Journal
Primary research
Effects of ketone bodies in Alzheimer’s disease in relation to neural hypometabolism, β-amyloid toxicity, and astrocyte function
Brain hypometabolism precedes clinical signs ofAlzheimer’s disease: Frackowiak et al. (1981) found a decline in cerebral bloodflow and mean cerebral oxygen utilization, i.e., hypometabolism, which is correlated with the severity of dementia. Global oxygen extraction ratio was not increased, providing evidence against chronic ischemia. Shortly afterward deLeon et al. (1983) found that aged patients with senile dementia showed consistent diminutions in regional glucose use compared to elderly normal persons, also with significant correlation between hypometabolism and decreased cognitive functioning. Thirteen additional studies (till 2009) all showed glucose hypometabolism (Cunnane et al. 2011), and since then glucose hypometabolism has repeatedly been confirmed in Alzheimer’s patients. In contrast, metabolism of ketone bodies is unaltered, at least in early stages of thedisease (Castellano et al. 2015).
Alzheimer’s disease as well as some forms of epilepsy can be treated more or less effectively with ketogenic diet. In epilepsy, it appears advantageous to administer the highest possible fraction of the patients’ calorie need in the form of ketone bodies, which may reduce glucose metabolism sufficiently to impair glutamate production in neurons. Much lower doses of ketone bodies can have therapeutic effect inAlzheimer’s disease by different mechanisms. Enabling ketone bodies to supply a fraction of needed ATP may partly compensate for the deficiency in glucose metabolism in Alzheimer’s patients. An alternative mechanism of action could be to prevent or reduce gliotransmitter release ofglutamate. Stimulation from subcortical nuclei can induce gliotransmitter release besides decreasing inflammation and enhancing metabolism.
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Impacts of Psychological Stress on Osteoporosis: Clinical Implications and Treatment Interactions
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Role of cortisol in the pathogenesis of postmenopausal osteoporosis: relationship to bone structure
Excess glucocorticoids are well recognised as a cause of osteoporosis; they inhibit osteoblast function and increase osteoblast and osteocyte apoptosis resulting in thinning of the trabeculae. The circadian rhythm of bone turnover, which is linked to cortisol rhythm, is abnormal in osteoporosis. Furthermore, some studies show abnormal cortisol metabolism in osteoporosis. The aim of our…
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Stress Factors Increase Osteoporosis: A ComparativeAssessment of Osteocalcin and Cortisol Levels in Menopausal Women
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Association of Menopausal Vasomotor Symptoms With Increased Bone Turnover During the Menopausal Transition
The purpose of this study was to determine the longitudinal association between menopausal vasomotor symptoms (VMS) and urinary N-telopeptide level (NTX) according to menopausal stage. We conclude that among early perimenopausal and late perimenopausal women, those with VMS had higher bone turnover than those without VMS. Prior to the final menstrual period, VMS may be a…
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Presence of vasomotor symptoms is associated with lower bone mineral density
Objective: To determine whether women with vasomotor symptoms (VMS) have lower bone mineral density (BMD) than women without VMS. Design We analyzed data from baseline to annual follow-up visit 5 for 2213 participants in the bone substudy of the Study of Women’s Health Across the Nation. At baseline, women were aged 42 to 52 years,…
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Osteocalcin, a promising marker of osteoporosis: evaluation in post-menopausal females with osteoporosis
Background: Osteocalcin, has high affinity for calcium. In osteoporotic women, deficiency of calcium may lead to lowering of the formation of hydroxyapatite crystals. Thus, in the state of hypo mineralization, free osteocalcin available in the circulation. Therefore, present study was designed to evaluate significance of serum osteocalcin in diagnosis of osteoporosis, and relationship between Serum Osteocalcin…
