Abstract
In humans, age-associated degrading changes, widely observed in molecular and cellular processes underly the time-dependent decline in spatial navigation, time perception, cognitive and psychological abilities, and memory. Cross-talk of biological, cognitive, and psychological clocks provides an integrative contribution to healthy and advanced aging. At the molecular level, genome, proteome, and lipidome instability are widely recognized as the primary causal factors in aging. We narrow attention to the roles of protein aging linked to prevalent amino acids chirality, enzymatic and spontaneous (non-enzymatic) post-translational modifications (PTMs SP), and non-equilibrium phase transitions. The homochirality of protein synthesis, resulting in the steady-state non-equilibrium condition of protein structure, makes them prone to multiple types of enzymatic and spontaneous PTMs, including racemization and isomerization. Spontaneous racemization leads to the loss of the balanced prevalent chirality. Advanced biological aging related to irreversible PTMs SP has been associated with the nontrivial interplay between somatic (molecular aging) and mental (psychological aging) health conditions. Through stress response systems (SRS), the environmental and psychological stressors contribute to the age-associated “collapse” of protein homochirality. The role of prevalent protein chirality and entropy of protein folding in biological aging is mainly overlooked. In a more generalized context, the time-dependent shift from enzymatic to the non-enzymatic transformation of biochirality might represent an important and yet underappreciated hallmark of aging. We provide the experimental arguments in support of the racemization theory of aging.
Highlights
At the molecular level, aging is associated with three primary classes of bio-molecules prone to spontaneous modifications: (1) nucleotides (NTs) within DNA sequence, (2) amino acids (AAs) within peptides and proteins and (3) lipid content of the membrane bilayers
Based on the above evidence, it is reasonable to conclude that spontaneous racemization may be a valuable molecular biomarker of age-associated neurodegenerative and psychiatric disorders
The combination of the above two factors provides the high probability of spontaneous age-associated post-translational modifications (PTMs) compromising mTOR function, explaining the known association of mTOR signaling with life span, aging, and age-related pathologies. mTOR is an illustrative example of many proteins containing racemizationprone AA residues, speaking to support the racemization hypothesis of aging
Summary
The consequences of psychological stresses linked to biological aging are evident at the organism, system, cellular, and molecular levels [2,3]. We will focus on the thermodynamics of protein folding in the age-dependent association with the function of the stress response system (SRS), and provide the experimental arguments in support of the racemization theory of aging. Age-as∆G. psychological underlying the decline in basic functions of the organism, including spatial navigation and where k is Boltzmann’s constant and W is the number of microstates that give rise to the macro-state of interest. Protein aging is a trade-off between the maintenance of prevalent chirality and spontaneous racemization From this integrative view, it is evident that the STS mediates the physiological and psychological outcomes of aging individuals
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