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Home › Research › Topics › tdp-43

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

  1. What Do Sugar, Gila Monsters, and the Therapeutic Dance Have in Common With GLP-1RA, Stroke, and Dementia? 2026-09-25
  2. Myo-inositol as a spectroscopic marker of neuroinflammation in frontotemporal lobar degeneration 2026-09-20
  3. 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.

  1. Modulation of p25 and inflammatory pathways by fisetin maintains cognitive function in Alzheimer's disease transgenic mice

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Aging cell 2013-12-17 Inflammation and the immune system

    Alzheimer's disease (AD) is the most common type of dementia.

  2. Triggering receptor expressed on myeloid cells 2 knockdown exacerbates aging-related neuroinflammation and cognitive deficiency in senescence-accelerated mouse prone 8 mice

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neurobiology of aging 2013-12-02 TREM2 and immune genetics

    As a major characteristic of aging process, neuroinflammation is involved in the pathogenesis of several aging-related diseases including Alzheimer's disease (AD).

  3. Human iPSC-based modeling of late-onset disease via progerin-induced aging

    ✓ Peer-reviewed alzhub usefulness score 53 out of 100. Cell stem cell 2013-12-01 Lewy body dementia

    Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) resets their identity back to an embryonic age and, thus, presents a significant hurdle for modeling late-onset disorders.

  4. Neuronal clearance of amyloid-β by endocytic receptor LRP1

    ✓ Peer-reviewed alzhub usefulness score 51 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2013-12-01 Brain tissue and pathology

    Alzheimer's disease (AD) is the most prevalent form of dementia in the elderly population.

  5. Pharmacologic inhibition of ROCK2 suppresses amyloid-β production in an Alzheimer's disease mouse model

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2013-12-01 Mild cognitive impairment

    Alzheimer's disease (AD) is the leading cause of dementia and has no cure.

  6. Sleep facilitates clearance of metabolites from the brain: glymphatic function in aging and neurodegenerative diseases

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Rejuvenation research 2013-12-01 Genetics

    Decline of cognition and increasing risk of neurodegenerative diseases are major problems associated with aging in humans.

  7. Hexanucleotide repeats in ALS/FTD form length-dependent RNA foci, sequester RNA binding proteins, and are neurotoxic

    ✓ Peer-reviewed alzhub usefulness score 55 out of 100. Cell reports 2013-11-27 Lewy body dementia

    The GGGGCC (G4C2) intronic repeat expansion within C9ORF72 is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).

  8. LIM homeobox 8 (Lhx8) is a key regulator of the cholinergic neuronal function via a tropomyosin receptor kinase A (TrkA)-mediated positive feedback loop

    ✓ Peer-reviewed alzhub usefulness score 37 out of 100. The Journal of biological chemistry 2013-11-21 Down syndrome and Alzheimer's

    Basal forebrain cholinergic neurons play an important role in cognitive functions such as learning and memory, and they are affected in several neurodegenerative diseases, including Alzheimer disease and Down syndrome.

  9. RAN proteins and RNA foci from antisense transcripts in C9ORF72 ALS and frontotemporal dementia

    ✓ Peer-reviewed alzhub usefulness score 57 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2013-11-18 Lewy body dementia

    The finding that a GGGGCC (G4C2) hexanucleotide repeat expansion in the chromosome 9 ORF 72 (C9ORF72) gene is a common cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) links ALS/FTD to a large group of unstable microsatellite diseases.

  10. Transmission of multiple system atrophy prions to transgenic mice

    ✓ Peer-reviewed alzhub usefulness score 52 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2013-11-11 Lewy body dementia

    Prions are proteins that adopt alternative conformations, which become self-propagating.

  11. Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degeneration

    ✓ Peer-reviewed alzhub usefulness score 53 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2013-10-29 Lewy body dementia

    Expanded hexanucleotide repeats in the chromosome 9 open reading frame 72 (C9orf72) gene are the most common genetic cause of ALS and frontotemporal degeneration (FTD).

  12. Bidirectional transcripts of the expanded C9orf72 hexanucleotide repeat are translated into aggregating dipeptide repeat proteins

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Acta neuropathologica 2013-10-17 Lewy body dementia

    Massive GGGGCC repeat expansion in the first intron of the gene C9orf72 is the most common known cause of familial frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS).

