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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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Processed foods are increasingly associated with the prevalence of neurodegenerative diseases, including Alzheimer disease (AD).
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Hippocampal pan-histone H3 crotonylation (H3Kcr) and H3K18cr were significantly upregulated in both 5xFAD and Aβ42-injected mice compared to controls.
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Late-onset Alzheimer disease (LOAD), the most common form of dementia among older adults, is a neurodegenerative disease characterized by brain amyloid-β (Aβ) plaque deposition and neurofibrillary tangles.
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Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are devastating neurodegenerative diseases that, despite the availability of symptomatic and modestly beneficial treatments, still lack therapies capable of halting disease progression.
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Alzheimer's disease (AD) and cancer are among the most devastating diseases worldwide.
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In AD-like mice surgery induced acute changes in amyloid-β; perioperative treatment with pVNS effectively reduced amyloid-β load, plaque sphericity, and neuronal loss.
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Frontotemporal dementia (FTD) is a group of early onset and progressive disorders, characterized by degeneration in the frontal and temporal lobes, and subsequent deterioration in cognition, personality, social behavior, and language, with aggregates of the RNA-binding protein TDP-43 being present in ~45% of the cases.
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39/100
Amyloid precursor protein (APP) is a key player in various neuronal functions but also the source for toxic Aβ that accumulates in the brain of Alzheimer patients.
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Autologous hematopoietic stem/progenitor cell (HSC)–gene therapy (GT) represents a promising therapeutic option for progranulin (PGRN)–related neurodegenerative diseases due to mutations in the PGRN encoding gene ( GRN ), such as frontotemporal dementia (FTD) and neuronal ceroid lipofuscinosis 11 (CLN11).
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AD patients exhibited increased expression of pyroptosis-related genes, supporting the involvement of pyroptosis in neurodegeneration.
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TAR DNA-binding protein 43 (TDP-43) dysfunction is a hallmark of several neurodegenerative diseases, including frontotemporal dementia, amyotrophic lateral sclerosis, and Alzheimer's disease.
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Methylglyoxal (MG), a reactive dicarbonyl metabolite associated with diabetes and metabolic disorders, contributes to carbonyl stress, neuroinflammation, and Alzheimer-like neurodegeneration.
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Tauopathies are neurodegenerative diseases characterized by accumulation of hyperphosphorylated tau protein (P-tau).
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Alzheimer's disease (AD) and vascular dementia (VaD) exhibit distinct neuropathological hallmarks, with AD defined by cortical amyloid plaques and neurofibrillary tangles, while VaD arises primarily from cerebrovascular disease (CeVD).
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Plasma Aβ levels and regional WMH burden are associated with glymphatic dysfunction as indicated by reduced ALPS.
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We show that TDP-43 activates GSK3 and promotes caspase-dependent cleavage of TDP-43, generating C-terminal fragments.
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Alzheimer's disease (AD) represents the most common cause of dementia and urgently requires sensitive biomarkers and effective therapies.
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Neuronal cytoplasmic aggregation and nuclear depletion of the TAR DNA-binding protein 43 (TDP-43) is the most characteristic pathology of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), causing toxicity through cytoplasmic gain and nuclear loss of function mechanisms.
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A key pathological feature of Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD) is the loss of nuclear localization and accumulation of cytoplasmic inclusions of TAR-DNA binding protein 43 (TDP-43).
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Intramembrane proteolysis by γ-secretase is critically implicated in Alzheimer disease pathogenesis by processing of its amyloid precursor protein substrate C99 into harmful amyloid-β peptide (Aβ) species.
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Cystatin C (CST3) colocalizes with amyloid-β (Aβ) around vessels in cerebral amyloid angiopathy (CAA).
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Epidemiological studies suggest that higher MedDiet adherence is associated with slower cognitive decline, reduced conversion from mild cognitive impairment to Alzheimer’s disease, and better motor and non-motor outcomes in Parkinson’s disease.
