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Longitudinal Characterization of Behavioral, Pathological, and Genomic Profiles in an Alzheimer’s Disease Mouse Model.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Longitudinal Characterization of Behavioral, Pathological, and Genomic Profiles in an Alzheimer’s Disease Mouse Model.
作者:	Kumar, Manasa.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, 2023
面頁冊數:	49 p.
附註:	Source: Masters Abstracts International, Volume: 84-08.
附註:	Advisor: Yan, Zhen.
Contained By:	Masters Abstracts International84-08.
標題:	Neurosciences.
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=30244675
ISBN:	9798371976178

Longitudinal Characterization of Behavioral, Pathological, and Genomic Profiles in an Alzheimer’s Disease Mouse Model.
Kumar, Manasa.

Longitudinal Characterization of Behavioral, Pathological, and Genomic Profiles in an Alzheimer’s Disease Mouse Model. - Ann Arbor : ProQuest Dissertations & Theses, 2023 - 49 p.

Source: Masters Abstracts International, Volume: 84-08.

Thesis (M.S.)--State University of New York at Buffalo, 2023.

This item must not be sold to any third party vendors.

Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder characterized by significant memory impairment and cognitive decline. Gradual onset of subclinical neurobiological and behavioral changes precede diagnosis by years, sometimes even decades. Our study aimed to longitudinally characterize behavioral, synaptic, morphological, and genomic profiles in the hyperphosphorylated P301S tau mouse model, to elucidate how dysfunction in these processes might account for any of the changes observed in AD. Insoluble total and hyperphosphorylated tau was found from 1-month-old mice. Transgenic mice showed spatial memory deficits from as early as 3-4 months of age, while recognition memory deficits and impaired sociability were seen at 5-6 months of age. Further, morphological analyses determined a decrease in dendritic arborization from 3 months of age in hippocampus of transgenic tau mice. Gene Ontology (GO) analysis of Differentially Expressed Genes (DEGs) revealed upregulated synaptic genes as the top affected category at 3 months of age in the hippocampus of transgenic tau mice, and this was later partially confirmed with RT/q-PCR. Taken together, these findings imply that there may be a compensatory mechanism at work at an early timepoint. It may also indicate that this overexpression of synaptic genes is resulting in an excitotoxic effect, which may be the driving force behind neurodegeneration observed in AD. Further study of these findings will contribute to the advancement of understanding pathophysiological mechanisms, and help preclinical detection and diagnosis, of AD and other tauopathies.

ISBN: 9798371976178Subjects--Topical Terms:

211508
Neurosciences.
Subjects--Index Terms:

Alzheimer's Disease

Longitudinal Characterization of Behavioral, Pathological, and Genomic Profiles in an Alzheimer’s Disease Mouse Model.
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506 $a This item must not be sold to any third party vendors.
520 $a Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder characterized by significant memory impairment and cognitive decline. Gradual onset of subclinical neurobiological and behavioral changes precede diagnosis by years, sometimes even decades. Our study aimed to longitudinally characterize behavioral, synaptic, morphological, and genomic profiles in the hyperphosphorylated P301S tau mouse model, to elucidate how dysfunction in these processes might account for any of the changes observed in AD. Insoluble total and hyperphosphorylated tau was found from 1-month-old mice. Transgenic mice showed spatial memory deficits from as early as 3-4 months of age, while recognition memory deficits and impaired sociability were seen at 5-6 months of age. Further, morphological analyses determined a decrease in dendritic arborization from 3 months of age in hippocampus of transgenic tau mice. Gene Ontology (GO) analysis of Differentially Expressed Genes (DEGs) revealed upregulated synaptic genes as the top affected category at 3 months of age in the hippocampus of transgenic tau mice, and this was later partially confirmed with RT/q-PCR. Taken together, these findings imply that there may be a compensatory mechanism at work at an early timepoint. It may also indicate that this overexpression of synaptic genes is resulting in an excitotoxic effect, which may be the driving force behind neurodegeneration observed in AD. Further study of these findings will contribute to the advancement of understanding pathophysiological mechanisms, and help preclinical detection and diagnosis, of AD and other tauopathies.
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