Most of the aging theories are monistic in nature, they omit numerous key factors of senescence during the process of model creation. There are two main categories of these theories: program theories and error (mutation) ones. Program theories imply the existence of internal or external programs that determine the aging process ab ovo. The error theories involve explicit or implicit the idea that aging would not happen without the destructive factors that cause errors, mutations, regulation disorders, and in turn these processes finally lead to disfunctions and senescence. The aim of this paper is to indicate that aging may be multifactorial and the process of senescence may be determined by the information level of the organization. This level itself changes during senescence (including the information level of the genom that also alters by time because of, e.g. its 'fluid' character). According to this approach the aging process is determined by the sum effects of internal (e.g. genom) and external (material, energy, information) factors, although there are some elements that bear more importance than others. Subsequently, the maximal life-span is probably determined by the principle of the weakest element of the chain. Because of the high complexity of the human body where different information systems superpose each other, the cooperation of the elements (counter-effects, regulation) have the same determining importance as the information level of the unit parts (cells) have. The further aim of this paper is to show that the roots of certain diseases (e.g. cancer) could firmly be linked to the aging process itself. This interpretation offers two ways of influencing the process of senescence. It could be influenced by maintaining the information level of the organism via optimization or by changing (elevating) this level. All the factors that help to prevent the decrease of the information level of the organism could act against aging and certain diseases, and vice versa: the factors which deteriorate the state of the information system could contribute to the acceleration of the aging process.
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http://dx.doi.org/10.1016/s0047-6374(00)00147-0 | DOI Listing |
Neurology
February 2025
Departments of Child Neurology and General Practice, University of Turku and Turku University Hospital, Finland.
Background And Objectives: Previous research has demonstrated increased brain amyloid plaque load in individuals with childhood-onset epilepsy in late middle age. However, the trajectory of this process is not yet known. The aim of this study was to determine whether individuals with a history of childhood-onset epilepsy show progressive brain aging in amyloid accumulation in late adulthood (Turku Adult Childhood-Onset Epilepsy study, TACOE).
View Article and Find Full Text PDFAlzheimers Dement (N Y)
January 2025
Centre for Healthy Brain Ageing (CHeBA), Discipline of Psychiatry and Mental Health, School of Clinical Medicine University of New South Wales Kensington New South Wales Australia.
Introduction: A lack of national consensus on the roles and responsibilities of Australian memory and cognition clinics contributes to the large variability seen across services. The introduction of guidelines and a quality assessment framework could facilitate greater harmonization and quality improvements.
Methods: We used a modified Delphi process to develop the guidelines.
Introduction: Melanopsin is a photopigment with roles in mediating sleep and circadian-related processes, which are often disrupted in Alzheimer's disease (AD). Melanopsin also impacts cognition and synaptogenesis. This study investigated the associations between melanopsin genetic variants, sleep, and markers of brain health.
View Article and Find Full Text PDFAlzheimers Dement (Amst)
January 2025
Department of Psychiatry Rambam Health Care Campus Haifa Israel.
Background: Late-life depression (LLD) is a heterogenous disorder related to cognitive decline and neurodegenerative processes, raising a need for the development of novel biomarkers. We sought to provide preliminary evidence for acoustic speech signatures sensitive to LLD and their relationship to depressive dimensions.
Methods: Forty patients (24 female, aged 65-82 years) were assessed with the Geriatric Depression Scale (GDS).
Acta Physiol (Oxf)
February 2025
Department of Medicine and Ageing Sciences, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.
Different physiological and pathological situations can produce alterations in the cell's endoplasmic reticulum (ER), leading to a condition known as ER stress, which can trigger an intricate intracellular signal transduction system known as the unfolded protein response (UPR). UPR is primarily tailored to restore proteostasis and ER equilibrium; otherwise, if ER stress persists, it can cause programmed cell death as a cytoprotective mechanism and drive inflammatory processes. Therefore, since intestinal cells strongly rely on UPR for their biological functions and unbalanced UPR has been linked to inflammatory, metabolic, and immune disorders, here we discussed the role of the UPR within the intestinal tract, focusing on the UPR contribution to inflammatory bowel disease development.
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