Depression and associated Alzheimer’s disease

Abstract The coexistence of depression with Alzheimer's disease (AD) has long been recognized. Data that illustrate the associations between peripheral and brain immune responses raise the possibility of shared pathophysiological mechanisms. Several studies suggested that depression can act as a potential risk factor for the progression of neurodegenerative disorders including AD. The existence of depressive symptoms may have a positive impact on the conversion of mild to severe dementia. It is reported that AD patients suffering from depression show more pronounced amyloid-beta plaques and neurofibrillary tangles in their brain as compared with AD patients without depression. Furthermore, individuals with genetic linkage to depression show more vulnerability toward the initiation of the neurodegenerative cascade. Recent evidence proposed that molecular mechanisms and cascades involve in the pathogenesis of depression such as HPA axis dysregulation, chronic inflammation, are also participate in the pathogenesis of AD. Particularly, impairment in the signaling of some neurotrophins, such as brain-derived neurotrophic factor and nerve growth factor. Furthermore, alteration in tumor necrosis factor-α and transforming growth factor signaling has been recognized as a common neurobiological link between AD and depression. In the present book chapter, we address the common molecular pathway and the neurological link between AD and depression.