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PubMed2004

The role of macroautophagy in the ageing process, anti-ageing intervention and age-associated diseases.

Macroautophagy is a degradation/recycling system ubiquitous in eukariotic cells, which generates nutrients during fasting under the control of amino acids and hormones, and contributes to the turnover and rejuvenation of cellular components (long-lived proteins, cytomembranes and organelles). Tight coupling between these two functions may be the weak point in cell housekeeping. Ageing denotes a post-maturational deterioration of tissues and organs with the passage of time, due to the progressive accumulation of the misfunctioning cell components because of oxidative damage and an age-dependent decline of turnover rate and housekeeping. Caloric restriction (CR) and lower insulin levels may slow down many age-dependent processes and extend lifespan. Recent evidence is reviewed showing that autophagy is involved in ageing and in the anti-ageing action of anti-ageing calorie restriction: function of autophagy declines during adulthood and is almost negligible at older age; CR prevents the age-dependent decline of autophagic proteolysis and improves the sensitivity of liver cells to stimulation of lysosomal degradation; protection of autophagic proteolysis from the age-related decline co-varies with the duration and level of anti-ageing food restriction like the effects of CR extending lifespan; the pharmacological stimulation of macroautophagy has anti-ageing effects. Besides the involvement in ageing, macroautophagy may have an essential role in the pathogenesis of many age-associated diseases. Higher protein turnover may not fully account for the anti-ageing effects of macroautophagy, and effects of macroautophagy on housekeeping of the cell organelles, antioxidant machinery of cell membranes and transmembrane cell signaling should also be considered.

Aging↗

PubMed1989

"You're only as old as you feel": self-perceptions of age, fears of aging, and life satisfaction from adolescence to old age.

We examined differences in subjective age identification from adolescence to old age and the relation between subjective age and fears about one's own aging and life satisfaction. Using a questionnaire format, 188 men and women from 14 to 83 years of age made judgments about how old they felt, looked, acted, and desired to be. Respondents also answered questions about their personal fears of aging and present life satisfaction. Results revealed that individuals in their teens held older subjective age identities, whereas during the early adult years, individuals maintained same age identities. Across the middle and later adult years, individuals reported younger age identities, and women experienced younger age identities than men across these adults years. Results also revealed that discrepancies between subjective and actual age were associated with personal fears of aging and life satisfaction, especially in younger men and women.

Adolescent↗

PubMed1994

[Bone mineral density of the lumbar spine and its relation to biological and lifestyle factors in middle-aged and aged Japanese women (Part 1). Relationship of age and menopause to bone mineral density of the lumbar spine measured by dual-energy X-ray absorptiometry].

Bone mineral density (BMD) of the lumbar spine in 198 community-dwelling Japanese women aged 35 years and over was measured by dual-energy X-ray absorptiometry to investigate the effects of aging and menopause on BMD. A highly significant negative correlation between age and BMD was observed in postmenopausal women as widely accepted. We found a weak but statistically significant negative correlation between age and BMD in even premenopausal women, suggesting that their bone loss had commenced before menopause. Marked decrement in BMD was seen during the first ten years after menopause. Menopause clearly accelerated bone loss in the lumbar spine. Two-way analysis of variance of BMD on age and menopausal status showed that these explanatory variables had a significantly decreasing effect on BMD independently of each other. Menopausal status had a greater sum of squares than age, which suggested that menopause played a greater role in bone loss than did aging. Early menopause has been implied as one of the risk factors for bone loss. The women aged 50 to 59 having encountered menopause before 49 years old exhibited significantly lower BMD than those of similar age who experienced menopause at age 49 and older. This difference in BMD was not observed in the women aged 60 and over. Early menopause was no more likely to be a risk factor for bone loss in the elderly women. We conclude that bone loss in the lumbar spine begins before menopause and is accelerated markedly by menopause for about ten years, and that menopause has a greater decreasing effect on the bone mass than does chronological age while each of them has an independent effect on the bone mass decrement.

Absorptiometry, Photon↗

PubMed1998

Growth hormone gene expression and secretion in aging rats is age dependent and not age-associated weight increase related.

