Amyloid Metabolism and Amyloid-Targeting Blood-Based Biomarkers of Alzheimer’s Disease

2020 ◽  
Vol 75 (3) ◽  
pp. 685-696
Author(s):  
Jung-Min Pyun ◽  
Min Ju Kang ◽  
Nayoung Ryoo ◽  
Jeewon Suh ◽  
Young Chul Youn ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Metabolism

Estrogen, beta-Amyloid Metabolism/Trafficking, and Alzheimer's Disease

2006 ◽  
Vol 1089 (1) ◽  
pp. 324-342 ◽  
Author(s):  
H. XU ◽  
R. WANG ◽  
Y.-W. ZHANG ◽  
X. ZHANG
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Beta Amyloid ◽  
Amyloid Metabolism

scholarly journals Obstructive sleep apnea may induce orexinergic system and cerebral β-amyloid metabolism dysregulation: is it a further proof for Alzheimer's disease risk?

2019 ◽  
Vol 56 ◽  
pp. 171-176 ◽  
Author(s):  
Claudio Liguori ◽  
Nicola Biagio Mercuri ◽  
Marzia Nuccetelli ◽  
Francesca Izzi ◽  
Alberto Cordella ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Disease Risk ◽  
Obstructive Sleep ◽  
Amyloid Metabolism ◽  
Β Amyloid

scholarly journals Imaging correlations of tau, amyloid, metabolism, and atrophy in typical and atypical Alzheimer's disease

2018 ◽  
Vol 14 (8) ◽  
pp. 1005-1014 ◽  
Author(s):  
Jennifer L. Whitwell ◽  
Jonathan Graff-Radford ◽  
Nirubol Tosakulwong ◽  
Stephen D. Weigand ◽  
Mary M. Machulda ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Metabolism ◽  
Atypical Alzheimer’S Disease

Caspases, amyloid metabolism and Alzheimer's disease

2000 ◽  
Vol 21 ◽  
pp. 136-137 ◽  
Author(s):  
Andrea C. LeBlanc ◽  
Beverly R. Akerman ◽  
Yan Zhang ◽  
Goodyer Cynthia ◽  
Catherine Bergeron
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Metabolism

scholarly journals Immune response and endocytosis pathways are associated with the resilience against Alzheimer’s disease

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Niccolò Tesi ◽  
Sven J. van der Lee ◽  
Marc Hulsman ◽  
Iris E. Jansen ◽  
Najada Stringa ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Immune Response ◽  
Genetic Variants ◽  
Genetic Risk ◽  
Risk Scores ◽  
Study Cohort ◽  
Increased Risk ◽  
Amyloid Metabolism ◽  
Β Amyloid

Abstract Developing Alzheimer’s disease (AD) is influenced by multiple genetic variants that are involved in five major AD-pathways. Per individual, these pathways may differentially contribute to the modification of the AD-risk. The pathways involved in the resilience against AD have thus far been poorly addressed. Here, we investigated to what extent each molecular mechanism associates with (i) the increased risk of AD and (ii) the resilience against AD until extreme old age, by comparing pathway-specific polygenic risk scores (pathway-PRS). We used 29 genetic variants associated with AD to develop pathway-PRS for five major pathways involved in AD. We developed an integrative framework that allows multiple genes to associate with a variant, and multiple pathways to associate with a gene. We studied pathway-PRS in the Amsterdam Dementia Cohort of well-phenotyped AD patients (N = 1895), Dutch population controls from the Longitudinal Aging Study Amsterdam (N = 1654) and our unique 100-plus Study cohort of cognitively healthy centenarians who avoided AD (N = 293). Last, we estimated the contribution of each pathway to the genetic risk of AD in the general population. All pathway-PRS significantly associated with increased AD-risk and (in the opposite direction) with resilience against AD (except for angiogenesis, p < 0.05). The pathway that contributed most to the overall modulation of AD-risk was β-amyloid metabolism (29.6%), which was driven mainly by APOE-variants. After excluding APOE variants, all pathway-PRS associated with increased AD-risk (except for angiogenesis, p < 0.05), while specifically immune response (p = 0.003) and endocytosis (p = 0.0003) associated with resilience against AD. Indeed, the variants in these latter two pathways became the main contributors to the overall modulation of genetic risk of AD (45.5% and 19.2%, respectively). The genetic variants associated with the resilience against AD indicate which pathways are involved with maintained cognitive functioning until extreme ages. Our work suggests that a favorable immune response and a maintained endocytosis pathway might be involved in general neuro-protection, which highlight the need to investigate these pathways, next to β-amyloid metabolism.

scholarly journals Immune response and endocytosis pathways are associated with the escape of Alzheimer’s Disease

2019 ◽  
Author(s):  
Niccolò Tesi ◽  
Sven J. van der Lee ◽  
Marc Hulsman ◽  
Iris E. Jansen ◽  
Najada Stringa ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Immune Response ◽  
Genetic Variants ◽  
Genetic Risk ◽  
Molecular Mechanisms ◽  
Risk Scores ◽  
Integrative Framework ◽  
Amyloid Metabolism ◽  
Population Controls

AbstractThe risk to develop and escape Alzheimer’s disease (AD) is influenced by a constellation of genetic variants, each associated with specific molecular pathways. Different pathways may differentially contribute to the modification of the AD-risk. We studied the molecular mechanisms that explain the extreme ends of the cognitive spectrum by comparing pathway-specific polygenic risk scores (pathway-PRS) in individuals with AD and those who escaped AD until old age. We used 29 genetic variants associated with AD to calculate pathway-PRS for five major pathways involved in AD. We developed an integrative framework that allows multiple genes to associate with a variant, and multiple pathways to associate with a gene. We studied pathway-PRS in patients with AD (N=1,909), population controls (N=1,654), and cognitively healthy centenarians who escaped AD (N=293). Last, we estimated the contribution of each pathway to the genetic risk of AD in the general population. All pathway-PRS significantly associated with increased AD-risk and escaping AD (p<0.05). The pathway that contributed the most to the overall modulation of AD-risk was b-amyloid metabolism (32%), driven mainly by APOE variants. After excluding APOE variants, all pathway-PRS associated with increased AD-risk (p<0.05), while specifically immune response (p=3.1×10−3) and endocytosis (p=3.8×10−4) associated with escaping AD. These pathways were the main contributors to the overall modulation of genetic risk of AD (41.3% and 21.4%, respectively). Our work suggests that immune response and endocytosis might be involved in general neuro-protective functions, and highlights the need to study these pathways, next to b-amyloid metabolism.

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