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tdp-43
1,157 studies tagged tdp-43, dated 1986-01-01 to 2026-09-25. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- What Do Sugar, Gila Monsters, and the Therapeutic Dance Have in Common With GLP-1RA, Stroke, and Dementia? 2026-09-25
- Myo-inositol as a spectroscopic marker of neuroinflammation in frontotemporal lobar degeneration 2026-09-20
- Laromestrocel preserves brain volume and cognitive function in Alzheimers disease by inhibiting neuroinflammation 2026-09-17
Studies
1,157 studies carry this tag.
Date range
1986 to 2026
Top journals
- The Journal of biological chemistry 109
- The Journal of neuroscience : the official journal of the Society for Neuroscience 42
- Proceedings of the National Academy of Sciences of the United States of America 39
- Neuron 28
- Nature 23
363 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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We identified 218 m6A sites significantly associated with the three diseases, highlighting 3,430 associations between m6A sites and gene expression.
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Loss-of-function mutations affecting the lysosomal protein progranulin are a leading cause of frontotemporal dementia.
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Autophagic markers beclin 1, LC3II and p62, and lysosome-related marker cathepsin B, all upregulated in AD astrocytes, were significantly reduced, while autophagic flux was rescued, by stabilizing 20 nm-MERCS.
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It has been demonstrated to have neuroprotective effects in cellular models of neurodegenerative diseases; however, its precise mechanism of action in alleviating tau pathology in Alzheimer's disease (AD), as well as its potential to improve cognitive deficits in animal models, has not yet been elucidated.
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Alzheimer’s disease (AD), the leading cause of senile dementia, lacks effective therapies.
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Extracellular vesicles (EVs) in plasma are composed of exosomes, microvesicles, and apoptotic bodies.
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Microglia-mediated neuroinflammation plays a crucial role in memory and cognitive deficits and the development of early mild cognitive impairment (MCI) associated with Alzheimer's disease (AD).
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Hippocampal and serum irisin levels were progressively reduced in CCH mice.
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Vascular dementia (VaD) is a neurodegenerative disorder characterized by chronic oxygen insufficiency, leading to the generation of oxygen-free radicals, inflammatory responses, disturbances in iron metabolism, lipid peroxidation, and other pathological changes that disrupt intracellular homeostasis.
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36/100
Aging is the greatest risk factor for learning and memory disorders; dementia prevalence significantly increases with age due to numerous molecular changes in the body.
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JOURNAL/nrgr/04.03/01300535-202606000-00056/figure1/v/2026-02-11T151048Z/r/image-tiff Cerebral small vessel disease is a major vascular contributor to cognitive impairment and dementia.
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Aβ 42 , TDP-43, and neurogranin show potential as blood-based biomarkers for cognitive decline and may provide insight into the pathogenesis of neurodegeneration.
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Transactive response DNA binding protein-43 (TDP-43)-mediated pathology is a hallmark of devastating neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
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The study included 356,173 participants (median age 56 years; 53.69% female).
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Extracellular vesicles (EVs) are membrane-enclosed nanoparticles released by most cell types, and from multiple sub-cellular compartments.
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High Resolution Image Download MS PowerPoint Slide Pathological aggregates of TDP-43 are implicated in Alzheimer’s disease, frontotemporal dementia, and amyotrophic lateral sclerosis.
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This study shows that WMHs do not significantly alter gray matter nicotinic signaling in directly connected regions.
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AMS-17 treatment improved cognitive function, enhanced blood-brain barrier (BBB) integrity, and promoted remyelination in VaD mice.
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Alzheimer disease (AD) is the most common form of dementia affecting more than 6 million people in the United States.
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Our results show that lecanemab exhibits high binding affinity to amyloid-β fibril structures that have a flexible N-terminus in common, as is the case for type I, type II and murine type III amyloid-β fibril polymorphs, which resemble or are identical to human structures observed in sporadic and familial cases of Alzheimer's disease, including a case with the Arctic (E22G) mutation.
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Nuclear clearance and cytoplasmic aggregation of TAR DNA-binding protein 43 (TDP-43) are observed in many neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
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TAR DNA-binding protein 43 (TDP-43) pathology is linked to the neurodegenerative disorders amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and Huntington disease (HD).
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The coronavirus disease 2019 (COVID-19) pandemic has been linked to long-term neurological effects with multifaceted complications of neurodegenerative diseases.
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Alzheimer’s disease (AD) remains a significant global health challenge with limited FDA-approved treatments, necessitating the search for novel preventive strategies.
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Alzheimer’s disease (AD) and related tauopathies such as frontotemporal dementia (FTD) or traumatic brain injury (TBI) are neurodegenerative disorders characterized by progressive loss of memory and cognitive function.
