Multicellular hypothesis for the pathogenesis of Alzheimer's disease.
FASEB J
; 31(5): 1792-1795, 2017 05.
Article
en En
| MEDLINE
| ID: mdl-28100644
ABSTRACT
Extensive abnormal interactions among microglia, astrocytes, and neurons of the CNS have been observed in proteinopathic neurodegenerative dementias of the elderly. These multicellular interactions are initiated by insoluble tangles of phosphorylated tau protein and plaques of amyloid peptides. Most research has focused on these neurotoxic proteins, but much less is known about the pathogenic roles of the responding resident and recruited neural cells. Principal interactions among the major 3 sets of CNS cells are herein considered at several levels in relation to cellular phenotypic alterations, mechanisms of cellular communication, and extent of involvement in the pathogenesis of Alzheimer's disease and related proteinopathic dementias. It remains to be determined which of these abnormal neurocellular phenomena are primary events and sufficiently contributory to neurodegeneration to be useful targets for therapy of senile dementias.-Goetzl, E. J., Miller, B. L. Multicellular hypothesis for the pathogenesis of Alzheimer's disease.
Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Péptidos beta-Amiloides
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Ovillos Neurofibrilares
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Placa Amiloide
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Enfermedad de Alzheimer
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Neuronas
Tipo de estudio:
Etiology_studies
Límite:
Animals
/
Humans
Idioma:
En
Revista:
FASEB J
Asunto de la revista:
BIOLOGIA
/
FISIOLOGIA
Año:
2017
Tipo del documento:
Article