GH secretion declines with age in rats and humans and a reduction in GH gene expression has been demonstrated in aging rats. GH secretion also diminishes in obesity; thus, the aim of this study was to determine whether GH decrease in aging rats is due to body weight gain or to aging. Three groups of male Wistar rats of different ages were studied (young, 3 months; middle-aged, 11 months; old, 27 months). The middle-aged group was established on a statistical analysis and corresponded to the youngest age at which body weight was not significantly different from the old (27 month) group. Thus, by using this group as control for comparison with animals with the same weight and an older age, the effects due to aging itself could be determined. Body weight (g, mean +/- sD) 3 months: 361 +/- 5.6; 11 months: 713 +/- 39; 27 months: 635 +/- 38. In comparison with 3-month-old rats, the 11-month-old animals showed no difference in pituitary GH messenger RNA (mRNA) accumulation and pituitary and serum IR-GH levels. Similarly IGF-I.a, IGF-I.b mRNA transcripts and IG-FBP-3 mRNA accumulation in the liver showed no significant differences between the two groups. On the contrary, when the 27-month-old rats were compared with the 11-month-old animals, lower levels of pituitary GH mRNA and serum and pituitary IR-GH were found. Pituitary GH mRNA decreased 37.5 +/- 7.7% P < 0.001, pituitary IR-GH content diminished (5.2 +/- 3.4 vs. 55 +/- 10.7 ng/mg of protein, P < 0.001) and serum IR-GH decreased (3.5 +/- 1.8 vs. 12.5 +/- 4.2 ng/ml, P < 0.01). Liver IGF-I.a and IGF-I.b mRNA transcripts accumulation and serum IGF-I were significantly diminished. IGF-I.b mRNA accumulation decreased 35.8 +/- 1.2% P < 0.05 and IGF-I.a 36 +/- 5.6% P < 0.05; serum IR-IGF-I levels diminished (759 +/- 152 vs. 1327 +/- 67 ng/ml, P < 0.05). Liver IGFBP-3 mRNA accumulation decreased 79 +/- 4.2% P < 0.001. These results indicate that the decrease in GH gene expression and secretion, as well as the expression of genes induced by GH such as IGF-I and IGFBP-3, is due to aging and not to the increase in body weight that takes place with aging.

Age Factors↗

PubMed2001

Attitudes of middle-aged women to aging: contribution of the Reactions to Aging Questionnaire.

Attitudes to aging in mid-life have been found to be a predictor of health and well-being. The main purpose of the study was to assess the contribution of the Reactions to Aging Questionnaire (RAQ) to the understanding of middle-aged women's attitudes towards their aging. An additional purpose was to expand the existing information regarding the dimensions of the new version of the RAQ. Middle-aged Melbourne women (n = 381) were asked to complete the RAQ, in addition to another attitudes-to-aging scale (Worries About Aging). Factor analysis of the RAQ was used to explore its dimensionality, and frequencies of responses were used to assess the spread of response of both instruments. The factors extracted in the factor analysis of the RAQ were interpretable and meaningful in terms of emotions related to aging. They were also similar to the factors described by previous data. The RAQ was more effective in its distribution ability than the Worries About Aging Scale. With some modifications, the RAQ may be more informative than was the Worries About Aging Scale in its ability to assess emotions, opinions and beliefs associated with aging in middle-aged women.

Aging↗

PubMed2000

Photodynamic therapy for neovascular age-related macular degeneration.

BACKGROUND: In neovascular age-related macular degeneration, new vessels grow under the retina, distorting vision and leading to scarring. This is further exacerbated if the blood vessels leak. Photodynamic therapy, originally used in cancer treatment, has been investigated as a way to treat the neovascular membranes without affecting the retina. OBJECTIVES: The aim of this review is to examine the evidence for the safety and effectiveness of photodynamic therapy in the treatment of neovascular age-related macular degeneration. SEARCH STRATEGY: We searched for trials in the Cochrane Eyes and Vision Group trials register (available in the Cochrane Controlled Trials Register), the Cochrane Controlled Trials Register, Medline and Embase. We used the Science Citation Index to search for reports that cited identified relevant study reports. We contacted experts in the field for further trials information, and we searched the reference lists of identified relevant studies for further trial reports. Searches were conducted in December 1999. SELECTION CRITERIA: We included randomised trials of photodynamic therapy in people with choroidal neovascularisation due to age-related macular degeneration. DATA COLLECTION AND ANALYSIS: Two reviewers extracted the data independently. Meta analysis was not performed. MAIN RESULTS: One published trial was identified. Outcome data were available at 12 months after the first treatment. Patients received an average of 3.7 treatments. The relative risk of losing three or more lines of visual acuity at 12 months comparing the intervention with the control group was 0.72 (95% confidence interval 0.61 to 0.86). The relative risk of losing six or more lines of visual acuity at 12 months comparing the intervention with the control group was 0.62 (95% confidence interval 0.44 to 0.87). Subgroup analyses suggest that the benefits may be confined to people with no occult choroidal neovascularisation. REVIEWER'S CONCLUSIONS: Photodynamic therapy in people with classic choroidal neovascularisation due to age-related macular degeneration is effective in preventing visual loss. This evidence is drawn from a subgroup analysis of 143 participants in one trial. Outcomes and potential adverse effects of this treatment should be monitored closely. There is no evidence that photodynamic therapy is beneficial for people with evidence of occult choroidal neovascularisation. These people should be offered treatment in the context of a randomised trial.