  13. Antisense transcripts of the expanded C9ORF72 hexanucleotide repeat form nuclear RNA foci and undergo repeat-associated non-ATG translation in c9FTD/ALS

    ✓ Peer-reviewed alzhub usefulness score 56 out of 100. Acta neuropathologica 2013-10-16 Lewy body dementia

    Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are devastating neurodegenerative disorders with clinical, genetic, and neuropathological overlap.

  14. Phagocytosis executes delayed neuronal death after focal brain ischemia

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2013-10-07 Inflammation and the immune system

    Delayed neuronal loss and brain atrophy after cerebral ischemia contribute to stroke and dementia pathology, but the mechanisms are poorly understood.

  15. Dipeptide repeat protein pathology in C9ORF72 mutation cases: clinico-pathological correlations

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Acta neuropathologica 2013-10-06 Brain tissue and pathology

    Hexanucleotide repeat expansion in C9ORF72 is the most common genetic cause of frontotemporal dementia and motor neuron disease.

  16. RNA toxicity from the ALS/FTD C9ORF72 expansion is mitigated by antisense intervention

    ✓ Peer-reviewed alzhub usefulness score 57 out of 100. Neuron 2013-10-01 Lewy body dementia

    A hexanucleotide GGGGCC repeat expansion in the noncoding region of the C9ORF72 gene is the most common genetic abnormality in familial and sporadic amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).

  17. Targeting RNA foci in iPSC-derived motor neurons from ALS patients with a C9ORF72 repeat expansion

    ✓ Peer-reviewed alzhub usefulness score 53 out of 100. Science translational medicine 2013-10-01 Lewy body dementia

    Amyotrophic lateral sclerosis (ALS) is a severe neurodegenerative condition characterized by loss of motor neurons in the brain and spinal cord.

  18. Interaction of FUS and HDAC1 regulates DNA damage response and repair in neurons

    ✓ Peer-reviewed alzhub usefulness score 55 out of 100. Nature neuroscience 2013-09-15 Lewy body dementia

    Defects in DNA repair have been extensively linked to neurodegenerative diseases, but the exact mechanisms remain poorly understood.

  19. CHF5074 reduces biomarkers of neuroinflammation in patients with mild cognitive impairment: a 12-week, double-blind, placebo-controlled study

    ✓ Peer-reviewed alzhub usefulness score 53 out of 100. Current Alzheimer research 2013-09-01 Inflammation and the immune system

    As neuroinflammation is an early event in the pathogenesis of Alzheimer' s disease, new selective antiinflammatory drugs could lead to promising preventive strategies.

  20. Cyclooxygenase-1-dependent prostaglandins mediate susceptibility to systemic inflammation-induced acute cognitive dysfunction

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2013-09-01 Clinical safety

    Systemic inflammatory events often precipitate acute cognitive dysfunction in elderly and demented populations.

  21. Microglial beclin 1 regulates retromer trafficking and phagocytosis and is impaired in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Neuron 2013-09-01 TREM2 and immune genetics

    Phagocytosis controls CNS homeostasis by facilitating the removal of unwanted cellular debris.

  22. Intracerebroventricular streptozotocin exacerbates Alzheimer-like changes of 3xTg-AD mice

    ✓ Peer-reviewed alzhub usefulness score 42 out of 100. Molecular neurobiology 2013-08-31 Risk genes beyond APOE

    Alzheimer's disease (AD) involves several possible molecular mechanisms, including impaired brain insulin signaling and glucose metabolism.

  23. A physical interaction between the adaptor proteins DOK3 and DAP12 is required to inhibit lipopolysaccharide signaling in macrophages

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Science signaling 2013-08-20 TREM2 and immune genetics

    DNAX-activating protein of 12 kD (DAP12) is an immunoreceptor tyrosine-based activation motif (ITAM)-containing adaptor protein found in myeloid cells and natural killer cells, and it couples to various receptors that mediate either cellular activation or inhibition.

  24. The polyphenol oleuropein aglycone protects TgCRND8 mice against Aß plaque pathology

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. PloS one 2013-08-08 Risk genes beyond APOE

    The claimed beneficial effects of the Mediterranean diet include prevention of several age-related dysfunctions including neurodegenerative diseases and Alzheimer-like pathology.

  25. Converging mechanisms in ALS and FTD: disrupted RNA and protein homeostasis

    ✓ Peer-reviewed alzhub usefulness score 58 out of 100. Neuron 2013-08-01 Lewy body dementia

    Breakthrough discoveries identifying common genetic causes for amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) have transformed our view of these disorders.

