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Inflammation occurs early during the Abeta deposition process in TgCRND8 mice.
Neurobiol Aging 2004; 25(7):861-71NA

Abstract

Alzheimer's disease (AD) is characterized by a progressive cognitive decline leading to dementia and involves the deposition of amyloid-beta (Abeta) peptides into senile plaques. Other neuropathological features that accompany progression of the disease include a decrease in synaptic density, neurofibrillary tangles, dystrophic neurites, inflammation, and neuronal cell loss. In this study, we report the early kinetics of brain amyloid deposition and its associated inflammation in an early onset transgenic mouse model of AD (TgCRND8) harboring the human amyloid precursor protein gene with the Indiana and Swedish mutations. Both diffuse and compact plaques were detected as early as 9-10 weeks of age. Abeta-immunoreactive (Abeta-IR) plaques (4G8-positive) appeared first in the neocortex and amygdala, then in the hippocampal formation, and lastly in the thalamus. Compact plaques (ThioS-positive) with an amyloid core were observed as early as diffuse plaques were detected, but in lower numbers. Amyloid deposition increased progressively with age. The formation of plaques was concurrent with the appearance of activated microglial cells and shortly followed by the clustering of activated astrocytes around plaques at 13-14 weeks of age. This TgCRND8 mouse model allows for a rapid, time-dependent study of the relationship between the fibrillogenic process and the inflammatory response during the brain amyloidogenic process.

Authors+Show Affiliations

Department of Medicine, Division of Experimental Medicine, McGill University, Montréal, Qué., Canada.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15212840

Citation

Dudal, Sherri, et al. "Inflammation Occurs Early During the Abeta Deposition Process in TgCRND8 Mice." Neurobiology of Aging, vol. 25, no. 7, 2004, pp. 861-71.
Dudal S, Krzywkowski P, Paquette J, et al. Inflammation occurs early during the Abeta deposition process in TgCRND8 mice. Neurobiol Aging. 2004;25(7):861-71.
Dudal, S., Krzywkowski, P., Paquette, J., Morissette, C., Lacombe, D., Tremblay, P., & Gervais, F. (2004). Inflammation occurs early during the Abeta deposition process in TgCRND8 mice. Neurobiology of Aging, 25(7), pp. 861-71.
Dudal S, et al. Inflammation Occurs Early During the Abeta Deposition Process in TgCRND8 Mice. Neurobiol Aging. 2004;25(7):861-71. PubMed PMID: 15212840.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inflammation occurs early during the Abeta deposition process in TgCRND8 mice. AU - Dudal,Sherri, AU - Krzywkowski,Pascale, AU - Paquette,Julie, AU - Morissette,Céline, AU - Lacombe,Diane, AU - Tremblay,Patrick, AU - Gervais,Francine, PY - 2002/12/16/received PY - 2003/06/25/revised PY - 2003/08/28/accepted PY - 2004/6/24/pubmed PY - 2004/9/24/medline PY - 2004/6/24/entrez SP - 861 EP - 71 JF - Neurobiology of aging JO - Neurobiol. Aging VL - 25 IS - 7 N2 - Alzheimer's disease (AD) is characterized by a progressive cognitive decline leading to dementia and involves the deposition of amyloid-beta (Abeta) peptides into senile plaques. Other neuropathological features that accompany progression of the disease include a decrease in synaptic density, neurofibrillary tangles, dystrophic neurites, inflammation, and neuronal cell loss. In this study, we report the early kinetics of brain amyloid deposition and its associated inflammation in an early onset transgenic mouse model of AD (TgCRND8) harboring the human amyloid precursor protein gene with the Indiana and Swedish mutations. Both diffuse and compact plaques were detected as early as 9-10 weeks of age. Abeta-immunoreactive (Abeta-IR) plaques (4G8-positive) appeared first in the neocortex and amygdala, then in the hippocampal formation, and lastly in the thalamus. Compact plaques (ThioS-positive) with an amyloid core were observed as early as diffuse plaques were detected, but in lower numbers. Amyloid deposition increased progressively with age. The formation of plaques was concurrent with the appearance of activated microglial cells and shortly followed by the clustering of activated astrocytes around plaques at 13-14 weeks of age. This TgCRND8 mouse model allows for a rapid, time-dependent study of the relationship between the fibrillogenic process and the inflammatory response during the brain amyloidogenic process. SN - 0197-4580 UR - https://www.unboundmedicine.com/medline/citation/15212840/Inflammation_occurs_early_during_the_Abeta_deposition_process_in_TgCRND8_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0197458003001945 DB - PRIME DP - Unbound Medicine ER -