Humans↗

PubMed1999

Dynamics of cognitive aging: distinguishing functional age and disease from chronologic age in a population.

This paper introduces a methodological approach to the dynamics of cognitively normal (i.e., successful) aging compared with aging accompanied by different types of cognitive impairment and dementia. Using secondary analysis of a national representative database (Canadian Study of Health and Aging, 1991-1992), the authors show that the occurrence of an adverse event (symptom, sign, or disease), or the accumulation of a number of events, may be modeled as a logistic function of chronologic age in a population. In the cognitively normal, a linear relation between the logarithm of the odds of events and chronologic age was present for the majority of symptoms and signs. This regression represents the accumulation of each sign in a cognitively successful, aging population. The authors then estimated which ages for this cognitively unimpaired group correspond to the odds of the occurrence of symptoms found for a cognitively impaired population at any given chronologic age. This may be regarded as functional age, based upon the accumulation of a particular functional deficit in the impaired population, analogous to the concept of frailty. The dynamics of aging are a complex process of accumulation of deficits (morbidity), whereby decline from some previously healthy level of synergistically associated symptoms and signs results in distinct patterns of disease and staging. The modeling of these dynamics takes us a step further toward the definition and refinement of disease and normal aging.

Aged↗

PubMed2006

Functional ability at age 75: is there an impact of physical inactivity from middle age to early old age?

The aim of this study is to analyze the impact of physical inactivity from middle age to early old age on functional ability at age 75. Physical activity is measured both as cumulated activity from age 50 to 60 to 70 and at three separate points in time. Three hundred eighty-seven men and women born in 1914 and living in seven municipalities in the western part of the County of Copenhagen were followed for 25 years with examinations in 1964, 1974, 1984 and 1989. Analyses were conducted with physical inactivity as an independent variable (accumulated and separately for each point in time) and smoking, sex, school education, household composition, chronic disease at baseline and functional ability at age 70 as possible confounders. There was a strong association between physical inactivity at age 70 and disability at age 75. However, the analyses showed no effect of cumulated physical inactivity from age 50 to 60 to 70 on disability at age 75 when adjusting for functional ability at age 70. Physical inactivity is a risk factor for disability among old people. Thus, old people should be encouraged to take up and maintain physical training throughout the aging process.

Aged↗

PubMed2006

Increasing sex difference in bone strength in old age: The Age, Gene/Environment Susceptibility-Reykjavik study (AGES-REYKJAVIK).

INTRODUCTION: It is important to identify possible pathological mechanisms that underlie the known sexual dimorphism in bone fragility in old age. In this cross-sectional population-based study, we use data from three different skeletal sites to examine sex differences in volumetric bone density, geometry and strength indices and determine whether sex differences in these bone strength measures continue to increase into very old age. MATERIALS AND METHODS: A total of 1715 elderly individuals (807 men and 908 women) age 67-93 years, participants in a population-based study, the Age, Gene/Environment Susceptibility-Reykjavik Study (AGES-REYKJAVIK) and not taking medications affecting bone metabolism, were studied. Quantitative computed tomography (QCT) was performed in the lumbar spine, hip and mid-femoral shaft to estimate volumetric trabecular, cortical and integral BMD, bone geometry and bone strength indices. Regression models were used to assess the effects of age and gender-adjustment for standing midlife height and current weight. RESULTS: At age 67-69 years, men had 24.9-31.7% larger cross-sectional bone size at measured sites than women. At all bone sites, women had two- to fivefold diminution in net bone mass with age compared to men but had comparable increments in bone size (1.8-6.0% per 10 years). This was reflected in significantly worse (more than twofold) bone strength measures with age in women, including compressive strength indices at the spine, femoral neck and trochanter and bending strength indices at the femoral neck. CONCLUSION: With the limitations of a cross-sectional study, our data support the hypothesis that sex differences in bone strength continue into old age. These sex differences appear to be due to greater net bone loss in women rather than due to greater bone gain in men.

