Investigating the mechanistic convergence of signaling systems linking arterial stiffening to dementia.

Aging affects the whole body and is linked with metabolic dysfunction, loss of cellular stress resistance and accumulation of cellular damage. Aging is one of the strongest risk factors for the development of both vascular stiffening and neurodegenerative diseases such as Alzheimer's disease (AD). Many of the pathologies linked to aging are now recognized as being highly characteristic of neurodegenerative diseases – suggesting that both vascular stiffening and AD progression may be interconnected via molecular aging pathologies. Protracted, highly complex processes such as aging require the coherent coordination of many different physiological processes. To orchestrate such complex events the body uses proteins termed 'hubs' that can control a multiplicity of physiological processes simultaneously. Our laboratory has already identified multiple 'hubs' within somatic aging networks and in this context we shall specifically investigate, using advanced informatics technologies, how certain key proteins may interconnect these two pathologies. The functional activity of such 'hub' proteins may represent an important target to study for aging, vascular and neurodegenerative research. We propose that the identification of the key age-dependent controlling factors, common between vascular stiffening and AD processes will reveal multiple important targets for future investigation and eventual therapeutic strategy design.

Keywords:DEMENTIA

Disciplines:Medicinal and biomolecular chemistry, Molecular and cell biology, Plant biology, Systems biology, Biophysics