Cited by 1,031Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Classification and basic pathology of Alzheimer disease

Duyckaerts, Charles, Delatour, Benoît, Potier, Marie-Claude·2009·Acta Neuropathologica

DOI 10.1007/s00401-009-0532-1

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Abstract

The lesions of Alzheimer disease include accumulation of proteins, losses of neurons and synapses, and alterations related to reactive processes. Extracellular Abeta accumulation occurs in the parenchyma as diffuse, focal or stellate deposits. It may involve the vessel walls of arteries, veins and capillaries. The cases in which the capillary vessel walls are affected have a higher probability of having one or two apoepsilon 4 alleles. Parenchymal as well as vascular Abeta deposition follows a stepwise progression. Tau accumulation, probably the best histopathological correlate of the clinical symptoms, takes three aspects: in the cell body of the neuron as neurofibrillary tangle, in the dendrites as neuropil threads, and in the axons forming the senile plaque neuritic corona. The progression of tau pathology is stepwise and stereotyped from the entorhinal cortex, through the hippocampus, to the isocortex. The neuronal loss is heterogeneous and area-specific. Its mechanism is still discussed. The timing of the synaptic loss, probably linked to Abeta peptide itself, maybe as oligomers, is also controversial. Various clinico-pathological types of Alzheimer disease have been described, according to the type of the lesions (plaque only and tangle predominant), the type of onset (focal onset), the cause (genetic or sporadic) and the associated lesions (Lewy bodies, vascular lesions, hippocampal sclerosis, TDP-43 inclusions and argyrophilic grain disease).

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Authors: Duyckaerts, C., Delatour, B., & Potier, M.-C.
Affiliations: Assistance Publique – Hôpitaux de Paris (FR)
Centre National de la Recherche Scientifique (FR)
Corresponding author: Duyckaerts, Charles
ORCID: Duyckaerts, Charles
Potier, Marie-Claude
Venue: Acta Neuropathologica
Publisher: Springer Science and Business Media LLC
Published: 2009-04-21
Volume: 118
Issue: 1
Pages: 5-36
ISSN: 0001-6322 (ISSN-L)
1432-0533
DOI: 10.1007/s00401-009-0532-1
OpenAlex: W2051218719
Semantic Scholar: 104c14d3e596d774b8dfad1eeab72d94930700f0
Cited by: 1,031
References: 362
Citations by year: 2026: 31 · 2025: 54 · 2024: 62 · 2023: 76 · 2022: 81 · 2021: 76 · 2020: 80 · 2019: 40 · 2018: 50 · 2017: 50 · 2016: 52 · 2015: 59 · 2014: 56 · 2013: 77 · 2012: 65
FWCI: 6.54
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Acta Neuropathologica (publishedVersion)
PubMed (publishedVersion)
HAL (submittedVersion)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: Alzheimer's disease, amyloid-beta deposition, tau pathology, neurofibrillary tangles, neuropil threads, amyloid plaques, synaptic loss, neuronal loss, APOE ε4, entorhinal cortex, hippocampus, Lewy bodies, hippocampal sclerosis, TDP-43 inclusions, argyrophilic grain disease, disease progression
MeSH terms: Alzheimer Disease, Animals, Brain, DNA-Binding Proteins, Gliosis, Humans, Nerve Degeneration, Synaptic Transmission, Neuronal Plasticity, Neurons, Sclerosis, Amyloid beta-Peptides, Lewy Bodies, Neurofibrillary Tangles, tau Proteins, Cell Death, Age of Onset, Disease Progression, Tauopathies, Neurogenesis, Plaque, Amyloid

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