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: ACTB: actin, beta; AD: Alzheimer disease; ADAM10: a disintegrin and metallopeptidase domain 10; ADGGA: acyl diacylglyceryl glucuronide; AHexSIS: acylhexosyl sitosterol; AHexSTS: acylhexosyl stigmasterol; AIF1/IBA1: allograft inflammatory factor 1; APP: amyloid beta precursor protein; ATG5: autophagy related 5; Aβ: amyloid β-protein; BACE1: beta-site APP cleaving enzyme 1; BASulfate: bile acid sulfate; BMP: bismonoacylglycerophosphate; CAR: acylcarnitine; CE: cholesteryl ester; Cer_NS: ceramide non-hydroxyfatty acid-sphingosine; CL: cardiolipin; CMA: chaperone-mediated autophagy; DAPI: 4',6-diamidino-2-phenylindole; DCAE: esterified deoxycholic acid; DEP: differentially expressed protein; DG: diacylglycerol; DGCC: diacylglyceryl-3-O-carboxyhydroxymethylcholine; DLG4/PSD95: discs large MAGUK scaffold protein 4; ECM: extracellular matrix; EtherLPC: ether-linked lysophosphatidylcholine; EtherLPE: ether-linked lysophosphatidylethanolamine; EtherMGDG: ether-linked monogalactosyldiacylglycerol; EtherOxPC: ether-linked oxidized phosphatidylcholine; EtherPC: ether-linked phosphatidylcholine; EtherPE: ether-linked phosphatidylethanolamine; EtherPG: ether-linked phosphatidylglycerol; EtherSMGDG: semino lipid; EtherTG: ether-linked triacylglycerol; FA: fatty acyls; FA: free fatty acid; FAHFA: fatty acid ester of hydroxyl fatty acid; FJC: fluoro-Jade C; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GDCAE: esterified glycodeoxycholic acid; GFAP: glial fibrillary acidic protein; GL: glycerolipids; GP: glycerophospholipids; HBMP: hemibismonoacylglycerophosphate; HexCer_NS: hexosylceramide non-hydroxyfatty acid-sphingosine; HSPA8/HSC70: heat shock protein 8; IP-MS: immunoprecipitation-mass spectrometry; KEGG: Kyoto Encyclopedia of Genes and Genomes; LAMP1: lysosomal-associated membrane protein 1; LAMP2A: lysosomal-associated membrane protein 2A; LDGCC: lysodiacylglyceryl-3-O-carboxyhydroxymethylcholine; LDs: lipid droplets; LNAPE: N-acyl-lysophosphatidylethanolamine; LNAPS: N-acyl-lysophosphatidylserine; LPA: lysophosphatidic acid; LPC: lyso-phophatidylcholine; LPE: lysophosphatidylethanolamine; LPG: lysophosphatidylglycerol; LPI: lysophosphatidylinositol; LPS: lysophosphatidylserine; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MGDG: monogalactosyldiacylglycerol; MWM: Morris Water Maze; OA: oleic acid; OFT: Open Field Test; OxPC: oxidized phosphatidylcholine; OxPG: oxidized phosphatidylglycerol; OxPI: oxidized phosphatidylinositol; OxPS: oxidiz
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A total of 62 RCTs comprising 200,068 participants were included.
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Dysregulation of the TAR DNA-binding protein 43 (TDP-43), including intraneuronal cytoplasmic mislocalisation and aggregation is a feature of multiple neurodegenerative diseases including amyotrophic lateral sclerosis (ALS), frontotemporal lobar dementia (FTLD), limbic-predominant age-related TDP-43 encephalopathy (LATE) and alzheimer’s disease (AD).
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We demonstrate that irisin promotes the expression of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), glial cell line-derived neurotrophic factor (GDNF), α5 subunits of integrin receptors and LDH5α, and stimulates transient activation of ERK 1/2 in astrocytes.
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33/100
Barnes Maze Acquisition was performed on males (N = 4-5/genotype) after habituation and several days training.
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Vascular dementia is the second most common form of dementia.
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Compared to controls, MAO-B immunoreactive area fraction was significantly increased in the frontal cortex and white matter of AD, CBD, and especially PiD and FTLD-TDP, but not PSP.
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Chronic psychological stress is a well-known risk factor for neurodegenerative diseases including Alzheimer disease (AD), yet the underlying mechanisms remain unclear.
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Acute and chronic treatment of JRMS reduced TDP-25 aggregation in a dose-dependent manner by ∼75% in cells.
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Primary cortical neurons with C9orf72 haploinsufficiency exhibit alterations in dendritic branching, indicating disrupted neuronal connectivity.