  26. Growth hormone-releasing hormone effects on brain γ-aminobutyric acid levels in mild cognitive impairment and healthy aging

    ✓ Peer-reviewed alzhub usefulness score 64 out of 100. JAMA neurology 2013-07-01 Treatments

    TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00257712.

  27. Sorting receptor SORLA--a trafficking path to avoid Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Journal of cell science 2013-06-26 Risk genes beyond APOE

    Excessive proteolytic breakdown of the amyloid precursor protein (APP) to neurotoxic amyloid β peptides (Aβ) by secretases in the brain is a molecular cause of Alzheimer disease (AD).

  28. Canonical Wnt signaling protects hippocampal neurons from Aβ oligomers: role of non-canonical Wnt-5a/Ca(2+) in mitochondrial dynamics

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Frontiers in cellular neuroscience 2013-06-25 Disease mechanisms

    Alzheimer's disease (AD) is the most common type of age-related dementia.

  29. Eukaryotic stress granules are cleared by autophagy and Cdc48/VCP function

    ✓ Peer-reviewed alzhub usefulness score 52 out of 100. Cell 2013-06-01 Lewy body dementia

    Stress granules and P bodies are conserved cytoplasmic aggregates of nontranslating messenger ribonucleoprotein complexes (mRNPs) implicated in the regulation of mRNA translation and decay and are related to RNP granules in embryos, neurons, and pathological inclusions in some degenerative diseases.

  30. Multiple risk pathways for schizophrenia converge in serine racemase knockout mice, a mouse model of NMDA receptor hypofunction

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2013-05-31 Hippocampus size on brain scans

    Schizophrenia is characterized by reduced hippocampal volume, decreased dendritic spine density, altered neuroplasticity signaling pathways, and cognitive deficits associated with impaired hippocampal function.

  31. Clathrin adaptor CALM/PICALM is associated with neurofibrillary tangles and is cleaved in Alzheimer's brains

    ✓ Peer-reviewed alzhub usefulness score 49 out of 100. Acta neuropathologica 2013-04-16 Genetics

    PICALM, a clathrin adaptor protein, plays important roles in clathrin-mediated endocytosis in all cell types.

  32. Variants in triggering receptor expressed on myeloid cells 2 are associated with both behavioral variant frontotemporal lobar degeneration and Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 52 out of 100. Neurobiology of aging 2013-04-09 TREM2 and immune genetics

    Recent evidence suggests that rare genetic variants within the TREM2 gene are associated with increased risk of Alzheimer's disease.

  33. The endogenous tryptophan metabolite and NAD+ precursor quinolinic acid confers resistance of gliomas to oxidative stress

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Cancer research 2013-04-02 Inflammation and the immune system

    Quinolinic acid is a product of tryptophan degradation and may serve as a precursor for NAD(+), an important enzymatic cofactor for enzymes such as the DNA repair protein PARP.

  34. Blocking the interaction between apolipoprotein E and Aβ reduces intraneuronal accumulation of Aβ and inhibits synaptic degeneration

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. The American journal of pathology 2013-03-13 Genetics

    Accumulation of β-amyloid (Aβ) in the brain is a key event in Alzheimer disease pathogenesis.

  35. Pomegranate polyphenols and extract inhibit nuclear factor of activated T-cell activity and microglial activation in vitro and in a transgenic mouse model of Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. The Journal of nutrition 2013-03-06 Risk genes beyond APOE

    Alzheimer disease (AD) brain is characterized by extracellular plaques of amyloid β (Aβ) peptide with reactive microglia.

  36. PI3-kinase/Akt/mTOR signaling: impaired on/off switches in aging, cognitive decline and Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 42 out of 100. Experimental gerontology 2013-03-05 Risk factors

    The normal on and off switching of the PI3-K (phosphoinositide 3-kinase)/Akt pathway, particularly by its major activators insulin and IGF-1 (insulin-like growth factor-1), is a powerful integrator of physiological responses rudimentary to successful aging.

  37. Advanced glycation end-products disrupt the blood-brain barrier by stimulating the release of transforming growth factor-β by pericytes and vascular endothelial growth factor and matrix metalloproteinase-2 by endothelial cells in vitro

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neurobiology of aging 2013-02-19 Disease mechanisms

    Diabetic encephalopathy is now accepted as an important complication of diabetes.

  38. Unconventional translation of C9ORF72 GGGGCC expansion generates insoluble polypeptides specific to c9FTD/ALS

    ✓ Peer-reviewed alzhub usefulness score 57 out of 100. Neuron 2013-02-12 Lewy body dementia

    Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are devastating neurodegenerative disorders with clinical, genetic, and neuropathological overlap.

