Articles tagged with Tau Proteins
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Researchers genetically engineered Toxoplasma gondii to produce and release therapeutic proteins in the human brain, bypassing the blood-brain barrier. The method has potential implications for treating diseases caused by protein deficiencies or abnormal expression.
Researchers discovered elevated levels of neurofilament light chain protein in Parkinson's disease and dementia with Lewy bodies, suggesting potential early detection methods. The study found different protein patterns between the prodromal stage and established diseases.
Researchers found that combining plasma p-tau217 and Aβ42/40 levels could predict early brain Aβ accumulation in people with subthreshold Aβ accumulation. These biomarkers may help screen participants for primary prevention trials.
Researchers from Jilin University provide a comprehensive overview of brain injury biomarkers, including neuron-specific enolase, ubiquitin C-terminal hydrolase-L1, and neurofilament proteins. These biomarkers can help identify brain injuries and predict disease progression.
Researchers have determined the structure of molecules within an Alzheimer's disease brain for the first time using cryo-electron tomography and fluorescence microscopy. This study revealed the molecular structure of tau protein and its arrangement with amyloid plaques, providing new insights into the pathology of the disease.
Researchers have discovered a new diagnostic method for PSP by analyzing protein biomarkers in spinal fluid, which could lead to earlier diagnosis and targeted therapies. The high-throughput technology allows for the measurement of thousands of proteins in a tiny drop of fluid, providing a promising solution for identifying the condition.
Researchers have developed a new nonhuman primate model that allows for the tracking and treatment of early-stage Alzheimer's disease. The study shows a six-month window in which disease progression can be measured, enabling preclinical testing of interventions targeting the tau protein.
Researchers have developed a blood test that can detect rare forms of dementia, such as frontotemporal dementia (FTD) and progressive supranuclear palsy (PSP), as well as amyotrophic lateral sclerosis (ALS). The test uses biomarkers, including tau and TDP-43 proteins, to identify underlying pathology.
Researchers at Johns Hopkins Medicine identified a potentially new biological target involving Aplp1, which drives the spread of Parkinson's disease-causing alpha-synuclein. The findings suggest targeting this interaction with drugs could slow Parkinson's disease progression and other neurodegenerative diseases.
Researchers used machine learning to integrate high-throughput transcriptomic, proteomic, metabolomic, and lipidomic profiles to identify four distinct molecular profiles of Alzheimer's Disease. These profiles were associated with varying levels of cognitive function and neuropathological features.
Researchers found that boosting mitochondrial health can combat protein clumping linked to both aging and Alzheimer's. The study identifies a core insoluble proteome enriched with numerous proteins not previously considered, offering new targets for exploration.
A new study reveals that people with Down syndrome are more prone to developing Alzheimer's disease due to the presence of an extra chromosome 21, which leads to increased amyloid deposits. As a result, cognitive decline occurs in their 50s, whereas autosomal dominant Alzheimer's typically starts later in life.
Researchers found TDP-43 drives nerve damage after injury and blocking cell surface protein KCNJ2 can correct faulty TDP-43, curbing nerve death. The study provides insights into traumatic brain injury and potential prevention methods.
A traumatic brain injury quadruples the risk of developing dementia and neurodegenerative diseases like ALS. USC scientists used lab-grown human brain structures called organoids to study TBI's effects. They identified a gene, KCNJ2, that helps protect nerve cells against injury.
A new blood test has been shown to diagnose Alzheimer's disease pathology as accurately as FDA-approved spinal fluid tests, making early diagnosis and treatment accessible to more people. The blood test measures levels of Alzheimer's proteins in the blood, detecting molecular signs of the disease even before symptoms appear.
A new blood test uses the biomarker BD-tau to predict functional outcomes in patients after ischemic stroke. Higher levels of BD-tau are associated with more severe outcomes.
Researchers found GV1001 decreases BACE and Aβ1-42 levels, reducing neurodegeneration and senescence in 3xTg-AD mice. It also increases survival, telomere length, and telomerase activity, contributing to improved lifespan.
Researchers connected cognitive and behavioral symptoms to protein buildup in the brain marking the disease. The study showed a clear relationship between CTE pathology and severity of cognitive and functional symptoms during life.
Researchers at Buck Institute for Research on Aging propose an alternate strategy for reversing memory problems in Alzheimer's disease by targeting the KIBRA protein. The findings suggest that KIBRA can rescue mechanisms that promote synapse resilience, potentially leading to improved memory function.
Researchers at Northwestern University have discovered that toxic short RNAs contribute to neuron death and DNA damage in Alzheimer's disease. Studies found that older individuals with superior memories have higher amounts of protective short RNA strands in their brains.
