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Home › Research › Topics › phosphorylated

phosphorylated

738 studies tagged phosphorylated, dated 1986-05-01 to 2026-10-19. Bibliography: BibTeX (.bib) · RIS (.ris)

Newest in this topic

  1. Genetic Architecture of Plasma Amyloid and Tau Biomarkers in the Amish 2026-10-19
  2. Elevation in Plasma p-tau217 Concentrations Among Blood Donors: An Exploratory Cross-Sectional Study 2026-09-24
  3. A Harmonized Visual Reading Framework for Tau PET Staging in Alzheimer Disease 2026-09-21

Studies

738 studies carry this tag.

Date range

1986 to 2026

Top journals

  • Neurology 52
  • Alzheimer s & Dementia 50
  • JAMA neurology 42
  • Brain : a journal of neurology 24
  • The Journal of biological chemistry 22

231 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. Neurodegenerative tauopathies

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Annual review of neuroscience 2001-01-01 Lewy body dementia

    The defining neuropathological characteristics of Alzheimer's disease are abundant filamentous tau lesions and deposits of fibrillar amyloid beta peptides.

  2. Tau filament formation in transgenic mice expressing P301L tau

    ✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of biological chemistry 2001-01-01 Lewy body dementia

    Mutations in the microtubule-associated protein tau, including P301L, are genetically coupled to hereditary frontotemporal dementia with parkinsonism linked to chromosome 17.

  3. Tau gene mutation K257T causes a tauopathy similar to Pick's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neuropathology and experimental neurology 2000-11-01 Disease mechanisms

    Exonic and intronic mutations in Tau cause neurodegenerative syndromes characterized by frontotemporal dementia and filamentous tau protein deposits.

  4. Tau protein isoforms, phosphorylation and role in neurodegenerative disorders

    ✓ Peer-reviewed alzhub usefulness score 54 out of 100. Brain research. Brain research reviews 2000-08-01 Lewy body dementia

    Tau proteins belong to the family of microtubule-associated proteins.

  5. In vitro polymerization of tau protein monitored by laser light scattering: method and application to the study of FTDP-17 mutants

    ✓ Peer-reviewed alzhub usefulness score 44 out of 100. Biochemistry 2000-05-01 Digital health tools

    Tau polymerization into the filaments that compose neurofibrillary tangles is seminal to the development of many neurodegenerative diseases.

  6. Progressive supranuclear palsy pathology caused by a novel silent mutation in exon 10 of the tau gene: expansion of the disease phenotype caused by tau gene mutations

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Brain : a journal of neurology 2000-05-01 Clinical safety

    Genetic mutations in the tau gene on chromosome 17 are known to cause frontotemporal dementias.

  7. Quantification of tau phosphorylated at threonine 181 in human cerebrospinal fluid: a sandwich ELISA with a synthetic phosphopeptide for standardization

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Neuroscience letters 2000-05-01 Lewy body dementia

    Hyperphosphorylation of the microtubule-associated protein tau is specifically found in those brain cells affected in several tauopathies.

  8. Tau gene mutation G389R causes a tauopathy with abundant pick body-like inclusions and axonal deposits

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of neuropathology and experimental neurology 1999-12-01 Disease mechanisms

    Exonic and intronic mutations in Tau cause familial neurodegenerative syndromes characterized by frontotemporal dementia and dysfunction of multiple cortical and subcortical circuits.

  9. Age-dependent emergence and progression of a tauopathy in transgenic mice overexpressing the shortest human tau isoform

    ✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neuron 1999-11-01 Lewy body dementia

    Filamentous tau aggregates are hallmarks of tauopathies, e.g., frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17) and amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC).

  10. Cellular co-localization of phosphorylated tau- and NACP/alpha-synuclein-epitopes in lewy bodies in sporadic Parkinson's disease and in dementia with Lewy bodies

    ✓ Peer-reviewed alzhub usefulness score 42 out of 100. Brain research 1999-10-01 Disparities

    The precursor of the non-Abeta-component of Alzheimer's disease (AD) amyloid (NACP, alpha-synuclein) aggregates into insoluble filaments of Lewy bodies (LBs) in Parkinson's disease (PD) and dementia with LBs (DLB).

  11. Frequency of tau mutations in three series of non-Alzheimer's degenerative dementia

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Annals of neurology 1999-08-01 Disease mechanisms

    Splice-site and missense mutations have been identified in tau associated with frontotemporal dementia with parkinsonism linked to chromosome 17.

  12. A mutation at codon 279 (N279K) in exon 10 of the Tau gene causes a tauopathy with dementia and supranuclear palsy

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Acta neuropathologica 1999-07-01 Disease mechanisms

    Recently intronic and exonic mutations in the Tau gene have been found to be associated with familial neurodegenerative syndromes characterized not only by a predominantly frontotemporal dementia but also by the presence of neurological signs consistent with the dysfunction of multiple subcortical neuronal circuitries.

