scientists have found that a Mediterranean-like dietary pattern with high intake of vegetables, legumes, and fish may reduce protein deposits in the brain and prevent brain atrophy. The study suggests that adhering to this diet could lower the risk of Alzheimer's disease and dementia.
A University of Colorado Boulder study reveals that tau aggregates interfere with RNA splicing, leading to neurodegeneration in Alzheimer's disease and other tauopathies. The findings provide new insights into the mechanism of action of tau tangles, shedding light on potential therapeutic targets.
Research from Lund University in Sweden suggests that women accumulate Alzheimer's-related protein tau at a higher rate than men. The study found a 75% higher accumulation rate of tau in women compared to men in the temporal lobe affected by the disease.