Behavioral and Neuronal Characterizations, across Ages, of the TgSwDI Mouse Model of Alzheimer’s Disease

Alzheimer’s disease (AD) is a neurodegenerative disorder that currently affects as many as 50 million people worldwide. It is neurochemically characterized by an aggregation of β-amyloid plaques and tau neurofibrillary tangles that result in neuronal dysfunction, cognitive decline, and a progressive...

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Main Authors: Natalie A. Tan, Angelica M. Alvarado Carpio, H. Craig Heller, Elsa C. Pittaras
Format: Article
Language:English
Published: MDPI AG 2023-12-01
Series:Genes
Subjects:
Online Access:https://www.mdpi.com/2073-4425/15/1/47
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author Natalie A. Tan
Angelica M. Alvarado Carpio
H. Craig Heller
Elsa C. Pittaras
author_facet Natalie A. Tan
Angelica M. Alvarado Carpio
H. Craig Heller
Elsa C. Pittaras
author_sort Natalie A. Tan
collection DOAJ
description Alzheimer’s disease (AD) is a neurodegenerative disorder that currently affects as many as 50 million people worldwide. It is neurochemically characterized by an aggregation of β-amyloid plaques and tau neurofibrillary tangles that result in neuronal dysfunction, cognitive decline, and a progressive loss of brain function. TgSwDI is a well-studied transgenic mouse model of AD, but no longitudinal studies have been performed to characterize cognitive deficits or β-amyloid plaque accumulation for use as a baseline reference in future research. Thus, we use behavioral tests (T-Maze, Novel Object Recognition (NOR), Novel Object Location (NOL)) to study long-term and working memory, and immunostaining to study β-amyloid plaque deposits, as well as brain size, in hippocampal, cerebellum, and cortical slices in TgSwDI and wild-type (WT) mice at 3, 5, 8, and 12 months old. The behavioral results show that TgSwDI mice exhibit deficits in their long-term spatial memory starting at 8 months old and in long-term recognition memory at all ages, but no deficits in their working memory. Immunohistochemistry showed an exponential increase in β-amyloid plaque in the hippocampus and cortex of TgSwDI mice over time, whereas there was no significant accumulation of plaque in WT mice at any age. Staining showed a smaller hippocampus and cerebellum starting at 8 months old for the TgSwDI compared to WT mice. Our data show how TgSwDI mice differ from WT mice in their baseline levels of cognitive function and β-amyloid plaque load throughout their lives.
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spelling doaj.art-47209f2342d9408ba361cb51230739262024-01-26T16:41:42ZengMDPI AGGenes2073-44252023-12-011514710.3390/genes15010047Behavioral and Neuronal Characterizations, across Ages, of the TgSwDI Mouse Model of Alzheimer’s DiseaseNatalie A. Tan0Angelica M. Alvarado Carpio1H. Craig Heller2Elsa C. Pittaras3Department of Biology, Stanford University, Stanford, CA 94305, USADepartment of Biology, Stanford University, Stanford, CA 94305, USADepartment of Biology, Stanford University, Stanford, CA 94305, USADepartment of Biology, Stanford University, Stanford, CA 94305, USAAlzheimer’s disease (AD) is a neurodegenerative disorder that currently affects as many as 50 million people worldwide. It is neurochemically characterized by an aggregation of β-amyloid plaques and tau neurofibrillary tangles that result in neuronal dysfunction, cognitive decline, and a progressive loss of brain function. TgSwDI is a well-studied transgenic mouse model of AD, but no longitudinal studies have been performed to characterize cognitive deficits or β-amyloid plaque accumulation for use as a baseline reference in future research. Thus, we use behavioral tests (T-Maze, Novel Object Recognition (NOR), Novel Object Location (NOL)) to study long-term and working memory, and immunostaining to study β-amyloid plaque deposits, as well as brain size, in hippocampal, cerebellum, and cortical slices in TgSwDI and wild-type (WT) mice at 3, 5, 8, and 12 months old. The behavioral results show that TgSwDI mice exhibit deficits in their long-term spatial memory starting at 8 months old and in long-term recognition memory at all ages, but no deficits in their working memory. Immunohistochemistry showed an exponential increase in β-amyloid plaque in the hippocampus and cortex of TgSwDI mice over time, whereas there was no significant accumulation of plaque in WT mice at any age. Staining showed a smaller hippocampus and cerebellum starting at 8 months old for the TgSwDI compared to WT mice. Our data show how TgSwDI mice differ from WT mice in their baseline levels of cognitive function and β-amyloid plaque load throughout their lives.https://www.mdpi.com/2073-4425/15/1/47Alzheimer’s diseaseTgSwDI mouse modelβ-amyloidimmunochemistrymemorymotor skills
spellingShingle Natalie A. Tan
Angelica M. Alvarado Carpio
H. Craig Heller
Elsa C. Pittaras
Behavioral and Neuronal Characterizations, across Ages, of the TgSwDI Mouse Model of Alzheimer’s Disease
Genes
Alzheimer’s disease
TgSwDI mouse model
β-amyloid
immunochemistry
memory
motor skills
title Behavioral and Neuronal Characterizations, across Ages, of the TgSwDI Mouse Model of Alzheimer’s Disease
title_full Behavioral and Neuronal Characterizations, across Ages, of the TgSwDI Mouse Model of Alzheimer’s Disease
title_fullStr Behavioral and Neuronal Characterizations, across Ages, of the TgSwDI Mouse Model of Alzheimer’s Disease
title_full_unstemmed Behavioral and Neuronal Characterizations, across Ages, of the TgSwDI Mouse Model of Alzheimer’s Disease
title_short Behavioral and Neuronal Characterizations, across Ages, of the TgSwDI Mouse Model of Alzheimer’s Disease
title_sort behavioral and neuronal characterizations across ages of the tgswdi mouse model of alzheimer s disease
topic Alzheimer’s disease
TgSwDI mouse model
β-amyloid
immunochemistry
memory
motor skills
url https://www.mdpi.com/2073-4425/15/1/47
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