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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-語言資料,手稿 : 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.
面頁冊數:	1 online resource (49 pages)
附註:	Source: Masters Abstracts International, Volume: 84-08.
Contained By:	Masters Abstracts International84-08.
標題:	Morphology. -
電子資源:	click for full text (PQDT)
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. - 1 online resource (49 pages)

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

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

Includes bibliographical references

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.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2024

Mode of access: World Wide Web

ISBN: 9798371976178Subjects--Topical Terms:

1183868
Morphology.
Subjects--Index Terms:

Alzheimer's DiseaseIndex Terms--Genre/Form:

554714
Electronic books.

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