Classification and basic pathology of Alzheimer disease

Duyckaerts, Charles; Delatour, Benoît; Potier, Marie-Claude

doi:10.1007/s00401-009-0532-1

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

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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In Lewy body dementia, Lewy related pathology affects corticolimbic regions and is often associated with concurrent Alzheimer type pathologic change.
“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]
Tau accumulation as intracellular neurofibrillary tangles is a hallmark feature of AD and is strongly associated with progressive neuronal loss and cognitive decline.
“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]
Aβ begins accumulating over a decade prior to clinical symptoms and comprises the cortical extracellular plaques characteristic of AD.
“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]
Aβ and tau play a pathogenic role in Alzheimer's disease.
“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]
Hyperphosphorylated tau accumulates as intraneuronal neurofibrillary tangles, a hallmark feature of AD pathology.
“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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Alzheimer and frontotemporal pathology in subsets of primary progressive aphasia
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Disease‐specific patterns of locus coeruleus cell loss
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Cell-cycle reentry and cell death in transgenic mice expressing nonmutant human tau isoforms
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“In transgenic mice overexpressing normal human tau, there are also signs of re-entry: tau accumulation could thus be the cause of the re-entry rather than its consequence [12].”
Background
Microglia in degenerative neurological disease
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Lymphatic drainage of the brain and the pathophysiology of neurological disease
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Staging of neurofibrillary pathology in Alzheimer's disease: A study of the BrainNet Europe Consortium
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ALZHEIMER’S DISEASE —AN ELECTRON MICROSCOPICAL STUDY
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Neuropathologic Substrate of Mild Cognitive Impairment
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Cell death in Alzheimer's disease evaluated by DNA fragmentation in situ
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Activation of caspase-3 in single neurons and autophagic granules of granulovacuolar degeneration in Alzheimer's disease. Evidence for apoptotic cell death.
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Two Types of Sporadic Cerebral Amyloid Angiopathy
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Oligomerization of Alzheimer's β-Amyloid within Processes and Synapses of Cultured Neurons and Brain
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Alzheimer disease models and human neuropathology: similarities and differences
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Self-citation
Enzymatically active lysosomal proteases are associated with amyloid deposits in Alzheimer brain.
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Morphometric Demonstration of Atrophic Changes in the Cerebral Cortex, White Matter, and Neostriatum in Huntington's Disease
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Alzheimer's disease-type neuronal tau hyperphosphorylation induced by Aβ oligomers
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Occurrence of neuropil threads in the senile human brain and in Alzheimer's disease: A third location of paired helical filaments outside of neurofibrillary tangles and neuritic plaques
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Concurrence of TDP-43, tau and α-synuclein pathology in brains of Alzheimer's disease and dementia with Lewy bodies
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Correlations of synaptic and pathological markers with cognition of the elderly
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Increased level of active GSK‐3β in Alzheimer’s disease and accumulation in argyrophilic grains and in neurones at different stages of neurofibrillary degeneration
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The Structural Basis of Monoclonal Antibody Alz50's Selectivity for Alzheimer's Disease Pathology
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Massive CA1/2 Neuronal Loss with Intraneuronal and N-Terminal Truncated Aβ42 Accumulation in a Novel Alzheimer Transgenic Model
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Parkinson Disease Neuropathology
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Locus coeruleus neurofibrillary degeneration in aging, mild cognitive impairment and early Alzheimer's disease
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Alzheimer's neurofibrillary pathology and the spectrum of cognitive function: Findings from the Nun Study
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Vascular Pathology in Alzheimer Disease: Correlation of Cerebral Amyloid Angiopathy and Arteriosclerosis/Lipohyalinosis with Cognitive Decline
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Activation of the classical complement pathway in brain tissue of Alzheimer patients
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MRI correlates of neurofibrillary tangle pathology at autopsy: A voxel-based morphometry study
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Cerebral amyloid angiopathy and its relationship to Alzheimer’s disease
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The human pineal gland and melatonin in aging and Alzheimer's disease
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Cholinergic nucleus basalis tauopathy emerges early in the aging‐MCI‐AD continuum
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Alzheimer Disease With Amygdala Lewy Bodies: A Distinct Form of α-Synucleinopathy