  13. Missense and silent tau gene mutations cause frontotemporal dementia with parkinsonism-chromosome 17 type, by affecting multiple alternative RNA splicing regulatory elements

    ✓ Peer-reviewed alzhub usefulness score 51 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1999-05-01 Lewy body dementia

    Frontotemporal dementia with parkinsonism, chromosome 17 type (FTDP-17) is caused by mutations in the tau gene, and the signature lesions of FTDP-17 are filamentous tau inclusions.

  14. Phylogenetic diversity of the expression of the microtubule-associated protein tau: implications for neurodegenerative disorders

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Brain research. Molecular brain research 1999-05-01 Disease mechanisms

    The microtubule-associated protein tau regulates the dynamic stability of the neuronal cytoskeleton by interacting with microtubules.

  15. Tau pathology in a family with dementia and a P301L mutation in tau

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of neuropathology and experimental neurology 1999-04-01 Disease mechanisms

    Familial forms of frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) have recently been associated with coding region and intronic mutations in the tau gene.

  16. A distinct familial presenile dementia with a novel missense mutation in the tau gene

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuroreport 1999-02-01 Disease mechanisms

    We report a Japanese family with early onset hereditary frontotemporal dementia and a novel missense mutation (Ser305Asn) in the tau gene.

  17. Increased tau in the cerebrospinal fluid of patients with frontotemporal dementia and Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 49 out of 100. Neuroscience letters 1999-01-01 Cognitive tests and assessment

    Cerebrospinal fluid (CSF) concentrations of tau protein were measured using an enzyme-linked immunosorbent assay which measures both normal and hyperphosphorylated tau.

  18. Mutation-specific functional impairments in distinct tau isoforms of hereditary FTDP-17

    ✓ Peer-reviewed alzhub usefulness score 59 out of 100. Science (New York, N.Y.) 1998-12-01 Lewy body dementia

    Tau proteins aggregate as cytoplasmic inclusions in a number of neurodegenerative diseases, including Alzheimer's disease and hereditary frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17).

  19. Pathogenic implications of mutations in the tau gene in pallido-ponto-nigral degeneration and related neurodegenerative disorders linked to chromosome 17

    ✓ Peer-reviewed alzhub usefulness score 51 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1998-10-01 Lewy body dementia

    Pallido-ponto-nigral degeneration (PPND) is one of the most well characterized familial neurodegenerative disorders linked to chromosome 17q21-22.

  20. Tau protein pathology in neurodegenerative diseases

    ✓ Peer-reviewed alzhub usefulness score 49 out of 100. Trends in neurosciences 1998-10-01 Lewy body dementia

    Abundant tau-positive neurofibrillary lesions constitute a defining neuropathological characteristic of Alzheimer's disease.

  21. Tau proteins with FTDP-17 mutations have a reduced ability to promote microtubule assembly

    ✓ Peer-reviewed alzhub usefulness score 49 out of 100. FEBS letters 1998-10-01 Lewy body dementia

    Recently exonic and intronic mutations in the gene for microtubule-associated protein tau have been discovered in cases of familial frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17).

  22. Association of missense and 5'-splice-site mutations in tau with the inherited dementia FTDP-17

    ✓ Peer-reviewed alzhub usefulness score 64 out of 100. Nature 1998-06-01 Lewy body dementia

    Thirteen families have been described with an autosomal dominantly inherited dementia named frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), historically termed Pick's disease.

  23. Mutation in the tau gene in familial multiple system tauopathy with presenile dementia

    ✓ Peer-reviewed alzhub usefulness score 57 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1998-06-01 Lewy body dementia

    Familial multiple system tauopathy with presenile dementia (MSTD) is a neurodegenerative disease with an abundant filamentous tau protein pathology.

  24. Tau is a candidate gene for chromosome 17 frontotemporal dementia

    ✓ Peer-reviewed alzhub usefulness score 58 out of 100. Annals of neurology 1998-06-01 Digital health tools

    Frontotemporal dementia with parkinsonism, chromosome 17 type (FTDP-17), a recently defined disease entity, is clinically characterized by personality changes sometimes associated with psychosis, hyperorality, and diminished speech output, disturbed executive function and nonfluent aphasia, bradykinesia, and rigidity.

  25. Familial multiple system tauopathy with presenile dementia: a disease with abundant neuronal and glial tau filaments

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1997-04-01 Disease mechanisms

    Neurofibrillary lesions made of hyperphosphorylated microtubule-associated protein tau constitute not only one of the defining neuropathological features of Alzheimer disease but also are present in a number of other neurodegenerative diseases with dementia.

  26. Vascular variant of prion protein cerebral amyloidosis with tau-positive neurofibrillary tangles: the phenotype of the stop codon 145 mutation in PRNP

    ✓ Peer-reviewed alzhub usefulness score 49 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1996-01-01 Brain tissue and pathology

    Deposition of PrP amyloid in cerebral vessels in conjunction with neurofibrillary lesions is the neuropathologic hallmark of the dementia associated with a stop mutation at codon 145 of PRNP, the gene encoding the prion protein (PrP).

  27. Tau protein in cerebrospinal fluid: a biochemical marker for axonal degeneration in Alzheimer disease?

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. Molecular and chemical neuropathology 1995-12-01 Getting a diagnosis

    Cerebrospinal fluid (CSF) biochemical markers for Alzheimer disease (AD) would be of great value to improve the clinical diagnostic accuracy of the disorder.

