scholarly journals Polygenic Risk for Alzheimer's Disease is not Associated with Cognitive Ability or Cognitive Aging in Non-Demented Older People

2014 ◽  
Vol 39 (3) ◽  
pp. 565-574 ◽  
Author(s):  
Sarah E. Harris ◽  
Gail Davies ◽  
Michelle Luciano ◽  
Antony Payton ◽  
Helen C. Fox ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Older People ◽  
Cognitive Ability ◽  
Cognitive Aging ◽  
Polygenic Risk

P4-240: Using polygenic risk score to predict Alzheimer's disease

2015 ◽  
Vol 11 (7S_Part_19) ◽  
pp. P872-P872 ◽  
Author(s):  
Valentina Escott-Price ◽  
Rebecca Sims ◽  
Denise Harold ◽  
Maria Vronskaya ◽  
Peter Holmans ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Score ◽  
Polygenic Risk Score ◽  
Polygenic Risk

ARMADA: Assessing reliable measurement in Alzheimer’s disease and cognitive aging project methods

2021 ◽  
Author(s):  
Sandra Weintraub ◽  
Tatiana Karpouzian‐Rogers ◽  
John Devin Peipert ◽  
Cindy Nowinski ◽  
Jerry Slotkin ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Aging ◽  
Reliable Measurement

scholarly journals Identification of Successful Cognitive Aging in the Alzheimer’s Disease Neuroimaging Initiative Study

2017 ◽  
Vol 59 (1) ◽  
pp. 101-111 ◽  
Author(s):  
Feng V. Lin ◽  
Xixi Wang ◽  
Rachel Wu ◽  
George W. Rebok ◽  
Benjamin P. Chapman ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Aging

scholarly journals Changes in cortical gene expression in the muscarinic M1 receptor knockout mouse: potential relevance to schizophrenia, Alzheimer’s disease and cognition

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Brian Dean ◽  
Elizabeth Scarr
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Ability ◽  
Noncoding Rna ◽  
Wild Type Mouse ◽  
Amyloid Precursor Protein Processing ◽  
Frontal Pole ◽  
Altered Expression ◽  
Receptor Knockout Mouse

AbstractPostmortem and neuroimaging studies show low levels of cortical muscarinic M1 receptors (CHRM1) in patients with schizophrenia which is significant because CHRM signalling has been shown to change levels of gene expression and cortical gene expression is altered in schizophrenia. We decided to identify CHRM1-mediated changes in cortical gene expression by measuring levels of RNA in the cortex of the Chrm1−/− mouse (n = 10), where there would be no signalling by that receptor, and in wild type mouse (n = 10) using the Affymetrix Mouse Exon 1.0 ST Array. We detected RNA for 15,501 annotated genes and noncoding RNA of which 1,467 RNAs were higher and 229 RNAs lower in the cortex of the Chrm1−/− mouse. Pathways and proteins affected by the changes in cortical gene expression in the Chrm1−/− are linked to the molecular pathology of schizophrenia. Our human cortical gene expression data showed 47 genes had altered expression in Chrm1−/− mouse and the frontal pole from patients with schizophrenia with the change in expression of 44 genes being in opposite directions. In addition, genes with altered levels of expression in the Chrm1−/− mouse have been shown to affect amyloid precursor protein processing which is associated with the pathophysiology of Alzheimer’s disease, and 69 genes with altered expression in the Chrm1−/− mouse are risk genes associated with human cognitive ability. Our findings argue CHRM1-mediated changes in gene expression are relevant to the pathophysiologies of schizophrenia and Alzheimer’s disease and the maintenance of cognitive ability in humans.

[P3-095]: THE USE OF POLYGENIC RISK SCORES (PRS) TO CHARACTERISE THE PRECLINICAL PHASE OF ALZHEIMER's DISEASE

2017 ◽  
Vol 13 (7S_Part_20) ◽  
pp. P970-P971
Author(s):  
Michelle K. Lupton ◽  
Margie Wright ◽  
Nick Martin ◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Scores ◽  
Polygenic Risk ◽  
Preclinical Phase
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