Persistent metabolic youth in the aging female brain

Sex differences influence brain morphology and physiology during both development and aging. Here we apply a machine learning algorithm to a multiparametric brain PET imaging dataset acquired in a cohort of 20- to 82-year-old, cognitively normal adults (n = 205) to define their metabolic brain age. We find that throughout the adult life span the female brain has a persistently lower metabolic brain age—relative to their chronological age—compared with the male brain. The persistence of relatively younger metabolic brain age in females throughout adulthood suggests that development might in part influence sex differences in brain aging. Our results also demonstrate that trajectories of natural brain aging vary significantly among individuals and provide a method to measure this.

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IC-P-129: Regional Brain Aerobic Glycolysis Across The Cognitively Normal Adult Life Span

Alzheimer s & Dementia ◽

10.1016/j.jalz.2016.06.159 ◽

2016 ◽

Vol 12 ◽

pp. P96-P96

Author(s):

Andrei G. Vlassenko

Keyword(s):

Life Span ◽

Aerobic Glycolysis ◽

Adult Life ◽

Normal Adult ◽

Adult Life Span ◽

Cognitively Normal ◽

Regional Brain

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Incorporating Ecological Momentary Assessment into multi-level investigations of adult development and aging: Promise and practical considerations

10.31234/osf.io/pc8tj ◽

2020 ◽

Author(s):

Jennifer Lee Crawford ◽

Tammy English ◽

Todd Samuel Braver

Keyword(s):

Adult Development ◽

Ecological Momentary Assessment ◽

Adult Life ◽

Individual Variability ◽

Aging Research ◽

Adult Life Span ◽

Age Related ◽

Development And Aging ◽

Ecological Momentary ◽

Momentary Assessment

Ecological momentary assessment (EMA) represents a promising approach to study adult development and aging. In contrast to laboratory-based studies, EMA involves the repeated sampling of experiences in daily life contexts, enabling investigators to gain access to dynamic processes (e.g., situational contexts, intra-individual variability) that are likely to strongly contribute to age-related change across the adult life-span. As such, EMA approaches complement the prevailing research methods to study age differences (e.g., experimental paradigms, neuroimaging), and offer the potential to replicate and extend findings from the laboratory to more naturalistic contexts. Following an overview of the methodological and conceptual strengths of EMA approaches in adult development and aging research, we provide a guide for researchers interested in implementing EMA studies. Together, this work will highlight the tremendous potential in combining EMA methods with other laboratory-based approaches in order to increase the robustness, replicability, and real-world implications of research findings.

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A Conserved MTMR Lipid Phosphatase Increasingly Suppresses Autophagy in Brain Neurons During Aging

10.21203/rs.3.rs-738913/v1 ◽

2021 ◽

Author(s):

Tibor Kovács ◽

Janka Szinyákovics ◽

Viktor Billes ◽

Gábor Murányi ◽

Virginia B. Varga ◽

...

Keyword(s):

Brain Aging ◽

Tyrosine Phosphatase ◽

Adult Life ◽

Fruit Fly ◽

Cellular Damage ◽

Adult Life Span ◽

Brain Neurons ◽

Lipid Phosphatase ◽

Age Related ◽

Cell Clearance

Abstract Aging is driven by the progressive, lifelong accumulation of cellular damage. Autophagy (cellular self-eating) functions as a major cell clearance mechanism to degrade such damages, and its capacity declines with age. Despite its physiological and medical significance, it remains largely unknown why autophagy becomes incapable of effectively eliminating harmful cellular materials at advanced ages. Here we show that age-associated defects in autophagic degradation occur at both early and late stages of the process. Furthermore, in the fruit fly Drosophila melanogaster, the myotubularin-related (MTMR) lipid phosphatase EDTP (egg-derived tyrosine phosphatase) known as an autophagy repressor gradually accumulates in brain neurons during the adult life span. The age-related increase in EDTP activity is associated with a growing DNA N6-adenine methylation at EDTP locus. MTMR14, the human counterpart of EDTP, also tends to accumulate with age in brain neurons. Thus, EDTP, and presumably MTMR14, promotes brain aging by increasingly suppressing autophagy throughout adulthood. We propose that EDTP and MTMR14 phosphatases operate as endogenous pro-aging factors setting the rate at which neurons age largely independently of environmental factors, and that autophagy is influenced by DNA N6-methyladenine levels.

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