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A variant of Alzheimer's disease with spastic paraparesis and unusual plaques due to deletion of exon 9 of presenilin 1
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Phenotype associated with APP duplication in five families
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In situ evidence for DNA fragmentation in Huntingtonʼs disease striatum and Alzheimerʼs disease temporal lobes
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Intraneuronal Aβ accumulation precedes plaque formation in β-amyloid precursor protein and presenilin-1 double-transgenic mice
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Alzheimer's disease: Tau proteins, the promoting factors of microtubule assembly, are major components of paired helical filaments
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Cell cycle markers in the hippocampus in Alzheimer's disease
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Progressive posterior cortical dysfunction
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PIB is a non-specific imaging marker of amyloid-beta (A ) peptide-related cerebral amyloidosis
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Complement activation in amyloid plaques in Alzheimer’s dementia
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Aβ Species Removal After Aβ 42 Immunization
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Synaptic Changes in Alzheimer's Disease
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Failure of Neuronal Maturation in Alzheimer Disease Dentate Gyrus
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The case described by Alois Alzheimer in 1911
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Co-Localization of Amyloid Beta and Tau Pathology in Alzheimer's Disease Synaptosomes
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Cholinergic Neuronal and Axonal Abnormalities Are Present Early in Aging and in Alzheimer Disease
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Amyloid β Protein Starting Pyroglutamate at Position 3 Is a Major Component of the Amyloid Deposits in the Alzheimer's Disease Brain
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Thrombin and Prothrombin Are Expressed by Neurons and Glial Cells and Accumulate in Neurofibrillary Tangles in Alzheimer Disease Brain
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Impaired Spine Stability Underlies Plaque-Related Spine Loss in an Alzheimer's Disease Mouse Model
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Alzheimer’s disease pathology influences severity and topographical distribution of cerebral amyloid angiopathy
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Cerebral Amyloid Induces Aberrant Axonal Sprouting and Ectopic Terminal Formation in Amyloid Precursor Protein Transgenic Mice
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Staging of Cytoskeletal and β-Amyloid Changes in Human Isocortex Reveals Biphasic Synaptic Protein Response during Progression of Alzheimer’s Disease
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Large amounts of neocortical βA4 deposits without neuritic plaques nor tangles in a psychometrically assessed, non-demented person
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Degenerative and vascular lesions of the brain have synergistic effects in dementia of the elderly
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Three-dimensional analysis of the relationship between synaptic pathology and neuropil threads in Alzheimer disease
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High sensitivity analysis of amyloid-beta peptide composition in amyloid deposits from human and PS2APP mouse brain
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Only cerebral capillary amyloid angiopathy correlates with Alzheimer pathology?a pilot study
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Reduction of acetylated alpha-tubulin immunoreactivity in neurofibrillary tangle-bearing neurons in Alzheimer's disease.
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Severely dystrophic axons at amyloid plaques remain continuous and connected to viable cell bodies
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Cholesterol Accumulates in Senile plaques of Alzheimer Disease patients and in Transgenic APPswMice
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Alzheimerʼs Disease
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Subtypes and differential laminar distributions of ?A4 deposits in Alzheimer's disease: relationship with the intellectual status of 26 cases
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Association of heparan sulfate proteoglycan with the neurofibrillary tangles of Alzheimer's disease
Perry, G. L., Siedlak, S. L., Richey, P. L., Kawai, M., Cras, P. P., Kalaria, R. N., Pg, G., Scardina, J. M., Cordell, B., & Greenberg, B. (1991) · Journal of Neuroscience · doi:10.1523/jneurosci.11-11-03679.1991 · Cited by 173 · see citing works
Neuroplasticity in Alzheimer's disease
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Multivariate network analysis of fiber tract integrity in Alzheimer’s disease
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No global neocortical nerve cell loss in brains from patients with senile dementia of Alzheimer's type.
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Subcellular Topography of Neuronal Aβ Peptide in APPxPS1 Transgenic Mice
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Visual Association Pathology in Preclinical Alzheimer Disease
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ALZHEIMER'S DISEASE: PAIRED HELICAL FILAMENTS AND CYTOMEMBRANES
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β‐Amyloid deposition and neurofibrillary tangle formation in the olfactory bulb in ageing and Alzheimer’s disease
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Neuronal cell death in Alzheimer's disease correlates with apoE uptake and intracellular Abeta stabilization.
