Cited by 1,455Neurology and Historical StudiesAlzheimer's disease research and treatmentsDementia and Cognitive Impairment Research

An english translation of alzheimer’s 1907 paper, “über eine eigenartige erkankung der hirnrinde”

Stelzmann, Rainulf A., Norman Schnitzlein, H., Reed Murtagh, F.·1995·Clinical Anatomy

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Crossref · 10.1002/ca.980080612

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7 of 7 references verified0 citation errors · 0 not checkable

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  • Senile amyloid plaques are formed by the extracellular nonvascular accumulation of Aβ40 and Aβ42 peptides that result from abnormal processing of amyloid precursor protein by the β- and γ-secretases and an imbalance in production and clearance pathways.

    “Senile amyloid plaques or “miliary foci” as described by Alzheimer in the description of Alzheimer’s disease and originally that same year by Oskar Fischer are formed by the extracellular nonvascular accumulation of Aβ40 and Aβ42 peptides that result from the abnormal processing of amyloid precursor protein by the β- and γ-secretases and an imbalance in the production and clearance pathways [1, 27”

    From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [1]

  • The presence of amyloid plaques and neurofibrillary tangles is still required for the pathological diagnosis of Alzheimer's disease.

    “today the presence of these amyloid plaques and neurofibrillary tangles are still required for a pathological diagnosis”

    From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [1]

  • Alzheimer's disease is associated with diverse phenotypic changes in microglia, resulting in distinct microglial states, including protective and harmful states.

    “Alzheimer’s disease is associated with diverse phenotypic changes in microglia5,6, resulting in distinct microglial states, including protective (aimed at amyloid clearance and neuroprotection7–9) and harmful (associated with microglia-driven neuroinflammation and toxicity)10,11.”
  • AD is the leading cause of dementia characterized by key neuronal hallmarks: extracellular deposition of Aβ plaques, formation of intracellular neurofibrillary tangles, and neuronal loss.

    “AD is the leading cause of dementia characterized by key neuronal hallmarks: extracellular deposition of Aβ plaques, formation of intracellular neurofibrillary tangles, and neuronal loss (1, 2).”
  • Alzheimer's disease is irreversible and presents with neurodegeneration caused by toxic aggregation of extracellular amyloid plaques and intracellular neurofibrillary tangles of hyperphosphorylated tau protein.

    “The disease is irreversible and presents with neurodegeneration caused by toxic aggregation of extracellular amyloid plaques, and intracellular neurofibrillary tangles of hyperphosphorylated tau protein [5].”

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Authors
Stelzmann, R. A., Norman Schnitzlein, H., & Reed Murtagh, F.
Affiliations
University of South Florida (US)
Venue
Clinical Anatomy
Publisher
Wiley
Published
1995-01
Volume
8
Issue
6
Pages
429-431
ISSN
  • 0897-3806 (ISSN-L)
  • 1098-2353
OpenAlex
W2010925911
Cited by
1,455
References
7
Citations by year
2026: 87 · 2025: 133 · 2024: 128 · 2023: 107 · 2022: 126 · 2021: 113 · 2020: 123 · 2019: 82 · 2018: 57 · 2017: 70 · 2016: 51 · 2015: 61 · 2014: 57 · 2013: 35 · 2012: 44
FWCI
0.24
Type
journal article
Language
en
Open access
closed
Locations
  • Clinical Anatomy (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Neurology › Neurology and Historical Studies
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, English translation, history of neurology
MeSH terms
Alzheimer Disease, Humans, Translations, History, 20th Century

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