RESUMO
The process of human ageing is significantly dependent upon events which are currently shaping humanity. One such event is the seemingly inexorable progress of technology, and specifically, digital communications technology. Technology and biology are tightly interconnected, and this has a direct relevance on how our own ageing mechanisms are evolving and adapting to the change. One way technology may affect biological ageing is based on the concept of information exposure which acts as a hormetic stimulus and up-regulates neuronal stress response pathways. In this way, neurons become increasingly more likely to acquire repair resources and function for longer, with a consequent overall improvement in healthy lifespan. At the same time, germline repair mechanisms may need to be downgraded in order to accommodate a tradeoff: a corresponding escalation of repairs in neurons. In this Opinion paper, it is discussed that how a meaningful and intentional integration with technology, which hormetically challenges our cognition, may redress the conflict for resources between the soma and the germline, and result in a reduction of age-related dysfunction in the subjects.
Assuntos
Envelhecimento , Cognição , Computadores , Meio Ambiente , Hormese , Desenvolvimento Industrial , Degeneração Neural , Neurônios/patologia , Fatores Etários , Envelhecimento/metabolismo , Envelhecimento/patologia , Envelhecimento/psicologia , Humanos , Modelos Neurológicos , Degeneração Neural/metabolismo , Degeneração Neural/patologia , Degeneração Neural/fisiopatologia , Degeneração Neural/psicologia , Regeneração Nervosa , Neurônios/metabolismo , Dinâmica não Linear , Estresse FisiológicoRESUMO
BACKGROUND/AIMS: Demyelination and axonal degeneration are the hallmarks of established white matter lesions (WML). The neurochemistry of ongoing WML is only partially known. We explored cerebrospinal fluid (CSF) substances as markers of brain tissue damage in relation to progression of WML rated on magnetic resonance imaging. METHODS: CSF from elderly individuals with WML was analyzed for amyloid markers, total τ, hyperphosphorylated τ, neurofilament protein light subunit, sulfatide and CSF/serum-albumin ratio. After 3 years, a follow-up magnetic resonance imaging was performed. Progression of WML was rated using the Rotterdam Progression Scale (RPS). RESULTS: 37 subjects (age 73.6 ± 4.6 years) were included. Subjects with more pronounced progression (RPS > 2; n = 15) had lower mean sulfatide concentration at baseline as compared to subjects with no or minimal progression (RPS 0-2; n = 22) according to univariate analyses (p = 0.009). Sulfatide was the only biomarker that predicted the RPS score according to regression analysis, explaining 18.9% of the total variance (r = 0.38, p = 0.015). CONCLUSION: The correlation of CSF sulfatide levels and RPS scores may reflect a remyelination response to the demyelination process associated with WML. Furthermore, the results strengthen the notion that WML pathology is different from that of Alzheimer's disease.