Dutch scientists identified five distinct biological variants of Alzheimer's disease through cerebrospinal fluid proteomics. These variants differ in protein production, immune system function and nerve cell growth, affecting disease progression and treatment responses.
Researchers at the University of Virginia Health System discovered that tau proteins damage brain cells by warping their nuclei, altering gene function and increasing tau production. This finding could lead to new treatments for Alzheimer's disease and other tauopathies.
Researchers found that a rare genetic mutation in the APOE gene, known as the Christchurch mutation, may prevent Alzheimer's dementia by severing the link between amyloid and tau accumulation. This discovery offers new hope for preventing the disease.
Researchers found lower levels of serotonin transporter and higher levels of amyloid-beta protein in brains of people with mild cognitive impairment, a potential target for treatments to slow or stop disease progression. Further research is needed to study the role of serotonin in disease progression.
Researchers investigate whether Tau proteins play a previously unsuspected role in energy management of neurons, potentially leading to new treatment options. The study aims to clarify the role of Tau in energy management and explore novel approaches to develop it into a target for therapies.
Tau protein forms nano-biomolecular condensates that dynamically cluster recycling synaptic vesicles, influencing synaptic function. This study highlights the importance of protein mapping in understanding neural transmission and synaptic plasticity.
A new study has identified specific genes associated with diet and brain structure in kingfishers, which are capable of diving at high speeds. The findings suggest that these birds have evolved unique traits to protect their brains from concussive forces.
A new trial combining an Alzheimer's medication with two other drugs may amplify its effects and arrest disease progression. The trial, funded by a $150M grant, will recruit 900 participants with early-onset Alzheimer's.
Scientists have identified a long non-coding RNA called SNHG8 that plays a crucial role in the development of toxic protein tangles in brain diseases like Alzheimer's. Replacing this RNA can prevent stress granule formation, which contributes to tau aggregation and brain damage.
Researchers identified a link between SARS-CoV-2 infection and Alzheimer's disease-like cognitive symptoms, triggered by Tau protein hyperphosphorylation. The study found increased Tau levels in infected cells, indicating pathological alterations to the protein.
A new blood-based test called p-tau217 has shown great promise in identifying Alzheimer's disease by stratifying patients into low, intermediate, and high-risk groups. The two-step workflow reduces the need for confirmatory testing in uncertain cases.
Researchers found that endogenous retroviruses, naturally present in the human genome, can influence the spread of tau aggregates between cells. This suggests that viral proteins could be potential targets for therapies to stop or slow neurodegeneration.
A new imaging technique, tau PET, has been shown to predict cognitive decline in Alzheimer's patients with greater accuracy than current methods. This breakthrough could lead to earlier diagnosis and treatment, improving patient outcomes.
A study published in Annals of Neurology suggests that a protein in spinal fluid can predict mild cognitive impairment and dementia years before symptoms appear. The findings may offer new targets for treating or preventing Alzheimer's disease and other dementias.
Researchers found that compounds in espresso, such as caffeine and trigonelline, can inhibit tau protein aggregation, a process linked to Alzheimer's. The study suggests potential benefits for neurodegenerative diseases.
The latest Alzheimer's drug, donanemab, has shown encouraging results in slowing cognitive decline by 35% compared to placebo in patients with low-to-intermediate levels of tau. However, its effectiveness is limited for those with more advanced disease, and risks include serious side effects such as amyloid-related imaging abnormalities.
A new biomarker, MTBR-tau243, tracks Alzheimer's disease progression by measuring levels of a specific form of tau in cerebrospinal fluid. The finding has major implications for diagnosing and staging the disease, and could accelerate the development of effective treatments.
ClearTau overcomes limitations of previous methods by producing Tau fibrils efficiently and consistently. This allows researchers to study the development of tauopathies and develop disease-specific therapeutics.
Researchers at Tel Aviv University have developed a novel approach to fight cancer by inducing cancer cells to produce a toxic protein using mRNA molecules. The treatment was successful in eliminating 44-60% of cancer cells in animal models, with no damage to healthy cells.
Researchers found that a combination of amyloid burden and blood markers of abnormal astrocyte activation can predict Alzheimer's disease progression. Testing for these biomarkers may help identify patients at risk, enabling earlier diagnosis and treatment.
Researchers have identified a novel model and therapy to mitigate the development of REM sleep behavior disorder, which affects over 3 million Americans. Dual orexin receptor antagonists have been shown to significantly reduce dream enactment behaviors, providing a promising new treatment option.
Researchers have discovered that toxic proteins, known as tau oligomers, are transported through synapses and contribute to the decline in brain function. The study found small clumps of tau oligomers inside synapses, which can spread through the brain and lead to neuron death.
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 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.
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.
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.