Articles tagged with Tau Proteins
A repurposed HIV drug has been found to restore the brain's autophagy function, helping prevent build-up of misfolded proteins and slowing disease progression in mouse models of Huntington's disease and dementia. This discovery provides clues to how this process could be slowed or prevented in humans.
A new genetic therapy, BIIB080, has been shown to safely lower levels of the harmful tau protein in patients with Alzheimer's disease. The trial found a greater than 50% reduction in tau protein concentrations after 24 weeks in treatment groups.
Targeting a specific antiviral pathway may one day offer a new way to treat or delay cognitive decline in Alzheimer's and frontotemporal dementia. Researchers found that inhibiting a key enzyme called cGAS can help neurons become resilient to tau protein buildup, a hallmark of these diseases.
Researchers have identified a possible way to help break the cycle between sleep disturbances and Alzheimer's disease. A small study found that people who took a sleeping aid experienced a drop in key Alzheimer's proteins.
Researchers at MIT have found a way to reverse neurodegeneration and symptoms of Alzheimer's disease by interfering with an overactive brain enzyme called CDK5. The peptide treatment reduced neurodegeneration, DNA damage, and improved behavior in mice with Alzheimer's.
Researchers at the University of Helsinki discovered a potential treatment for Alzheimer's disease and frontotemporal dementia using a PREP inhibitor. The PREP inhibitor reduced Tau accumulation and toxicity in cellular models and mice with tauopathy, improving cognitive skills.
Researchers at Karolinska Institutet have discovered that a type of sugar molecule in blood is associated with the level of tau protein, a critical factor in severe dementia. Measuring blood glycan levels can predict Alzheimer's disease risk to 80% accuracy, almost a decade before symptoms appear.
A new study from Mass General Brigham researchers found that early menopause may be a risk factor for Alzheimer's disease dementia. However, women who received hormone therapy around the time of menopause onset did not experience an increased risk of dementia. The study suggests that timing is crucial when it comes to hormone therapy, ...
A study by Washington University School of Medicine suggests targeting T cells to prevent neurodegeneration and treat Alzheimer's disease. The research indicates that microglia partner with T cells to cause brain damage in the disease, and blocking their entry can avoid most neurodegeneration.
Researchers at UTHSC are working on a project to find the first therapeutic intervention to prevent frontotemporal dementia or slow its progression in a mouse model linked with the condition. They aim to use DNAzymes to target pathological tau aggregates, which cause cognitive impairment and progressive neuropathological symptoms.
Researchers at Washington University in St. Louis have developed a non-invasive method called sonobiopsy that uses focused ultrasound to release neurodegenerative biomarkers into the blood, facilitating diagnosis of conditions like Alzheimer’s disease. The technique has shown promising results in releasing tau proteins and another biom...
Researchers have developed a novel blood-based biomarker, brain-derived tau (BD-tau), that specifically measures non-phosphorylated tau originating from the brain. This breakthrough addresses an unmet need for a blood test that tracks neurodegenerative changes in Alzheimer's disease but not in other dementias.
A recent study suggests that the gut microbiome affects brain behavior, immune cells and neurodegeneration. Altering the gut microbiome could be an effective way to prevent or treat neurodegenerative diseases like Alzheimer’s.
A new nanopore-based sensing device explores the aggregation of tau and tubulin proteins in neurodegenerative diseases such as Alzheimer's and Parkinson's. The device provides volume information about protein molecules and their states at the single-molecule level, offering insights into protein binding and aggregation.
Researchers at UT Health San Antonio identified a new inflammatory trigger in Alzheimer's disease and progressive supranuclear palsy, involving 'jumping genes' that form double-stranded RNA mimicking viral infections. This discovery opens new doors for understanding astrocyte biology and their role in transposable element control.
A new biomarker test, called BD-tau, can detect Alzheimer's disease neurodegeneration in blood samples with high accuracy. The test outperforms current methods and correlates well with CSF biomarkers, providing a valuable tool for improved diagnosis and clinical trial design.
A new biomarker has been identified with up to 89% accuracy for corticobasal degeneration, a primary tauopathy. The discovery could accelerate progress toward therapies for this rare brain disease, which is often misdiagnosed due to similar symptoms.
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 from Indiana University School of Medicine identified the protein bassoon as a key contributor to tau neurotoxicity in Alzheimer's disease. The study found that bassoon stabilizes the tau seed, allowing it to propagate in the brain and exacerbate neurodegeneration.
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.