Chronic Mild Stress Assay Leading to Early Onset and Propagation of Alzheimer’s Disease Phenotype in Mouse Models

2016 ◽  
pp. 241-246 ◽  
Author(s):  
Mar Cuadrado-Tejedor ◽  
Ana García-Osta
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Models ◽  
Early Onset ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Disease Phenotype

Chronic Mild Stress Accelerates the Onset and Progression of the Alzheimer's Disease Phenotype in Tg2576 Mice

2012 ◽  
Vol 28 (3) ◽  
pp. 567-578 ◽  
Author(s):  
Mar Cuadrado-Tejedor ◽  
Ana Ricobaraza ◽  
Diana Frechilla ◽  
Rafael Franco ◽  
Alberto Pérez-Mediavilla ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Disease Phenotype ◽  
Tg2576 Mice

Transgenic mouse models of Alzheimer's disease: phenotype and mechanisms of pathogenesis

2001 ◽  
Vol 67 ◽  
pp. 195-202 ◽  
Author(s):  
Karen Duff
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Transgenic Mice ◽  
Amyloid Precursor Protein ◽  
Transgenic Mouse ◽  
Mouse Models ◽  
Precursor Protein ◽  
Transgenic Mouse Models ◽  
Disease Phenotype

A range of transgenic mice have been created to model Alzheimer's disease. These include mice expressing human forms of the amyloid precursor protein, the presenilins and, more recently, tau. Several of the models develop features of the disease including amyloid pathology, cholinergic deficits, neurodegeneration and cognitive impairment. Progress in the characterization and use of these model animals is discussed.

scholarly journals Genetic dissection of down syndrome-associated alterations in APP/amyloid-β biology using mouse models

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Justin L. Tosh ◽  
◽  
Elena R. Rhymes ◽  
Paige Mumford ◽  
Heather T. Whittaker ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Down Syndrome ◽  
Amyloid Precursor Protein ◽  
Mouse Models ◽  
Early Onset ◽  
Amyloid Β ◽  
Chromosome 21 ◽  
Extra Copy ◽  
Early Onset Alzheimer’S Disease

AbstractIndividuals who have Down syndrome (caused by trisomy of chromosome 21), have a greatly elevated risk of early-onset Alzheimer’s disease, in which amyloid-β accumulates in the brain. Amyloid-β is a product of the chromosome 21 gene APP (amyloid precursor protein) and the extra copy or ‘dose’ of APP is thought to be the cause of this early-onset Alzheimer’s disease. However, other chromosome 21 genes likely modulate disease when in three-copies in people with Down syndrome. Here we show that an extra copy of chromosome 21 genes, other than APP, influences APP/Aβ biology. We crossed Down syndrome mouse models with partial trisomies, to an APP transgenic model and found that extra copies of subgroups of chromosome 21 gene(s) modulate amyloid-β aggregation and APP transgene-associated mortality, independently of changing amyloid precursor protein abundance. Thus, genes on chromosome 21, other than APP, likely modulate Alzheimer’s disease in people who have Down syndrome.

P4-273: Impairment Of Adolescent Hippocampal Plasticity In Mouse Models For Alzheimer's Disease Precedes Disease Phenotype

2009 ◽  
Vol 5 (4S_Part_17) ◽  
pp. e10-e10
Author(s):  
Daniela Hartl ◽  
Lei Mao ◽  
Claus Zabel ◽  
Joachim Klose
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Models ◽  
Disease Phenotype ◽  
Hippocampal Plasticity

scholarly journals Genetic dissection of Down syndrome-associated alterations in APP/amyloid-β biology using mouse models

2020 ◽  
Author(s):  
Justin L. Tosh ◽  
Ellie Rhymes ◽  
Paige Mumford ◽  
Heather T. Whittaker ◽  
Laura J. Pulford ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Down Syndrome ◽  
Amyloid Precursor Protein ◽  
Mouse Models ◽  
Early Onset ◽  
Amyloid Β ◽  
Chromosome 21 ◽  
Extra Copy ◽  
Early Onset Alzheimer’S Disease

AbstractIndividuals who have Down syndrome (caused by trisomy of chromosome 21), have a greatly elevated risk of early-onset Alzheimer’s disease, in which amyloid-β accumulates in the brain. Amyloid-β is a product of the chromosome 21 gene APP (amyloid precursor protein) and the extra copy or ‘dose’ of APP is thought to be the cause of this early-onset Alzheimer’s disease. However, other chromosome 21 genes likely modulate disease when in three-copies in people with Down syndrome. Here we show that an extra copy of chromosome 21 genes, other than APP, influences APP/Aβ biology. We crossed Down syndrome mouse models with partial trisomies, to an APP transgenic model and found that extra copies of subgroups of chromosome 21 gene(s) modulate amyloid-β aggregation and APP transgene-associated mortality, independently of changing amyloid precursor protein abundance. Thus, genes on chromosome 21, other than APP, likely modulate Alzheimer’s disease in people who have Down syndrome.

Distinct social-behavioral changes in frontotemporal dementia and early onset Alzheimer's disease

2014 ◽  
Author(s):  
Joseph P. Barsuglia ◽  
Michelle J. Mather ◽  
Hemali V. Panchal ◽  
Aditi Joshi ◽  
Elvira Jimenez ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Frontotemporal Dementia ◽  
Early Onset ◽  
Behavioral Changes ◽  
Early Onset Alzheimer’S Disease
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