Age Distribution↗

PubMed2005

Cause-specific mortality in old age in relation to body mass index in middle age and in old age: follow-up of the Whitehall cohort of male civil servants.

BACKGROUND: The relevance of body mass index (BMI) to cause-specific mortality in old age is uncertain. OBJECTIVES: To examine cause-specific 5 year mortality in old age by BMI in old age and middle age (40-69 years). METHODS: Cox proportional hazards for mortality rates among 4862 former male civil servants in relation to quartiles of BMI measured when screened in 1968-70 and when resurveyed in 1997-98 (median age 76 years). RESULTS: The association between all-cause mortality after resurvey and BMI in old age was U-shaped with hazard ratios (HRs) of 1.3 (95% CI 1.1-1.5) for the lightest and heaviest categories relative to the middle two. Among 'healthy' men the lightest (<22.7 kg/m2) had greatest all-cause mortality. The heaviest men (>26.6 kg/m2) had increased risk of cardiovascular disease (CVD) mortality in the first two years or for the whole period if never-smokers. Respiratory mortality was inversely associated with BMI in old age [adjusted HR for trend per BMI category increase 0.6 (0.5-0.7)] but cancer mortality lacked a clear pattern. Net gain or loss of 10 kg or more between middle and old age was a strong predictor of all-cause and CVD mortality. CONCLUSIONS: The shape of the association between BMI in old age and mortality differs by cause of death. Major weight change over time is a warning signal for higher CVD mortality. Having BMI<22.7 kg/m2 in old age is associated with above-average mortality rates even if apparently healthy.

Aged↗

PubMed1987

Sociological research on age, aging and the aged in the Netherlands.

A review is given of the socio-gerontological research in the Netherlands. According to a frame work, organising this area of research, first an overview is presented of the studies on age and ageing and next the research on the aged is summarized. The research on age and ageing is limited. Some publications analyse the social meaning of age, some cohort studies have been conducted and recently the life course approach is getting attention. Concerning the research on the aged, the main areas studied are: living circumstances, age stratification, family and social contacts, housing, work and retirement, formal and informal care, death and dying. Since 1970 the amount of socio-gerontological research has increased. It became prominent in the eighties with the promotional activities of a special committee for gerontological research. Several universities are identified with their special areas in the sociology of ageing and the aged.

Adult↗

PubMed1998

AGEs and their interaction with AGE-receptors in vascular disease and diabetes mellitus. I. The AGE concept.

OBJECTIVE: This is the first part of a bipartite review that summarizes the rising knowledge on the molecular mechanisms underlying the action of advanced glycation endproducts (AGEs) and their contribution to diabetic complications and vascular disease. While the first part presented here focusses on AGE formation, the second part will describe the AGE-protein/receptor interactions and their role in mediating AGE-dependent intracellular signalling. RESULTS: Nonenzymatic glycation, in which reducing sugars are covalently attached to free amino groups and ultimately form AGEs, has been found to occur during normal aging and at accelerated rate in diabetes mellitus. Oxidation, accompanying glycation in vivo, further supports chemical modifications. AGE formation and protein crosslinking are irreversible processes that alter the structural and functional properties of proteins, lipid components and nucleic acids. AGE modifications do not only change the physicochemical properties of the afflicted molecules, but also induce cellular signalling, activation of transcription factors and subsequent gene expression in vitro and in vivo. CONCLUSIONS: AGEs elicit a wide range of cell-mediated responses that might contribute to the pathogenesis of diabetic complications, vascular and renal disease and Alzheimer's disease. Substances that inhibit AGE formation, reduce oxidative stress or destroy already formed crosslinks may limit the progression of disease and may offer new tools for therapeutic interventions in the therapy of AGEs mediated disease.