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Increased phosphorylation of TDP-43 is a pathological hallmark of several neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
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Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD) are two neurodegenerative disorders that share common genes and pathomechanisms and are referred to as the ALS-FTD spectrum.
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Both the Keto and ADF groups demonstrated significant weight loss, but cognitive performance improved most notably in the ADF group, in association with reduced inflammation.
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Alterations in transactivating response region DNA-binding protein 43 (TDP-43) are prevalent in amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and other neurological disorders.
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One of the major consequences of diabetes mellitus that has gained attention due to its rising incidence is cognitive impairment.
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Mitochondrial dysfunction plays a preponderant role in the development of Alzheimer disease (AD).
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At baseline, Aβ+ participants showed higher CP FWf, increased white matter hyperintensity (WMH) volume, and decreased diffusion tensor image analysis along the perivascular space (DTI-ALPS).
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The results showed that T. chuii extracts could protect neuronal cells from neurotoxic damage, especially against L-glutamate and H2O2.
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Presenilin 1 (PSEN1) mutations are the leading cause of early-onset Alzheimer disease (EOAD).
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46/100
TDP-43_SAA was positive in 29/65 patients with sporadic MND, 9/21 patients with genetic MND, 6/17 OND patients and 3/22 controls.
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Recent reports suggest dysregulation of the N6-methyladenosine (m6A) RNA modification may contribute to the pathology of neurodegenerative diseases.
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Brain deposition of transactive response DNA-binding protein 43 (TDP-43) is a feature of neurodegenerative syndromes.
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Mutations in the TARDBP gene encoding TDP-43 protein are linked to loss of function in neurons and familial frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS).
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Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy associated with repetitive head impact (RHI) exposure.
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Frontotemporal dementia is a debilitating neurodegenerative disorder characterized by frontal and temporal lobe degeneration, resulting in behavioral changes, language difficulties, and cognitive decline.
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41/100
Natural products (NPs) are considered to be the oldest medicine in human history and numerous NPs have been investigated to search for therapeutic agents in various diseases.
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Microglia are the resident immune cells in the brain and have pivotal roles in neurodevelopment and neuroinflammation 1,2 .
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TDP-43 protein is an RNA-binding protein linked to amyotrophic lateral sclerosis, frontotemporal dementia, and Alzheimer disease.
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We found that ICVIGF-1 administration protected working memory demonstrated as (1) reduced latency to reach the platform, and reduced swimming distance in trials 3 (p < 0.05) and 4 (p < 0.01) on days 45 and 90 post-injection and (2) a short-term (up to 45 days post-injection) enhancement of reference memory, manifested by a reduction in swimming distance and latency (p < 0.05).
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Alzheimer’s disease (AD), the term “dementia”, describes a specific neuropathology together with the development and progression of age-related cognitive and functional loss.
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43/100
We identified a significant genome-wide association with p-S65-Ub for rs429358 (apolipoprotein E ε4 [APOE4]) and a suggestive association for rs6480922 (ZMIZ1).
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35/100
Neurodegeneration in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) results from both gain of toxicity and loss of normal function of the RNA-binding protein TDP-43, but their mechanistic connection remains unclear.
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40/100
Repulsive guidance molecule-a (RGMa) has emerged as a significant therapeutic target in a variety of neurological disorders, including neurodegenerative diseases and acute conditions.
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Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD) are overwhelmingly linked to TDP-43 dysfunction.
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BackgroundAlzheimer's disease (AD) causes cognitive function disorder and has become the preeminent cause of dementia.
From across this tag
10 of the 1,153 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Null mutations in progranulin cause ubiquitin-positive frontotemporal dementia linked to chromosome 17q21
- Cryptic splicing in synaptic and membrane excitability genes links TDP-43 loss to neuronal dysfunction
- Calcineurin/NFAT Signaling in Activated Astrocytes Drives Network Hyperexcitability in Aβ-Bearing Mice
- Histological and imunohistochemical alterations of hippocampus and prefrontal cortex in a rat model of Alzheimer like-disease with a preferential role of the flavonoid "hesperidin"
- LINE-1 retrotransposition in a mouse TDP-43 model of neurodegeneration marks motor cortex neurons for cell-intrinsic and cell non-autonomous programmed cell death
- Deficiency in LRP6-mediated Wnt signaling contributes to synaptic abnormalities and amyloid pathology in Alzheimer's disease
- Genome-wide association study identifies two loci influencing plasma neurofilament light levels
- Alpha-synuclein is part of a diverse and highly conserved interaction network that includes PARK9 and manganese toxicity
- Astrocytes produce the antiinflammatory and neuroprotective agent hydrogen sulfide
- Microbial translocation is associated with increased monocyte activation and dementia in AIDS patients