ABSTRACT
Recent clinical and epidemiological observations point to a correlation between disorders of energy metabolism, such as obesity and diabetes, and cognitive decline and dementia. Many studies indicate that these age-related conditions closely interact with each other, but the underlying molecular and physiological mechanisms for such correlations are largely unknown. Insulin and leptin, hormones classically implicated in diabetes and obesity, are gaining increasing attention for their participation in cognitive processes and memory. Disrupted signaling by those hormones is associated with impaired brain function. The current review discusses how restoration of insulin and leptin signaling in the brain may attenuate neuronal damage and promote cognition. We further discuss potential therapeutic approaches involving the use of insulin and leptin as cognitive enhancers in the context of metabolic disorders and Alzheimer's disease. This article is part of the special issue entitled 'The Quest for Disease-Modifying Therapies for Neurodegenerative Disorders'.
Subject(s)
Alzheimer Disease/drug therapy , Alzheimer Disease/psychology , Insulin/therapeutic use , Leptin/therapeutic use , Metabolic Diseases/drug therapy , Metabolic Diseases/psychology , Nootropic Agents/pharmacology , Animals , Biomarkers , Energy Metabolism/drug effects , HumansABSTRACT
Non-specific lymphocytic myocarditis (NLM) is frequently observed in baboons within the endemic range of Trypanosoma cruzi. We sought to determine whether T. cruzi infection is a cause of baboon NLM. We evaluated serial histologic sections of cardiac muscle, blood cultures, immunohistochemistry, serology, polymerase chain reaction, and clinical pathology from 31 baboons with NLM to determine whether T. cruzi infection is associated with NLM. Eleven baboons with no evidence of T. cruzi infection by serology and no NLM were used as controls. Seropositivity for T. cruzi was 45% in baboons with NLM compared with a 2-3% colony prevalence. NLM lesion severity was significantly higher in seropositive than seronegative baboons with NLM. NLM was significantly more common in older baboons. No statistical association between NLM and sex, weight, or clinical pathology was found. These results suggest an association between NLM and T. cruzi infection in the baboon.
Subject(s)
Chagas Cardiomyopathy/veterinary , Monkey Diseases/parasitology , Papio , Trypanosoma cruzi/isolation & purification , Animals , Chagas Cardiomyopathy/parasitology , Female , Male , Myocardium/pathologyABSTRACT
BACKGROUND: There is little information available concerning trichobezoars in the non-human primate literature. METHODS: We evaluated 118 cases of trichobezoar in baboons over a 29-year period at the Southwest National Primate Research Center. RESULTS: The anatomic locations affected in decreasing order were the stomach, small intestine, cecum, esophagus and colon. The most common clinical history was weight loss. The most frequent associated pathology included gastrointestinal inflammation and ulceration, emaciation, peritonitis, intussusception, pneumonia, and aspiration. Trichobezoars were the cause of death in nine baboons and the reason for euthanasia in 12. Females were 2.14 times more likely than males to be affected. The greater the percentage of group housing time, the more likely the baboon is to develop trichobezoars. CONCLUSIONS: The baboon may present a useful model to evaluate the etiology, genetic predisposition, physiopathology, neurobiology, and treatment response of trichobezoars.