Diabetes Mellitus↗

PubMed2006

How do health and biological age influence chronological age and sex differences in cognitive aging: moderating, mediating, or both?

Much research on cognitive competence in normal older adults has documented age and sex differences. The authors used new cross-sectional data from the Victoria Longitudinal Study (VLS) (n=386; age 61 to 95 years) to examine how health and biological age influence age and sex differences in cognitive aging. The authors found evidence for both moderating and mediating influences. Age differences were moderated by health status, such that the negative effects of age were most pronounced among participants of relatively better health. Sex differences were moderated by health and were more pronounced among participants reporting comparatively poorer health. Although health mediated a notable amount of age-related cognitive variation, BioAge mediated considerably more variance, even after statistical control for differences in health. A complex pattern emerged for the mediation of sex differences: Although BioAge accounted for sex-related variation in cognitive performance, health operated to suppress these differences. Overall, both health and BioAge predicted cognitive variation independently of chronological age.

Aged↗

PubMed1987

Interactions of aged gametes: in vitro fertilization using in vitro-aged sperm and in vivo-aged ova in the mouse.

A study of varying combinations of in vitro-aged sperm and in vivo-aged ova at 3 hr intervals from 0-24 hr resulted in failures at different steps of the fertilization process during in vitro fertilization of mouse ova. Significant decreases caused by sperm aging, ova aging, and sperm X ova aging interaction were found in sperm penetration. Pronuclear formation was not affected by sperm aging and was enhanced by ova aging, and there was a significant effect of sperm X ova aging interaction. Sperm aging significantly influenced the prometaphase stage of the fertilization process. Therefore, it is suggested that the detrimental fertilization effects resulting from aging gametes are due to different mechanisms in sperm and ova, that these mechanisms are affected at different times, and that they affect different steps in the fertilization process.

Aging↗

PubMed1998

Age-related changes in rodent cortical acetylcholine and cognition: main effects of age versus age as an intervening variable.

Evidence from aged and demented humans has stimulated research on the effects of age on the integrity of cortical cholinergic afferents in rodents. However, a comprehensive review of the available data does not consistently support the hypothesis that normal aging in rodents robustly affects the function of basal forebrain cholinergic projections to the cortex. These data indicate the limited significance of age as an independent experimental variable in research on age-related changes in cortical acetylcholine and associated behavioral or cognitive functions. Alternatively, recent studies demonstrated that normal aging in rodents potently interacts with the consequences of experimental manipulations of this system. Thus, aging acts as an intervening variable in experiments designed to elucidate age-related changes in the vulnerability and restorative capacity of this neuronal system after injury and degenerative processes. Investigations of the interactions between the effects of age and the capacity of the cholinergic systems to respond to detrimental processes reveal robust consequences of aging on cortical acetylcholine and the cognitive functions mediated by this neuronal system.

Acetylcholine↗

PubMed1991

Age, disease, and changing sex hormone levels in middle-aged men: results of the Massachusetts Male Aging Study.

To evaluate the hypothesis that endocrine profiles change with aging independently of specific disease states, we examined the age trends of 17 major sex hormones, metabolites, and related serum proteins in 2 large groups of adult males drawn from the Massachusetts Male Aging Study, a population-based cross-sectional survey of men aged 39-70 yr conducted in 1986-89. Group 1 consisted of 415 men who were free of obesity, alcoholism, all prescription medication, prostate problems, and chronic illness (cancer, coronary heart disease, hypertension, diabetes, and ulcer). Group 2 consisted of 1294 men who reported 1 or more of the above conditions. Each age trend was satisfactorily described by a constant percent change per yr between ages 39-70 yr. Free testosterone declined by 1.2%/yr, and albumin-bound testosterone by 1.0%/yr. Sex hormone-binding globulin (SHBG), the major serum carrier of testosterone, increased by 1.2%/yr, with the net effect that total serum testosterone declined more slowly (0.4%/yr) than the free or albumin-bound pools alone. Among the major androgens and metabolites, androstane-3 alpha,17 beta-diol (androstanediol; 0.8%/yr) and androstanediol glucuronide (0.6%/yr) declined less rapidly than free testosterone, while 5 alpha-dihydrotestosterone remained essentially constant between ages 39-70 yr. Androstenedione declined at 1.3%/yr, a rate comparable to that of free testosterone, while the adrenal androgen dehydroepiandrosterone (3.1%/yr) and its sulfate (2.2%/yr) declined 2-3 times more rapidly. The levels of testosterone, SHBG, and several androgen metabolites followed a parallel course in groups 1 and 2, remaining consistently 10-15% lower in group 2 across the age range of the study. Subgroup analyses suggested that obese subjects might be responsible for much of the group difference in androgen level. Serum concentrations of estrogens and cortisol did not change significantly with age or differ between groups. Of the pituitary gonadotropins, FSH increased at 1.9%/yr, LH increased at 1.3%/yr, and PRL declined at 0.4%/yr, with no significant difference between groups 1 and 2.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed2002