  28. Investigation of tau-2 positive microglia-like cells in the subcortical nuclei of human neurodegenerative disorders

    ✓ Peer-reviewed alzhub usefulness score 37 out of 100. Neuroscience letters 1995-06-01 Biomarkers

    An anti-tau monoclonal antibody tau-2 was demonstrated to react with the cells which characteristically appeared in the subcortical nuclei of certain neurodegenerative disorders.

  29. Glycated tau protein in Alzheimer disease: a mechanism for induction of oxidant stress

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1994-08-01 Disease mechanisms

    The stability of proteins that constitute the neurofibrillary tangles and senile plaques of Alzheimer disease suggests that they would be ideal substrates for nonenzymatic glycation, a process that occurs over long times, even at normal levels of glucose, ultimately resulting in the formation of advanced glycation end products (AGEs).

  30. Levels of normal and abnormally phosphorylated tau in different cellular and regional compartments of Alzheimer disease and control brains

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. FEBS letters 1994-08-01 Tau biomarkers

    Microtubule associated protein tau is abnormally phosphorylated in Alzheimer disease (AD) brain.

  31. The extent of phosphorylation of fetal tau is comparable to that of PHF-tau from Alzheimer paired helical filaments

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Brain research 1993-11-01 Drug development

    The relationship between Alzheimer's disease (AD) and expression of fetal proteins was examined by: (i) determining the phosphate content of tau prepared from fetal brains (F-tau); (ii) comparing F-tau, tau from normal adult human brains (N-tau) and tau from paired helical filaments in AD brains (PHF-tau) for phosphate content; and (iii) testing the reactivity of F-tau with five antibodies known to recognize PHF-tau.

  32. Identification of nuclear tau isoforms in human neuroblastoma cells

    ✓ Peer-reviewed alzhub usefulness score 42 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1990-11-01 Down syndrome and Alzheimer's

    The tau proteins have been reported only in association with microtubules and with ribosomes in situ, in the normal central nervous system.

  33. Defined neurofilament, tau, and beta-amyloid precursor protein epitopes distinguish Alzheimer from non-Alzheimer senile plaques

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1990-03-01 Risk genes beyond APOE

    Eight antisera and one monoclonal antibody to synthetic peptides that corresponded to domains extending over the entire length of the beta-amyloid precursor protein (beta-APP), and an antiserum to the full-length 695-amino acid form of the beta-APP, were raised to probe the composition of the core and corona of senile plaques (SPs).

  34. Multiple isoforms of human microtubule-associated protein tau: sequences and localization in neurofibrillary tangles of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 52 out of 100. Neuron 1989-10-01 Disease mechanisms

    The researchers determined the sequences of human tau protein isoforms that feature amino-terminal insertions.

  35. Accumulation of abnormally phosphorylated tau precedes the formation of neurofibrillary tangles in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Brain research 1989-01-01 Brain tissue and pathology

    The intraneuronal accumulation of paired helical filaments in the form of neurofibrillary tangles is one hallmark of the brain pathology in Alzheimer's disease.

  36. Neurofibrillary tangles in Alzheimer's disease and progressive supranuclear palsy: antigenic similarities and differences. Microtubule-associated protein tau antigenicity is prominent in all types of tangles

    ✓ Peer-reviewed alzhub usefulness score 42 out of 100. Acta neuropathologica 1987-01-01 Disparities

    The antigenic profile of neurofibrillary tangles (NFT) in Alzheimer's disease (AD), senile dementia of Alzheimer type (SDAT), progressive supranuclear palsy (PSP) and in non-demented aged humans was investigated by light and electron microscopic immunocytochemistry using antisera and monoclonal antibodies to tubulin, microtubule-associated proteins (MAP1, MAP2 and tau), neurofilament proteins and determinants unique to Alzheimer paired helical filaments (PHF).

  37. Abnormal phosphorylation of the microtubule-associated protein tau (tau) in Alzheimer cytoskeletal pathology.

    ✓ Peer-reviewed alzhub usefulness score 55 out of 100. Proceedings of the National Academy of Sciences 1986-07-01 Disease mechanisms

    A monoclonal antibody to the microtubule-associated protein tau (tau) labeled some neurofibrillary tangles and plaque neurites, the two major locations of paired-helical filaments (PHF), in Alzheimer disease brain.

  38. Microtubule-associated protein tau. A component of Alzheimer paired helical filaments.

    ✓ Peer-reviewed alzhub usefulness score 51 out of 100. Journal of Biological Chemistry 1986-05-01 Disease mechanisms

    Microtubule-associated protein tau was purified from bovine brain microtubules by either (1) phosphocellulose chromatography, (2) heat treatment at pH 6.4, (3) heat treatment at pH 2.7, (4) heat treatment at pH 2.7 followed by extraction with perchloric acid and precipitation with glycerol, or (5) by precipitation with ammonium sulfate followed by extraction with perchloric acid.

From across this tag

9 of the 733 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 9. The same 9 appear here every time.

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