The DOI matches its Crossref record; 362 of the 362 references it cites were found in a registry or an index.
Classification and basic pathology of Alzheimer disease
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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“In Lewy body dementia, Lewy related pathology affects corticolimbic regions and is often associated with concurrent Alzheimer type pathologic change [120, 121].”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [121]
In the citing paper
“Meanwhile, tau accumulation as intracellular neurofibrillary tangles (NFTs) is another hallmark feature of AD and strongly associated with progressive neuronal loss and cognitive decline [3].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [3]
In the citing paper
“Aβ, which begins accumulating over a decade prior to clinical symptoms, comprises the cortical extracellular plaques characteristic of AD [3].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [3]
In the citing paper
“A wealth of evidence suggests these proteins play a pathogenic role in disease.”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [3]
In the citing paper
“Hyperphosphorylated tau accumulates as intraneuronal NFTs, a hallmark feature of AD pathology [3].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [3]
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Metadata
- 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
- Venue
- Acta Neuropathologica
- Published
- 2009-04-21
- Volume
- 118
- Issue
- 1
- Pages
- 5-36
- ISSN
- 0001-6322 (ISSN-L)
- 1432-0533
- 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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