Alzheimer's disease (AD) remains a global health challenge. Previous studies have reported linkages between AD and multiple behavioural risk exposures, however, the underlying biological mechanisms and crucial genes of gene expression patterns driven by behavioural risks on the onset or progression of AD remains ambiguous. In this study, we performed an integrated analysis on the influence of behavioural risks including smoking, excessive alcohol consumption, physical inactivity, and non-healthy dietary pattern on AD with a comprehensive strategy. Our results demonstrated that multiple behavioural risk exposures could independently or collectively influence diverse hierarchical levels of gene expression patterns through multiple biological mechanisms such as Wnt, mitogen-activated protein kinase (MAPK), AMP-activated protein kinase (AMPK), nuclear factor (NF)-κB, phosphatidylinositol 3-kinase (PI3K)-Akt, and insulin (INS) signalling pathways-mediated pathological processes, thereby prodromally or intermediately impacting AD. Our study provided insights into understanding the association of behavioural risk exposures with AD and informative support for further studies.
Keyphrases
- protein kinase
- gene expression
- pi k akt
- signaling pathway
- nuclear factor
- global health
- alcohol consumption
- cell proliferation
- air pollution
- dna methylation
- type diabetes
- toll like receptor
- human health
- cell cycle arrest
- public health
- physical activity
- stem cells
- oxidative stress
- risk assessment
- case control
- cognitive decline
- skeletal muscle
- immune response
- mild cognitive impairment
- breast cancer risk
- weight gain