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Olfactory tau pathology in Alzheimer disease and mild cognitive impairment
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The role of microglial cells and astrocytes in fibrillar plaque evolution in transgenic APPSW mice
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Fibrous Astrocytes in Senile Dementia of the Alzheimer Type
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Extracellular neurofibrillary tangles reflect neuronal loss and provide further evidence of extensive protein cross-linking in Alzheimer disease
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Neurofibrillary tangle-predominant dementia: comparison with classical Alzheimer disease
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Interlaboratory Comparison of Neuropathology Assessments in Alzheimerʼs Disease: A Study of the Consortium to Establish a Registry for Alzheimerʼs Disease (CERAD)
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Role of the neuropathology of Alzheimer disease in dementia in the oldest-old
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Neuropil Threads Occur in Dendrites of Tangle—Bearing Nerve Cells
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Abortive apoptosis in Alzheimer's disease
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Alzheimer's disease: Advances in clinical and basic research
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Laminar distribution of neocortical senile plaques in senile dementia of the alzheimer type
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Modeling the Relation Between Neurofibrillary Tangles and Intellectual Status
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Senile Dementia with Tangles (Tangle Predominant Form of Senile Dementia)
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Three-Dimensional Tomographic Imaging and Characterization of Iron Compounds within Alzheimer's Plaque Core Material
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The neuropathological diagnosis of Alzheimer's disease
DeTure, M. A., & Dickson, D. W. (2019) · Molecular Neurodegeneration · doi:10.1186/s13024-019-0333-5 · Cited by 3,329 · see citing works
“In Lewy body dementia, Lewy related pathology affects corticolimbic regions and is often associated with concurrent Alzheimer type pathologic change [120, 121].”
Background
Alzheimer Disease: An Update on Pathobiology and Treatment Strategies
Long, J. M., & Holtzman, D. M. (2019) · Cell · doi:10.1016/j.cell.2019.09.001 · Cited by 3,204 · see citing works
Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature
Nelson, P. T., Alafuzoff, I., Bigio, E. H., Bouras, C., Braak, H., Cairns, N. J., Castellani, R. J., Crain, B. J., Davies, P., Tredici, K. D., et al. (2012) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0b013e31825018f7 · Cited by 2,050 · see citing works
“Excellent reviews are available about the molecular characteristics of NFTs and A A Ps (27, 28).”
BackgroundSelf-citation
Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets
Gao, C., Jiang, J., Tan, Y., & Chen, S. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01588-0 · Cited by 1,616 · see citing works
Alzheimer's disease: Targeting the Cholinergic System
H. Ferreira-Vieira, T., M. Guimaraes, I., R. Silva, F., & M. Ribeiro, F. (2016) · Current Neuropharmacology · doi:10.2174/1570159x13666150716165726 · Cited by 1,551 · see citing works
Distinct Tau Prion Strains Propagate in Cells and Mice and Define Different Tauopathies
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Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future
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Prion-like transmission of protein aggregates in neurodegenerative diseases
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Tau and tauopathies
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Motor deficits, neuron loss, and reduced anxiety coinciding with axonal degeneration and intraneuronal Aβ aggregation in the 5XFAD mouse model of Alzheimer's disease.
Jawhar, S., Trawicka, A., Jenneckens, C., Bayer, T. A., & Wirths, O. (2012) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2010.05.027 · Cited by 623 · see citing works
Cerebrospinal fluid secretion by the choroid plexus
Damkier, H. H., Brown, P. D., & Praetorius, J. (2013) · Physiological Reviews · doi:10.1152/physrev.00004.2013 · Cited by 606 · see citing works
Alzheimer's disease as homeostatic responses to age-related myelin breakdown
Bartzokis, G. (2011) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2009.08.007 · Cited by 546 · see citing works
Lipid peroxidation triggers neurodegeneration: A redox proteomics view into the Alzheimer disease brain
Sultana, R., Perluigi, M., & Butterfield, D. A. (2013) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2012.09.027 · Cited by 478 · see citing works
Resveratrol Mitigates Lipopolysaccharide- and Aβ-Mediated Microglial Inflammation by Inhibiting the TLR4/NF-Κb/STAT Signaling cascade
Capiralla, H., Vingtdeux, V., Zhao, H., Sankowski, R., Al‐Abed, Y., Davies, P., & Marambaud, P. (2012) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2011.07594.x · Cited by 426 · see citing works
Locus coeruleus volume and cell population changes during Alzheimer's disease progression: A stereological study in human postmortem brains with potential implication for early‐stage biomarker discovery
Theofilas, P., Ehrenberg, A. J., Dunlop, S., Di Lorenzo Alho, A. T., Nguy, A., Leite, R. E. P., Rodriguez, R. D., Mejia, M. B., Suemoto, C. K., Ferretti-Rebustini, R. E. D. L., et al. (2017) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2016.06.2362 · Cited by 416 · see citing works
α-synuclein in the pathophysiology of Alzheimer’s disease
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Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease
Gouras, G. K., Tampellini, D., Takahashi, R. H., & Capetillo-Zarate, E. (2010) · Acta Neuropathologica · doi:10.1007/s00401-010-0679-9 · Cited by 372 · see citing works
What Is Nuclear Factor Kappa B (NF-κB) Doing in and to the Mitochondrion?