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Pathological inclusions of the C-terminal domain (CTD) of TAR DNA binding protein-43 (TDP-43) are neurodegenerative hallmarks in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia, yet CTD's aggregation propensity complicates structural characterization of native TDP-43.
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Lewy body dementia (LBD), which includes Parkinson's disease dementia and dementia with Lewy bodies, is characterized by progressive cognitive decline, α-synuclein (α-Syn) aggregation, and concurrent microglial activation and neuroinflammation.
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Acupuncture ameliorated cognitive impairment in VD rats, reduced hippocampal neuronal damage and apoptosis, downregulated pro-apoptotic proteins (cleaved-caspase 3 and Bax), and upregulated anti-apoptotic Bcl-2.
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Neuro-inflammation was not reduced between the neflamapimod and placebo groups, and no change was observed in [18F]-DPA-714 PET.
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Recent evidence indicates the presence of micro- and nanoplastics in the human brain, with higher accumulation observed in patients with dementia.
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M1 specifically enhanced uptake of Aβ fibrils through reduction of intracellular cAMP levels, without affecting monomeric or oligomeric Aβ internalization.
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Dementia is a growing global health concern in aging societies, leading to a progressive decline in cognitive function that severely impairs daily life.
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Lewy body dementias (LBD), comprising dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD), are defined by misfolded α-synuclein aggregation.
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The pathological loss of nuclear TDP-43 is a hallmark of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), leading to extensive alterations in RNA metabolism and a broad number of neuronal transcripts.
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The findings demonstrate that administration of S1P analogs cP1P and P1P at 0.1 mg/kg and 1 mg/kg significantly reduced Aβ burden by inhibiting the amyloidogenic pathway and decreasing hyperphosphorylated tau protein levels in the mouse brain.
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41/100
Synaptic loss is strongly associated with cognitive decline in Alzheimer's disease (AD).
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33/100
Astrocytes are a source of IL-15 in AD, particularly near localized Aβ pathology, and neurons are poised to respond.
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This is primarily a mouse-model study (in amyloid-plaque mouse models such as 5xFAD, with some human tissue validation) identifying a newly recognized, protective state of brain immune cells (microglia) that expresses genes normally associated with the immune system's lymphocytes.
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Neurodegenerative disorders alter mitochondrial functions, including the production of reactive oxygen species (ROS).
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Chronic cerebral hypoperfusion (CCH) profoundly affects patient well-being and has been proposed as a risk factor for cognitive impairment and dementia.
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Two regions achieved genome-wide significance with TDP-43: apolipoprotein E (APOE) and TMEM106B. Three loci reached genome-wide significance with HS: APOE, TMEM106B, and granulin precursor (GRN).
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180 patients (46 %) developed delirium and 70% of these had dementia.
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Post-ischemic brain neurodegeneration with subsequent neuroinflammation is a major cause of mortality, permanent disability, and the development of Alzheimer’s disease type dementia in the absence of appropriate treatment.
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.
- Causal effect of infectious mononucleosis on neurodegenerative diseases: A Mendelian randomization study
- Resveratrol mediates mechanical allodynia through modulating inflammatory response via the TREM2-autophagy axis in SNI rat model
- Epileptic seizures induced by pentylenetetrazole kindling accelerate Alzheimer-like neuropathology in 5×FAD mice
- Microglial activation in the right amygdala-entorhinal-hippocampal complex is associated with preserved spatial learning in AppNL-G-F mice
- A novel dual GLP-1/GIP receptor agonist alleviates cognitive decline by re-sensitizing insulin signaling in the Alzheimer icv. STZ rat model
- Targeting the HDAC2/HNF-4A/miR-101b/AMPK Pathway Rescues Tauopathy and Dendritic Abnormalities in Alzheimer's Disease
- Netrin-1 interacts with amyloid precursor protein and regulates amyloid-beta production
- Induction of apolipoprotein E mRNA in the hippocampus of the gerbil after transient global ischemia
- Amyloid beta interaction with receptor for advanced glycation end products up-regulates brain endothelial CCR5 expression and promotes T cells crossing the blood-brain barrier
- Laromestrocel preserves brain volume and cognitive function in Alzheimers disease by inhibiting neuroinflammation