scholarly journals AppGene Dosage Modulates Endosomal Abnormalities of Alzheimer's Disease in a Segmental Trisomy 16 Mouse Model of Down Syndrome

2003 ◽  
Vol 23 (17) ◽  
pp. 6788-6792 ◽  
Author(s):  
Anne M. Cataldo ◽  
Suzana Petanceska ◽  
Corrinne M. Peterhoff ◽  
Nicole B. Terio ◽  
Charles J. Epstein ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Down Syndrome ◽  
Mouse Model ◽  
Trisomy 16

scholarly journals The role of calbindin‐D28k in a mouse model of Down syndrome‐related Alzheimer's disease

2020 ◽  
Vol 16 (S2) ◽  
Author(s):  
Eric D. Hamlett ◽  
Steven L. Carroll ◽  
Ann‐Charlotte Granholm
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Down Syndrome ◽  
Mouse Model ◽  
Calbindin D28k

Impaired Sustained Attention and Error-Induced Stereotypy in the Aged Ts65Dn Mouse: A Mouse Model of Down Syndrome and Alzheimer's Disease.

2004 ◽  
Vol 118 (6) ◽  
pp. 1196-1205 ◽  
Author(s):  
Lori L. Driscoll ◽  
Jenna C. Carroll ◽  
Jisook Moon ◽  
Linda S. Crnic ◽  
David A. Levitsky ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Down Syndrome ◽  
Mouse Model ◽  
Sustained Attention ◽  
Ts65dn Mouse

scholarly journals Normalizing the gene dosage of Dyrk1A in a mouse model of Down syndrome rescues several Alzheimer's disease phenotypes

2017 ◽  
Vol 106 ◽  
pp. 76-88 ◽  
Author(s):  
Susana García-Cerro ◽  
Noemí Rueda ◽  
Verónica Vidal ◽  
Sara Lantigua ◽  
Carmen Martínez-Cué
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Down Syndrome ◽  
Mouse Model ◽  
Gene Dosage ◽  
Disease Phenotypes

scholarly journals Long‐term effects of maternal choline supplementation on CA1 pyramidal neuron gene expression in the Ts65Dn mouse model of Down syndrome and Alzheimer's disease

2019 ◽  
Vol 33 (9) ◽  
pp. 9871-9884 ◽  
Author(s):  
Melissa J. Alldred ◽  
Helen M. Chao ◽  
Sang Han Lee ◽  
Judah Beilin ◽  
Brian E. Powers ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Down Syndrome ◽  
Mouse Model ◽  
Pyramidal Neuron ◽  
Long Term Effects ◽  
Ts65dn Mouse ◽  
Ca1 Pyramidal Neuron

Down syndrome, Alzheimer's disease and the trisomy 16 mouse

1988 ◽  
Vol 11 (9) ◽  
pp. 390-394 ◽  
Author(s):  
J COYLE ◽  
M OSTERGRANITE ◽  
R REEVES ◽  
J GEARHART
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Down Syndrome ◽  
Trisomy 16

scholarly journals Sex Differences in the Cholinergic Basal Forebrain in the Ts65Dn Mouse Model of Down Syndrome and Alzheimer's Disease

2013 ◽  
Vol 24 (1) ◽  
pp. 33-44 ◽  
Author(s):  
Christy M. Kelley ◽  
Brian E. Powers ◽  
Ramon Velazquez ◽  
Jessica A. Ash ◽  
Stephen D. Ginsberg ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sex Differences ◽  
Down Syndrome ◽  
Mouse Model ◽  
Basal Forebrain ◽  
Ts65dn Mouse ◽  
Cholinergic Basal Forebrain

scholarly journals Oxidative Phosphorylation Is Dysregulated Within the Basocortical Circuit in a 6-month old Mouse Model of Down Syndrome and Alzheimer’s Disease

2021 ◽  
Vol 13 ◽  
Author(s):  
Melissa J. Alldred ◽  
Sang Han Lee ◽  
Grace E. Stutzmann ◽  
Stephen D. Ginsberg
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Down Syndrome ◽  
Mouse Model ◽  
Oxidative Phosphorylation ◽  
Basal Forebrain ◽  
Complex I ◽  
Neurological Dysfunction ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Oxidative Phosphorylation Pathway

Down syndrome (DS) is the primary genetic cause of intellectual disability (ID), which is due to the triplication of human chromosome 21 (HSA21). In addition to ID, HSA21 trisomy results in a number of neurological and physiological pathologies in individuals with DS, including progressive cognitive dysfunction and learning and memory deficits which worsen with age. Further exacerbating neurological dysfunction associated with DS is the concomitant basal forebrain cholinergic neuron (BFCN) degeneration and onset of Alzheimer’s disease (AD) pathology in early mid-life. Recent single population RNA sequencing (RNA-seq) analysis in the Ts65Dn mouse model of DS, specifically the medial septal cholinergic neurons of the basal forebrain (BF), revealed the mitochondrial oxidative phosphorylation pathway was significantly impacted, with a large subset of genes within this pathway being downregulated. We further queried oxidative phosphorylation pathway dysregulation in Ts65Dn mice by examining genes and encoded proteins within brain regions comprising the basocortical system at the start of BFCN degeneration (6 months of age). In select Ts65Dn mice we demonstrate significant deficits in gene and/or encoded protein levels of Complex I-V of the mitochondrial oxidative phosphorylation pathway in the BF. In the frontal cortex (Fr Ctx) these complexes had concomitant alterations in select gene expression but not of the proteins queried from Complex I-V, suggesting that defects at this time point in the BF are more severe and occur prior to cortical dysfunction within the basocortical circuit. We propose dysregulation within mitochondrial oxidative phosphorylation complexes is an early marker of cognitive decline onset and specifically linked to BFCN degeneration that may propagate pathology throughout cortical memory and executive function circuits in DS and AD.

Amelioration of Tau Pathology by Anle138b Rescues Neuronal Function in a Mouse Model of Human Alzheimer's Disease Tau

2019 ◽  
Author(s):  
M Deussing ◽  
T Blume ◽  
L Kaiser ◽  
F Probst ◽  
F Overhoff ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Neuronal Function ◽  
Tau Pathology
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