Hippocampal and cognitive alterations precede amyloid deposition in a mouse model of al- zheimer’s disease

Although there is strong evidence about neuronal and glial disturbances at advanced stages of Alzheimer’s disease, less attention has been directed to early, pre-amyloid changes that could contribute to the progression of the disease. We evaluated neuronal and glial morphological changes and behavio...

Descripción completa

Guardado en:

Detalles Bibliográficos
Publicado:	2014
Materias:	Alzheimer’s disease Glia Hippocampus Memory Neurogenesis Transgenic mice amyloid brain protein protein precursor amyloid precursor protein APP protein, human synaptophysin Alzheimer disease amygdaloid nucleus animal experiment animal model animal tissue Article behavior disorder cognitive defect controlled study dentate gyrus emotionality hippocampus immunohistochemistry mouse nerve cell nonhuman oncogene c fos amyloid plaque animal anxiety disorder astrocyte C57BL mouse disease course disease model genetics human isolation and purification metabolism mild cognitive impairment nervous system development pathology physiology transgenic mouse Alzheimer Disease Amyloid beta-Protein Precursor Animals Anxiety Disorders Astrocytes Dentate Gyrus Disease Models, Animal Disease Progression Humans Mice, Inbred C57BL Mice, Transgenic Mild Cognitive Impairment Neurons Plaque, Amyloid Synaptophysin
Acceso en línea:	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00257680_v74_n4_p282_Beauquis http://hdl.handle.net/20.500.12110/paper_00257680_v74_n4_p282_Beauquis
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

