RESUMO
Polycystic ovary syndrome (PCOS) is the most common endocrinopathy among reproductive-aged women, and it typically presents during adolescence. The objective of this review is to describe the clinical manifestations of PCOS in adolescent girls and the underlying basis for the altered reproductive physiology. Recognising adolescents at risk for PCOS and taking the appropriate steps to reduce circulating androgen levels is critical in reducing the clinical symptomatology of this disorder, and the development of adulthood infertility, diabetes, and metabolic syndrome in patients with PCOS.
Assuntos
Hormônio Liberador de Gonadotropina/metabolismo , Hiperandrogenismo/metabolismo , Distúrbios Menstruais/fisiopatologia , Síndrome do Ovário Policístico/metabolismo , Síndrome do Ovário Policístico/fisiopatologia , Puberdade/fisiologia , Adolescente , Adulto , Androgênios/metabolismo , Anovulação/metabolismo , Hormônio Antimülleriano/metabolismo , Criança , Desidroepiandrosterona/metabolismo , Feminino , Hormônio Foliculoestimulante/metabolismo , Humanos , Hiperandrogenismo/prevenção & controle , Hiperinsulinismo/metabolismo , Hormônio Luteinizante/efeitos dos fármacos , Hormônio Luteinizante/metabolismo , Ciclo Menstrual/metabolismo , Distúrbios Menstruais/metabolismo , Obesidade/metabolismo , Ovário/diagnóstico por imagem , Ovário/patologia , Ovário/fisiopatologia , Síndrome do Ovário Policístico/diagnóstico por imagem , Progesterona/farmacologia , Progesterona/fisiologia , Fatores de Risco , Globulina de Ligação a Hormônio Sexual/metabolismo , Testosterona/sangue , UltrassonografiaRESUMO
The amyloid beta-protein precursor gives rise to the amyloid beta-protein, the principal constituent of senile plaques and a cytotoxic fragment involved in the pathogenesis of Alzheimer disease. Here we show that amyloid beta-protein precursor was proteolytically cleaved by caspases in the C terminus to generate a second unrelated peptide, called C31. The resultant C31 peptide was a potent inducer of apoptosis. Both caspase-cleaved amyloid beta-protein precursor and activated caspase-9 were present in brains of Alzheimer disease patients but not in control brains. These findings indicate the possibility that caspase cleavage of amyloid beta-protein precursor with the generation of C31 may be involved in the neuronal death associated with Alzheimer disease.