Albensi, B. C. (2019) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2019.00154 · Cited by 341 · see citing works
Chronic stress and glucocorticoids: From neuronal plasticity to neurodegeneration
Vyas, S., Rodrigues, A. J., Silva, J. M., Tronche, F., Almeida, O. F. X., Sousa, N., & Sotiropoulos, I. (2016) · Neural Plasticity · doi:10.1155/2016/6391686 · Cited by 297 · see citing works
Emerging roles of innate and adaptive immunity in Alzheimer’s disease
Chen, X., & Holtzman, D. M. (2022) · Immunity · doi:10.1016/j.immuni.2022.10.016 · Cited by 297 · see citing works
Oxidative stress and β-amyloid protein in Alzheimer’s disease
Cai, Z., Zhao, B., & Ratka, A. (2011) · NeuroMolecular Medicine · doi:10.1007/s12017-011-8155-9 · Cited by 279 · see citing works
Contributions of Brain Insulin Resistance and Deficiency in Amyloid-Related Neurodegeneration in Alzheimerʼs Disease
de la Monte, S. M. (2012) · Drugs · doi:10.2165/11597760-000000000-00000 · Cited by 265 · see citing works
Regional dynamics of amyloid-β deposition in healthy elderly, mild cognitive impairment and Alzheimer’s disease: a voxelwise PiB–PET longitudinal study
Villain, N., Chételat, G., Grassiot, B., Bourgeat, P., Jones, G., Ellis, K. A., Ames, D., Martins, R. N., Eustache, F., Salvado, O., et al. (2012) · Brain · doi:10.1093/brain/aws125 · Cited by 255 · see citing works
Efficacy and Safety of A Liposome-Based Vaccine against Protein Tau, Assessed in Tau.P301L Mice That Model Tauopathy
Theunis, C., Crespo-Biel, N., Gafner, V., Pihlgren, M., López-Deber, M. P., Reis, P., Hickman, D. T., Adolfsson, O., Chuard, N., Ndao, D. M., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0072301 · Cited by 259 · see citing works
“be high in cognitively normal individuals [7,9–11].”
Background
Tau seeding activity begins in the transentorhinal/entorhinal regions and anticipates phospho-tau pathology in Alzheimer’s disease and PART
Kaufman, S. K., Del Tredici, K., Thomas, T. L., Braak, H., & Diamond, M. I. (2018) · Acta Neuropathologica · doi:10.1007/s00401-018-1855-6 · Cited by 259 · see citing works
Soluble Aβ Seeds Are Potent Inducers of Cerebral β-Amyloid Deposition
Langer, F., Eisele, Y. S., Fritschi, S. K., Staufenbiel, M., Walker, L. C., & Jucker, M. (2011) · The Journal of Neuroscience · doi:10.1523/jneurosci.3088-11.2011 · Cited by 237 · see citing works
4-Hydroxy-2-nonenal, a reactive product of lipid peroxidation, and neurodegenerative diseases: a toxic combination illuminated by redox proteomics studies
Perluigi, M., Coccia, R., & Butterfield, D. A. (2012) · Antioxidants & Redox Signaling · doi:10.1089/ars.2011.4406 · Cited by 229 · see citing works
Dynamic changes in myelin aberrations and oligodendrocyte generation in chronic amyloidosis in mice and men
Behrendt, G., Baer, K., Buffo, A., Curtis, M. A., Faull, R. L., Rees, M. I., Götz, M., & Dimou, L. (2013) · Glia · doi:10.1002/glia.22432 · Cited by 219 · see citing works
Does Alzheimer's disease begin in the brainstem?
