Factors associated with depression during the perimenopausal transition.

BACKGROUND: This paper examines the factors associated with depressive symptoms during the perimenopausal transition, to increase the understanding about the etiology of perimenopausal depression. METHOD: Seventy-six peri- and early postmenopausal women with or without current depressive symptoms were recruited (mean, 49.5 years; standard deviation, 4.3). Participants completed a series of questionnaires relating to depression (Beck Depression Inventory-II), perimenopausal symptoms (Greene Climacteric Scale), social support, life events, history of mood disorders, exercise regime, and questions regarding lifestyle and well-being. FINDINGS: Univariate relationships between predictors and depression scores were assessed. All significant variables at this level (history of depression, history of premenstrual syndrome, recent negative life events, aerobic exercise, social support, and somatic symptoms) were then analyzed via multiple regression. The presence of recent negative life events, a history of depression, and severity of somatic symptoms of perimenopause were all found to predict unique variance in depression scores. There was also a trend toward a protective role of aerobic exercise. CONCLUSIONS: This study confirmed the role of negative life events, previous depression history, and somatic complaints in the development of depressive symptoms during perimenopause. Further exploration of this relationship is warranted.

What factors determine whether a woman becomes depressed during the perimenopause?

Perimenopause has long been associated with psychological distress, both anecdotally and clinically. Research has identified this time as a period of increased risk for both first-episode depression and for depression reoccurrence. However, we know that the majority of women do not experience these difficulties during perimenopause. This review examines the current research literature looking at the factors associated with depression during perimenopause, with a view to identifying those factors which are protective and those factors which predict increased risk. From the literature, it is evident that some women have a hormonal vulnerability to mood disorders. However, this does not account for the phenomenon of perimenopausal depression in and of itself. Rather, there appears to be a complex interplay between hormonal vulnerability, the psychosocial resources one has (coping skills and social support), their overall well-being (exercise and other lifestyle factors) and the demands on their coping resources (stressful life events). The complexity of the relationship between perimenopause and depression means that there is a need to look beyond either as a sole explanation of mood during midlife. Education is required for both general practitioners and for women regarding the individual risks of psychological distress during perimenopause, as well as the knowledge of the life factors which we know to be protective.

Hormonal therapies for new onset and relapsed depression during perimenopause.

In recent years the perimenopause has become recognised as a 'window of vulnerability' for women's mood. The risk of depression during perimenopause is high and treatment failure is common. Perimenopausal depression encompasses both new onset (first episode) depression occurring during perimenopause as well as a relapse during perimenopause in women with a history of depression. Perimenopausal depression is increasingly recognised as a new subtype of depression with specific clinical characteristics. Current treatments for perimenopausal depression have high failure rates, multiple adverse effects and potentially damaging long term consequences. This review examines both new onset and relapsed depression during perimenopause, biological mechanisms of perimenopausal depression, and the role of hormonal therapies.

Strength and functional characteristics of men and women 65 years and older.

BACKGROUND: Resistance training programs for older adults (>65 years) are an effective method to counteract the loss of muscle mass, strength, and function associated with aging. Nevertheless, limited normative strength and functional data exist for the comparison and stratification of older adults. Therefore, the purpose of this study was to establish normative strength and functional data for males and females 64-69 years, 70-74 years, and 75+ years old, using commonly available equipment and procedures. METHODS: At total of 110 males and 191 females completed upper and lower body strength and functional performance testing. Measurements were compared across gender and age groups (65-69, 70-74, and 75+ years). RESULTS: All strength measures, absolute and relative (to body and lean muscle mass), were significantly (p < 0.01) greater in males compared with females. Additionally, younger participants were stronger (p < 0.01) compared with older participants. Similar findings were observed for the functional performance tests. Quartile ranking for relative strength and functional measures provides comparative data for clinical and research assessments. CONCLUSIONS: This study provides additional normative data for strength and functional performance in males and females aged 65-69, 70-74, and 75+ years and confirms lower performance in females and with aging even when adjusted for lean muscle mass.

Memory loss caused by beta-amyloid protein is rescued by a beta(3)-adrenoceptor agonist.

Accumulation of the neurotoxic beta-amyloid protein (Abeta) in the brain is a key step in the pathogenesis of Alzheimer's disease (AD). Although transgenic mouse models of AD have been developed, there is a clear need for a validated animal model of Abeta-induced amnesia which can be used for toxicity testing and drug development. Intracranial injections of Abeta(1-42) impaired memory in a single trial discriminative avoidance learning task in chicks. Memory inhibition was closely associated with the state of aggregation of the Abeta peptide, and a scrambled-sequence of Abeta(1-42) peptide failed to impair memory. Abeta had little effect on labile (short-term and intermediate) memory, but blocked consolidation of memory into long-term storage mimicking the type of anterograde amnesia that occurs in early AD. Since noradrenaline exerts a modulatory influence on labile memory in the chick, we examined the effects of two beta-adrenoceptor (AR) agonists on Abeta-induced amnesia. A beta(3)-AR agonist (CL316243), but not a beta(2)-AR agonist, rescued Abeta-induced memory loss, suggesting the need for further studies on the role of beta(3)-ARs in AD.

Rescue of Abeta(1-42)-induced memory impairment in day-old chick by facilitation of astrocytic oxidative metabolism: implications for Alzheimer's disease.

Administration of small oligomeric beta-amyloid (Abeta)(1-42) 45 min before one-trial bead discrimination learning in day-old chicks abolishes consolidation of learning 30 min post-training (Gibbs et al. Neurobiol. Aging, in press). Administration of the beta3-adrenergic agonist CL316243, which specifically stimulates astrocytic but not neuronal glucose uptake, rescues Abeta impaired memory. Weakly reinforced training can be consolidated by various metabolic substrates and we have demonstrated neuronal dependence on oxidative metabolism of glucose soon after training versus astrocytic glucose dependence 20 min later. Based on these findings we examined whether different metabolic substrates were able to counteract memory inhibition by Abeta(1-42). Although lactate, the medium-chain fatty acid octanoate, and the ketone body beta-hydroxybutyrate consolidated weakly reinforced training when injected close to learning, none of them were able to salvage Abeta-impaired memory; at this early time. All three metabolites and the astrocytic-specific acetate consolidated weak learning and rescued Abeta-impaired memory when injected 10-20 min post-training. However, neither glucose nor insulin rescued memory when injected at 20 min. Rescue of memory by providing astrocytes with alternative substrates for oxidative metabolism suggests that Abeta(1-42) exerts its amnestic effects specifically by impairing astrocytic glycolysis.