  39. Astrocyte pathology and the absence of non-cell autonomy in an induced pluripotent stem cell model of TDP-43 proteinopathy

    ✓ Peer-reviewed alzhub usefulness score 51 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2013-02-11 Lewy body dementia

    Glial proliferation and activation are associated with disease progression in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar dementia.

  40. Ferulic acid is a nutraceutical β-secretase modulator that improves behavioral impairment and alzheimer-like pathology in transgenic mice

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. PloS one 2013-02-08 Risk genes beyond APOE

    Amyloid precursor protein (APP) proteolysis is required for production of amyloid-β (Aβ) peptides that comprise β-amyloid plaques in brains of Alzheimer's disease (AD) patients.

  41. γ-Secretase modulator (GSM) photoaffinity probes reveal distinct allosteric binding sites on presenilin

    ✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2013-02-08 Risk genes beyond APOE

    γ-Secretase is an intramembrane aspartyl protease that cleaves the amyloid precursor protein to produce neurotoxic β-amyloid peptides (i.e. Aβ42) that have been implicated in the pathogenesis of Alzheimer disease.

  42. The C9orf72 GGGGCC repeat is translated into aggregating dipeptide-repeat proteins in FTLD/ALS

    ✓ Peer-reviewed alzhub usefulness score 59 out of 100. Science (New York, N.Y.) 2013-02-07 Lewy body dementia

    Expansion of a GGGGCC hexanucleotide repeat upstream of the C9orf72 coding region is the most common cause of familial frontotemporal lobar degeneration and amyotrophic lateral sclerosis (FTLD/ALS), but the pathomechanisms involved are unknown.

  43. Prion protein-mediated toxicity of amyloid-β oligomers requires lipid rafts and the transmembrane LRP1

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. The Journal of biological chemistry 2013-02-05 Risk genes beyond APOE

    Soluble oligomers of the amyloid-β (Aβ) peptide cause neurotoxicity, synaptic dysfunction, and memory impairments that underlie Alzheimer disease (AD).

  44. ALS-linked TDP-43 mutations produce aberrant RNA splicing and adult-onset motor neuron disease without aggregation or loss of nuclear TDP-43

    ✓ Peer-reviewed alzhub usefulness score 53 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2013-02-04 Lewy body dementia

    Transactivating response region DNA binding protein (TDP-43) is the major protein component of ubiquitinated inclusions found in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) with ubiquitinated inclusions.

  45. Chronic high levels of the RCAN1-1 protein may promote neurodegeneration and Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Free radical biology & medicine 2013-01-29 Down syndrome and Alzheimer's

    The RCAN1 gene encodes three different protein isoforms: RCAN1-4, RCAN1-1L, and RCAN1-1S. RCAN1-1L is the RCAN1 isoform predominantly expressed in human brains.

  46. An N-terminal fragment of the prion protein binds to amyloid-β oligomers and inhibits their neurotoxicity in vivo

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. The Journal of biological chemistry 2013-01-28 Disease mechanisms

    A hallmark of Alzheimer disease (AD) is the accumulation of the amyloid-β (Aβ) peptide in the brain.

  47. Toll-like receptor 4 stimulation with the detoxified ligand monophosphoryl lipid A improves Alzheimer's disease-related pathology

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2013-01-15 Inflammation and the immune system

    Alzheimer's disease (AD) is the most common cause of dementia worldwide.

  48. Cathepsin F mutations cause Type B Kufs disease, an adult-onset neuronal ceroid lipofuscinosis

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. Human molecular genetics 2013-01-07 Disparities

    Kufs disease, an adult-onset neuronal ceroid lipofuscinosis, is challenging to diagnose and genetically heterogeneous.

  49. Natural cannabinoids improve dopamine neurotransmission and tau and amyloid pathology in a mouse model of tauopathy

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of Alzheimer's disease : JAD 2013-01-01 Disease mechanisms

    Cannabinoids are neuroprotective in models of neurodegenerative dementias.

  50. Deferoxamine inhibits iron induced hippocampal tau phosphorylation in the Alzheimer transgenic mouse brain

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neurochemistry international 2012-12-20 Risk genes beyond APOE

    Prior work has shown that iron interacts with hyperphosphorylated tau, which contributes to the formation of neurofibrillary tangles (NFTs) in Alzheimer's disease (AD), whereas iron chelator desferrioxamine (DFO) slows down the clinical progression of the cognitive decline associated with this disease.

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