Classification and basic pathology of Alzheimer disease

The lesions of Alzheimer disease include accumulation of proteins, losses of neurons and synapses, and alterations related to reactive processes. Extracellular Aβ accumulation occurs in the parenchyma as diffuse, focal or stellate deposits. It may involve the vessel walls of arteries, veins and capi...

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Published in	Acta neuropathologica Vol. 118; no. 1; pp. 5 - 36
Main Authors	Duyckaerts, Charles, Delatour, Benoît, Potier, Marie-Claude
Format	Journal Article
Language	English
Published	Berlin/Heidelberg Springer-Verlag 01.07.2009 Springer Nature B.V
Subjects	Age of Onset Alzheimer Disease - classification Alzheimer Disease - diagnosis Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Amyloid beta-Peptides - metabolism Animals Brain - blood supply Brain - metabolism Brain - pathology Cell Death Disease Progression DNA-Binding Proteins - metabolism Gliosis - complications Humans Lewy Bodies - pathology Medicine Medicine & Public Health Nerve Degeneration - pathology Neurofibrillary Tangles - metabolism Neurofibrillary Tangles - pathology Neurogenesis Neuronal Plasticity Neurons - pathology Neurons - physiology Neurosciences Pathology Peptides Plaque, Amyloid - pathology Proteins Review Sclerosis Synaptic Transmission tau Proteins - metabolism Tauopathies - pathology Tauopathies - physiopathology Entorhinal Cortex Cerebral Amyloid Angiopathy Senile Plaque Alzheimer Disease Neuritic Plaque
Online Access	Get full text
ISSN	0001-6322 1432-0533 1432-0533
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 Aβ 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 apoε 4 alleles. Parenchymal as well as vascular Aβ 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 Aβ 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).
AbstractList	The lesions of Alzheimer disease include accumulation of proteins, losses of neurons and synapses, and alterations related to reactive processes. Extracellular Aβ 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 apoε 4 alleles. Parenchymal as well as vascular Aβ 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 Aβ 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). 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). The lesions of Alzheimer disease include accumulation of proteins, losses of neurons and synapses, and alterations related to reactive processes. Extracellular A beta 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 apo epsilon 4 alleles. Parenchymal as well as vascular A beta 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 A beta 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). 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).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).
Author	Duyckaerts, Charles Potier, Marie-Claude Delatour, Benoît
Author_xml	– sequence: 1 givenname: Charles surname: Duyckaerts fullname: Duyckaerts, Charles email: charles.duyckaerts@psl.aphp.fr, charles.duyckaerts@psl.ap-hop-paris.fr organization: Laboratoire de Neuropathologie Escourolle, APHP, Hôpital de La Salpêtrière et Université Pierre et Marie Curie, Paris Universitas, Team 103, Inserm UMRS 975, CNRS UMR 7225, Centre de Recherche Institut du Cerveau et de la Moëlle – sequence: 2 givenname: Benoît surname: Delatour fullname: Delatour, Benoît organization: Team 103, Inserm UMRS 975, CNRS UMR 7225, Centre de Recherche Institut du Cerveau et de la Moëlle – sequence: 3 givenname: Marie-Claude surname: Potier fullname: Potier, Marie-Claude organization: Team 103, Inserm UMRS 975, CNRS UMR 7225, Centre de Recherche Institut du Cerveau et de la Moëlle
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/19381658$$D View this record in MEDLINE/PubMed
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Publisher	Springer-Verlag Springer Nature B.V
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SubjectTerms	Age of Onset Alzheimer Disease - classification Alzheimer Disease - diagnosis Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Amyloid beta-Peptides - metabolism Animals Brain - blood supply Brain - metabolism Brain - pathology Cell Death Disease Progression DNA-Binding Proteins - metabolism Gliosis - complications Humans Lewy Bodies - pathology Medicine Medicine & Public Health Nerve Degeneration - pathology Neurofibrillary Tangles - metabolism Neurofibrillary Tangles - pathology Neurogenesis Neuronal Plasticity Neurons - pathology Neurons - physiology Neurosciences Pathology Peptides Plaque, Amyloid - pathology Proteins Review Sclerosis Synaptic Transmission tau Proteins - metabolism Tauopathies - pathology Tauopathies - physiopathology
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Title	Classification and basic pathology of Alzheimer disease
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