RESUMO
This review discussed the importance of mutated tau, amyloid and neuroinflammatory factors and microglia in Alzheimer disease. In particular tau, CD4 and TNF alpha were included in the review and the colocalizations of these factors were highlighted. It is important to realize the Alzheimer disease may result from the interactions of these factors. Some of these factors may coexist at the same region and at the same time e.g. mutated tau and amyloid in plaques. A summary scheme of etiology leading to the disease was included.
Assuntos
Doença de Alzheimer/genética , Proteínas Amiloidogênicas/genética , Mutação , Placa Amiloide/genética , Proteínas tau/genética , Doença de Alzheimer/diagnóstico , Doença de Alzheimer/imunologia , Doença de Alzheimer/patologia , Proteínas Amiloidogênicas/imunologia , Animais , Encéfalo/imunologia , Encéfalo/patologia , Antígenos CD4/genética , Antígenos CD4/imunologia , Morte Celular , Expressão Gênica , Humanos , Inflamação , Microglia/imunologia , Microglia/patologia , Placa Amiloide/diagnóstico , Placa Amiloide/imunologia , Placa Amiloide/patologia , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/imunologia , Proteínas tau/imunologiaRESUMO
Serotonin (5-hydroxytryptamine, 5-HT) is well known to be closely associated with emotional disorders, such as depression and schizophrenia. The seven main members of 5-HT receptor family including the different subtypes are involved in the functional pathways in the brain and their balance in activity helps to maintain the normal mental stability. As any detrimental changes in the 5-HT system is believed to alter emotion in human, different drugs including serotonin reuptake inhibitors (SSRIs) are nowadays commonly used as anti- depressives. In this review, 5-HT(1A) and 5-HT(2A) receptors and serotonergic positive cells in the human were highlighted in particular. It is hoped that this review will give a map of these major 5-HT receptors and serotonergic neurons in the human CNS to facilitate further deciphering of their functions.