scholarly journals Effectiveness of a condensed protocol for disclosing APOE genotype and providing risk education for Alzheimer disease

2012 ◽  
Vol 14 (8) ◽  
pp. 742-748 ◽  
Author(s):  
J. Scott Roberts ◽  
◽  
Clara A. Chen ◽  
Wendy R. Uhlmann ◽  
Robert C. Green
Keyword(s):  
Alzheimer Disease ◽  
Apoe Genotype ◽  
Risk Education

Histopathology and APOE genotype of the first Alzheimer disease patient, Auguste D.

Neurogenetics ◽  
1998 ◽  
Vol 1 (3) ◽  
pp. 223-228 ◽  
Author(s):  
M. B. Graeber ◽  
S. Kösel ◽  
E. Grasbon-Frodl ◽  
H. J. Möller ◽  
P. Mehraein
Keyword(s):  
Alzheimer Disease ◽  
Disease Patient ◽  
Apoe Genotype ◽  
Alzheimer Disease Patient

Impact of APOE genotype on neuropathologic and neurochemical markers of Alzheimer disease

Neurology ◽  
2004 ◽  
Vol 62 (11) ◽  
pp. 1977-1983 ◽  
Author(s):  
P. Tiraboschi ◽  
L. A. Hansen ◽  
E. Masliah ◽  
M. Alford ◽  
L. J. Thal ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Apoe Genotype

scholarly journals Blood and Brain Transcriptome Analysis Reveals APOE Genotype-mediated and Immune-related Pathways Involved in Alzheimer Disease

2021 ◽  
Author(s):  
Rebecca Panitch ◽  
Junming Hu ◽  
Weiming Xia ◽  
David A Bennett ◽  
Thor D Stein ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Blood Brain Barrier ◽  
Vascular Injury ◽  
Apoe Genotype ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Differentially Expressed ◽  
Brain Barrier ◽  
Gene Set Enrichment ◽  
Gene Set

Abstract Background: While Alzheimer disease (AD) is generally considered as a brain disorder, blood biomarkers may be useful for diagnosis and prediction of AD brain pathology. The APOE ε4 allele has shown cerebrovascular effects including acceleration of blood brain barrier breakdown. Methods: We evaluated differential expression of previously established AD genes in brains from 344 pathologically confirmed AD cases and 232 controls and in blood from 112 pathologically confirmed AD cases and 67 controls from the Religious Orders Study and Memory and Aging Project. Differential gene expression between AD cases and controls was analyzed in the blood and brain jointly using a multivariate approach in the total sample and within APOE genotype groups. Gene set enrichment analysis was performed within APOE genotype groups using the results from the combined blood and brain analyses to identify biologically important pathways. Gene co-expression networks in brain and blood samples were investigated using weighted correlation network analysis. Top ranked genes from networks and pathways were further evaluated with vascular injury traits. Results: We observed differentially expressed genes with P<0.05 in both brain and blood for established AD genes INPP5D (upregulated) and HLA-DQA1 (downregulated). PIGHP1 and FRAS1 were differentially expressed at the transcriptome-wide level (P<3.3x10 -6 ) within ε2/ε3 and ε3/ε4 groups, respectively. Gene-set enrichment analysis revealed 21 significant pathways (false discovery rate P<0.05) in at least one APOE genotype group. Ten pathways were significantly enriched in the ε3/ε4 group, and six of these were unique to these subjects. Four pathways were enriched for AD upregulated genes in the ε3/ε4 group and AD downregulated genes in ε4 lacking subjects. We identified a co-expressed gene network in brain that reproduced in blood and showed higher average expression in ε4 carriers. Twenty-three genes from pathway and network analyses were significantly associated at P<0.05 with at least one vascular injury trait. Conclusion: These results suggest that APOE genotype contributes to unique expression network profiles in both blood and brain. Several genes in these networks are associated with measures of vascular injury and potentially contribute to ε4’s effect on the blood brain barrier.

scholarly journals Microglial Activation in Alzheimer Disease: Association with APOE Genotype

2006 ◽  
Vol 8 (3) ◽  
pp. 439-447 ◽  
Author(s):  
Rupert Egensperger ◽  
Siegfried Kösel ◽  
Ulrich Eitzen ◽  
Manuel B. Graeber
Keyword(s):  
Alzheimer Disease ◽  
Microglial Activation ◽  
Apoe Genotype ◽  
Disease Association

scholarly journals Cholesterol, APOE genotype, and Alzheimer disease: An epidemiologic study of Nigerian Yoruba

Neurology ◽  
2006 ◽  
Vol 66 (2) ◽  
pp. 223-227 ◽  
Author(s):  
K. Hall ◽  
J. Murrell ◽  
A. Ogunniyi ◽  
M. Deeg ◽  
O. Baiyewu ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Epidemiologic Study ◽  
Apoe Genotype

scholarly journals Does hearing loss lead to dementia? A review of the literature

2020 ◽  
Author(s):  
Yosra Nadhimi ◽  
Daniel Llano
Keyword(s):  
Hearing Loss ◽  
Alzheimer Disease ◽  
Noise Exposure ◽  
Human Subjects ◽  
Apoe Genotype ◽  
Microvascular Disease ◽  
Causal Link ◽  
Ample Evidence ◽  
Therapeutic Implications ◽  
Auditory Cognition

Recent studies have revealed a correlation between aging-related hearing loss and the likelihood of developing Alzheimer Disease. However, it is not yet known if the correlation simply reflects the fact that these two disorders share common risk factors or whether there is a causal link between them. The answer to this question carries therapeutic implications. Unfortunately, it is not possible to study the question of causality between aging-related hearing loss and dementia in human subjects. Here, we evaluate the research surrounding induced-hearing loss in animal models on non-auditory cognition to help infer if there is any causal evidence linking hearing loss and a more general dementia. We find ample evidence that induction of hearing loss in animals produces cognitive decline, particularly hippocampal dysfunction. The data suggest that noise-exposure produces a toxic milieu in the hippocampus consisting of a spike in glucocorticoid levels, elevations of mediators of oxidative stress and excitotoxicity, which as a consequence induce cessation of neurogenesis, synaptic loss and tau hyperphosphorylation. These data suggest that hearing loss can lead to pathological hallmarks similar to those seen in Alzheimer’s Disease and other dementias. However, the rodent data do not establish that hearing loss on its own can induce a progressive degenerative dementing illness. Therefore, we conclude that an additional “hit”, such as aging, APOE genotype, microvascular disease or others, may be necessary to trigger an ongoing degenerative process such as Alzheimer Disease.

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