Age trends in the level of serum testosterone and other hormones in middle-aged men: longitudinal results from the Massachusetts male aging study.

We used longitudinal data from the Massachusetts Male Aging Study, a large population-based random-sample cohort of men aged 40-70 yr at baseline, to establish normative age trends for serum level of T and related hormones in middle-aged men and to test whether general health status affected the age trends. Of 1,709 men enrolled in 1987-1989, 1,156 were followed up 7-10 yr afterward. By repeated-measures statistical analysis, we estimated simultaneously the cross-sectional age trend of each hormone between subjects within the baseline data, the cross-sectional trend between subjects within the follow-up data, and the longitudinal trend within subjects between baseline and follow-up. Total T declined cross-sectionally at 0.8%/yr of age within the follow-up data, whereas both free and albumin-bound T declined at about 2%/yr, all significantly more steeply than within the baseline data. Sex hormone-binding globulin increased cross-sectionally at 1.6%/yr in the follow-up data, similarly to baseline. The longitudinal decline within subjects between baseline and follow-up was considerably steeper than the cross-sectional trend within measurement times for total T (1.6%/yr) and bioavailable T (2-3%/yr). Dehydroepiandrosterone, dehydroepiandrosterone sulfate, cortisol, and estrone showed significant longitudinal declines, whereas dihydrotestosterone, pituitary gonadotropins, and PRL rose longitudinally. Apparent good health, defined as absence of chronic illness, prescription medication, obesity, or excessive drinking, added 10-15% to the level of several androgens and attenuated the cross-sectional trends in T and LH but did not otherwise affect longitudinal or cross-sectional trends. The paradoxical finding that longitudinal age trends were steeper than cross-sectional trends suggests that incident poor health may accelerate the age-related decline in androgen levels.

Adult↗

PubMed2005

Age, hormones, and cognitive functioning among middle-aged and elderly men: cross-sectional evidence from the Massachusetts Male Aging Study.

BACKGROUND: This study examines interrelationships among age, hormones, and cognition for middle-aged and elderly men, and tests whether hormones predict lower cognitive functioning and mediate the age-cognition relationship. METHODS: We analyzed Time 2 data from the Massachusetts Male Aging Study, a population-based cohort study. Selection criteria included complete information on cognition and hormones (n = 981). Cognitive measures included working memory (Backward Digit Span test), speed/attention (Digit Symbol Substitution test), and spatial ability (Figural Relations test). Hormones included free testosterone, total testosterone, dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), androstanediol glucuronide (3 alpha-A-diol-gluc), luteinizing hormone (LH), follicle-stimulating hormone (FSH), sex hormone-binding globulin (alternatively known as a "binding protein") (SHBG), prolactin (PRL), estrone (E1), and cortisol (CRT). Age was measured in years. Adjusted analyses added educational attainment, health conditions and behaviors, body mass index, and depression. RESULTS: Older age was associated with lower cognitive functioning. In unadjusted models, logged free and total testosterone, DHEA, and DHEAS related to higher functioning in at least one cognitive domain; logged FSH, SHBG, and LH related to lower functioning in at least one cognitive domain; and logged E1, CRT, and PRL were not significant. In adjusted models, logged hormones did not relate to cognitive function except for logged E1 and CRT, which had negative effects. Logged hormones did not mediate the age-cognition relationship. CONCLUSIONS: The direct effects of hormones on cognition are not significant when salient factors are considered. Further, hormones do not mediate the age-cognition relationship; it is necessary to look to other explanatory pathways.

Age Factors↗