Simic, G., Stanic, G., Mladinov, M., Jovanov‐Milosevic, N., Kostovic, I., & Hof, P. R. (2009) · Neuropathology and Applied Neurobiology · doi:10.1111/j.1365-2990.2009.01038.x · Cited by 204 · see citing works
A role for tau at the synapse in Alzheimer’s disease pathogenesis
Pooler, A. M., Noble, W., & Hanger, D. P. (2014) · Neuropharmacology · doi:10.1016/j.neuropharm.2013.09.018 · Cited by 203 · see citing works
RETRACTED ARTICLE: Brain-derived exosomes from dementia with Lewy bodies propagate α-synuclein pathology
Ngolab, J., Trinh, I., Rockenstein, E., Mante, M., Florio, J., Trejo, M., Masliah, D., Adame, A., Masliah, E., & Rissman, R. A. (2017) · Acta Neuropathologica Communications · doi:10.1186/s40478-017-0445-5 · Cited by 200 · see citing works
Retracted
Deregulation of excitatory neurotransmission underlying synapse failure in Alzheimer's disease
Paula‐Lima, A. C., Brito‐Moreira, J., & Ferreira, S. T. (2013) · Journal of Neurochemistry · doi:10.1111/jnc.12304 · Cited by 170 · see citing works
Efficacy and safety of immunization with phosphorylated tau against neurofibrillary tangles in mice
Boimel, M., Grigoriadis, N., Lourbopoulos, A., Haber, E., Abramsky, O., & Rosenmann, H. (2010) · Experimental Neurology · doi:10.1016/j.expneurol.2010.05.010 · Cited by 174 · see citing works
Alzheimer’s Disease: Exploring the Landscape of Cognitive Decline
Tenchov, R., Sasso, J. M., & Zhou, Q. A. (2024) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.4c00339 · Cited by 170 · see citing works
Immunohistological detection of Chlamydia pneumoniae in the Alzheimer's disease brain
Hammond, C. J., Hallock, L. R., Howanski, R. J., Appelt, D. M., Little, C. S., & Balin, B. J. (2010) · BMC Neuroscience · doi:10.1186/1471-2202-11-121 · Cited by 156 · see citing works
The Role of Telomerase Protein TERT in Alzheimer's Disease and in Tau-Related Pathology In Vitro
Spilsbury, A., Miwa, S., Attems, J., & Saretzki, G. (2015) · The Journal of Neuroscience · doi:10.1523/jneurosci.2925-14.2015 · Cited by 140 · see citing works
Oxidative modification of lipoic acid by HNE in Alzheimer disease brain
Hardas, S. S., Sultana, R., Clark, A. M., Beckett, T. L., Szweda, L. I., Murphy, M. P., & Butterfield, D. A. (2013) · Redox Biology · doi:10.1016/j.redox.2013.01.002 · Cited by 120 · see citing works
Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau
Rayaprolu, S., Higginbotham, L., Bagchi, P., Watson, C. M., Zhang, T., Levey, A. I., Rangaraju, S., & Seyfried, N. T. (2021) · Neuropsychopharmacology · doi:10.1038/s41386-020-00840-3 · Cited by 118 · see citing works
Is synaptic loss a unique hallmark of Alzheimer’s disease?
Scheff, S. W., Neltner, J. H., & Nelson, P. T. (2014) · Biochemical Pharmacology · doi:10.1016/j.bcp.2013.12.028 · Cited by 118 · see citing works
Histological underpinnings of grey matter changes in fibromyalgia investigated using multimodal brain imaging
Pomares, F. B., Funck, T., Feier, N. A., Roy, S., Daigle-Martel, A., Ceko, M., Narayanan, S., Araujo, D., Thiel, A., Stikov, N., et al. (2017) · The Journal of Neuroscience · doi:10.1523/jneurosci.2619-16.2016 · Cited by 108 · see citing works
Alzheimer’s Disease and Glaucoma: Mechanistic Similarities and Differences
Ghiso, J. A. (2013) · Journal of Glaucoma · doi:10.1097/ijg.0b013e3182934af6 · Cited by 107 · see citing works
PICALM and Alzheimer’s Disease: An Update and Perspectives
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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: Health Sciences › Medicine › Physiology › 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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