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[Brain lesions, pathogenic and etiologic hypotheses of Alzheimer's disease].
Rev Prat. 1998 Nov 01; 48(17):1873-8.RP

Abstract

The main lesions of Alzheimer's disease are: 1. amyloid deposits, labelled by antibodies directed against the A beta peptide (core of the senile plaques, diffuse deposits and amyloid angiopathy), 2. neurofibrillary lesions labelled by anti-tau antibodies (neurofibrillary tangles, neuropil threads, crown of the senile plaques) and 3. loss of neurons and synapses. The distribution of neurofibrillary pathology is hierarchical: they begin in the entorhinal cortex, progress along the anterograde corticocortical pathways toward the multimodal and unimodal associative cortices to reach, in the most severe cases, the primary cortices. Amyloid lesions are more diffuse, rapidly affecting all the cortical areas. The density of neurofibrillary tangles in the cerebral cortex is correlated with the severity of dementia. Neuritic plaques, synaptic and neuronal loss also contribute to the intellectual deterioration. There are various causes of Alzheimer's disease (several mutations, trisomy 21, repeated head trauma as in dementia pugilistica): it should be considered a syndrome. Its pathophysiology is complex and involves several proteins (e.g. amyloid protein precursor, tau protein, presenilins 1 and 2, and apolipoprotein E).

Authors+Show Affiliations

Laboratoire de neuropathologie, Raymond-Escourolle, Hôpital de La Salpêtrière, Paris.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
English Abstract
Journal Article

Language

fre

PubMed ID

9854388

Citation

Dessi, F, et al. "[Brain Lesions, Pathogenic and Etiologic Hypotheses of Alzheimer's Disease]." La Revue Du Praticien, vol. 48, no. 17, 1998, pp. 1873-8.
Dessi F, Colle MA, Hauw JJ, et al. [Brain lesions, pathogenic and etiologic hypotheses of Alzheimer's disease]. Rev Prat. 1998;48(17):1873-8.
Dessi, F., Colle, M. A., Hauw, J. J., & Duyckaerts, C. (1998). [Brain lesions, pathogenic and etiologic hypotheses of Alzheimer's disease]. La Revue Du Praticien, 48(17), 1873-8.
Dessi F, et al. [Brain Lesions, Pathogenic and Etiologic Hypotheses of Alzheimer's Disease]. Rev Prat. 1998 Nov 1;48(17):1873-8. PubMed PMID: 9854388.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Brain lesions, pathogenic and etiologic hypotheses of Alzheimer's disease]. AU - Dessi,F, AU - Colle,M A, AU - Hauw,J J, AU - Duyckaerts,C, PY - 1998/12/17/pubmed PY - 1998/12/17/medline PY - 1998/12/17/entrez SP - 1873 EP - 8 JF - La Revue du praticien JO - Rev Prat VL - 48 IS - 17 N2 - The main lesions of Alzheimer's disease are: 1. amyloid deposits, labelled by antibodies directed against the A beta peptide (core of the senile plaques, diffuse deposits and amyloid angiopathy), 2. neurofibrillary lesions labelled by anti-tau antibodies (neurofibrillary tangles, neuropil threads, crown of the senile plaques) and 3. loss of neurons and synapses. The distribution of neurofibrillary pathology is hierarchical: they begin in the entorhinal cortex, progress along the anterograde corticocortical pathways toward the multimodal and unimodal associative cortices to reach, in the most severe cases, the primary cortices. Amyloid lesions are more diffuse, rapidly affecting all the cortical areas. The density of neurofibrillary tangles in the cerebral cortex is correlated with the severity of dementia. Neuritic plaques, synaptic and neuronal loss also contribute to the intellectual deterioration. There are various causes of Alzheimer's disease (several mutations, trisomy 21, repeated head trauma as in dementia pugilistica): it should be considered a syndrome. Its pathophysiology is complex and involves several proteins (e.g. amyloid protein precursor, tau protein, presenilins 1 and 2, and apolipoprotein E). SN - 0035-2640 UR - https://www.unboundmedicine.com/medline/citation/9854388/[Brain_lesions_pathogenic_and_etiologic_hypotheses_of_Alzheimer's_disease]_ L2 - https://medlineplus.gov/alzheimersdisease.html DB - PRIME DP - Unbound Medicine ER -