id	paper:paper_00257680_v74_n4_p282_Beauquis
record_format	dspace
spelling	paper:paper_00257680_v74_n4_p282_Beauquis2023-06-08T14:53:41Z Hippocampal and cognitive alterations precede amyloid deposition in a mouse model of al- zheimer’s disease Alzheimer’s disease Glia Hippocampus Memory Neurogenesis Transgenic mice amyloid brain protein protein precursor amyloid precursor protein APP protein, human synaptophysin Alzheimer disease amygdaloid nucleus animal experiment animal model animal tissue Article behavior disorder cognitive defect controlled study dentate gyrus emotionality hippocampus immunohistochemistry mouse nerve cell nonhuman oncogene c fos Alzheimer disease amyloid plaque animal anxiety disorder astrocyte C57BL mouse disease course disease model genetics hippocampus human isolation and purification metabolism mild cognitive impairment nervous system development pathology physiology transgenic mouse Alzheimer Disease Amyloid beta-Protein Precursor Animals Anxiety Disorders Astrocytes Dentate Gyrus Disease Models, Animal Disease Progression Hippocampus Humans Mice, Inbred C57BL Mice, Transgenic Mild Cognitive Impairment Neurogenesis Neurons Plaque, Amyloid Synaptophysin Although there is strong evidence about neuronal and glial disturbances at advanced stages of Alzheimer’s disease, less attention has been directed to early, pre-amyloid changes that could contribute to the progression of the disease. We evaluated neuronal and glial morphological changes and behavioral disturbances in PDAPP-J20 transgenic (Tg) mice, carrying mutated human APP gene (amyloid precursor protein), at 5 months of age, before brain amyloid deposition occurs. Using NeuN immunohistochemistry we found decreased numbers of pyramidal and granular neurons in the hippocampus associated with a reduction of hippocampal volume in Tg mice compared with controls. Neurogenesis was impaired, evidenced by means of DCX immunohistochemistry in the dentate gyrus. In the CA3 region we found a decreased density of synaptophysin, suggesting synaptic disturbance, but no changes were found in CA1 synaptic spine density. Using confocal microscopy we observed decreased number and cell complexity of GFAP+ astrocytes, indicating potential glial atrophy. Cognitive impairment (novel location recognition test) and increased anxiety (open field) were detected in Tg mice, associated with more c-Fos+ nuclei in the amygdala, possibly indicating a role for emotionality in early stages of the disease. The study of early alterations in the course of amyloid pathology could contribute to the development of diagnostic and preventive strategies. © 2014, MEDICINA (Buenos Aires). All Rights Reserved. 2014 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00257680_v74_n4_p282_Beauquis http://hdl.handle.net/20.500.12110/paper_00257680_v74_n4_p282_Beauquis
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	Alzheimer’s disease Glia Hippocampus Memory Neurogenesis Transgenic mice amyloid brain protein protein precursor amyloid precursor protein APP protein, human synaptophysin Alzheimer disease amygdaloid nucleus animal experiment animal model animal tissue Article behavior disorder cognitive defect controlled study dentate gyrus emotionality hippocampus immunohistochemistry mouse nerve cell nonhuman oncogene c fos Alzheimer disease amyloid plaque animal anxiety disorder astrocyte C57BL mouse disease course disease model genetics hippocampus human isolation and purification metabolism mild cognitive impairment nervous system development pathology physiology transgenic mouse Alzheimer Disease Amyloid beta-Protein Precursor Animals Anxiety Disorders Astrocytes Dentate Gyrus Disease Models, Animal Disease Progression Hippocampus Humans Mice, Inbred C57BL Mice, Transgenic Mild Cognitive Impairment Neurogenesis Neurons Plaque, Amyloid Synaptophysin
spellingShingle	Alzheimer’s disease Glia Hippocampus Memory Neurogenesis Transgenic mice amyloid brain protein protein precursor amyloid precursor protein APP protein, human synaptophysin Alzheimer disease amygdaloid nucleus animal experiment animal model animal tissue Article behavior disorder cognitive defect controlled study dentate gyrus emotionality hippocampus immunohistochemistry mouse nerve cell nonhuman oncogene c fos Alzheimer disease amyloid plaque animal anxiety disorder astrocyte C57BL mouse disease course disease model genetics hippocampus human isolation and purification metabolism mild cognitive impairment nervous system development pathology physiology transgenic mouse Alzheimer Disease Amyloid beta-Protein Precursor Animals Anxiety Disorders Astrocytes Dentate Gyrus Disease Models, Animal Disease Progression Hippocampus Humans Mice, Inbred C57BL Mice, Transgenic Mild Cognitive Impairment Neurogenesis Neurons Plaque, Amyloid Synaptophysin Hippocampal and cognitive alterations precede amyloid deposition in a mouse model of al- zheimer’s disease
topic_facet	Alzheimer’s disease Glia Hippocampus Memory Neurogenesis Transgenic mice amyloid brain protein protein precursor amyloid precursor protein APP protein, human synaptophysin Alzheimer disease amygdaloid nucleus animal experiment animal model animal tissue Article behavior disorder cognitive defect controlled study dentate gyrus emotionality hippocampus immunohistochemistry mouse nerve cell nonhuman oncogene c fos Alzheimer disease amyloid plaque animal anxiety disorder astrocyte C57BL mouse disease course disease model genetics hippocampus human isolation and purification metabolism mild cognitive impairment nervous system development pathology physiology transgenic mouse Alzheimer Disease Amyloid beta-Protein Precursor Animals Anxiety Disorders Astrocytes Dentate Gyrus Disease Models, Animal Disease Progression Hippocampus Humans Mice, Inbred C57BL Mice, Transgenic Mild Cognitive Impairment Neurogenesis Neurons Plaque, Amyloid Synaptophysin
description	Although there is strong evidence about neuronal and glial disturbances at advanced stages of Alzheimer’s disease, less attention has been directed to early, pre-amyloid changes that could contribute to the progression of the disease. We evaluated neuronal and glial morphological changes and behavioral disturbances in PDAPP-J20 transgenic (Tg) mice, carrying mutated human APP gene (amyloid precursor protein), at 5 months of age, before brain amyloid deposition occurs. Using NeuN immunohistochemistry we found decreased numbers of pyramidal and granular neurons in the hippocampus associated with a reduction of hippocampal volume in Tg mice compared with controls. Neurogenesis was impaired, evidenced by means of DCX immunohistochemistry in the dentate gyrus. In the CA3 region we found a decreased density of synaptophysin, suggesting synaptic disturbance, but no changes were found in CA1 synaptic spine density. Using confocal microscopy we observed decreased number and cell complexity of GFAP+ astrocytes, indicating potential glial atrophy. Cognitive impairment (novel location recognition test) and increased anxiety (open field) were detected in Tg mice, associated with more c-Fos+ nuclei in the amygdala, possibly indicating a role for emotionality in early stages of the disease. The study of early alterations in the course of amyloid pathology could contribute to the development of diagnostic and preventive strategies. © 2014, MEDICINA (Buenos Aires). All Rights Reserved.
title	Hippocampal and cognitive alterations precede amyloid deposition in a mouse model of al- zheimer’s disease
title_short	Hippocampal and cognitive alterations precede amyloid deposition in a mouse model of al- zheimer’s disease
title_full	Hippocampal and cognitive alterations precede amyloid deposition in a mouse model of al- zheimer’s disease
title_fullStr	Hippocampal and cognitive alterations precede amyloid deposition in a mouse model of al- zheimer’s disease
title_full_unstemmed	Hippocampal and cognitive alterations precede amyloid deposition in a mouse model of al- zheimer’s disease
title_sort	hippocampal and cognitive alterations precede amyloid deposition in a mouse model of al- zheimer’s disease
publishDate	2014
url	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00257680_v74_n4_p282_Beauquis http://hdl.handle.net/20.500.12110/paper_00257680_v74_n4_p282_Beauquis
_version_	1768542876184084480

Hippocampal and cognitive alterations precede amyloid deposition in a mouse model of al- zheimer’s disease

Ejemplares similares