Early Life Stress, Depression And Parkinson's Disease: A New Approach

Abstract

This review aims to shed light on the relationship that involves exposure to early life stress, depression and Parkinson's disease (PD). A systematic literature search was conducted in Pubmed, MEDLINE, EBSCOHost and Google Scholar and relevant data were submitted to a meta-analysis . Early life stress may contribute to the development of depression and patients with depression are at risk of developing PD later in life. Depression is a common non-motor symptom preceding motor symptoms in PD. Stimulation of regions contiguous to the substantia nigra as well as dopamine (DA) agonists have been shown to be able to attenuate depression. Therefore, since PD causes depletion of dopaminergic neurons in the substantia nigra, depression, rather than being just a simple mood disorder, may be part of the pathophysiological process that leads to PD. It is plausible that the mesocortical and mesolimbic dopaminergic pathways that mediate mood, emotion, and/or cognitive function may also play a key role in depression associated with PD. Here, we propose that a medication designed to address a deficiency in serotonin is more likely to influence motor symptoms of PD associated with depression. This review highlights the effects of an antidepressant, Fluvoxamine maleate, in an animal model that combines depressive-like symptoms and Parkinsonism.

Keywords: Depression; Dopamine; Early stress; Fluvoxamine maleate; Parkinson’s disease.

Fig. 1

The HPA axis and the main hormones secreted by each gland in the axis. CRH: corticotropin releasing hormone. ACTH: adrenocorticotropic hormone. A stressor (e.g., a threat to the life of the organism) triggers the paraventricular nucleus of the hypothalamus to synthesize and secrete CRH, which binds to specific receptors in the anterior pituitary. This stimulates the synthesis and release of ACTH which is released into the circulatory system. ACTH triggers the synthesis and secretion of glucocorticoids (cortisol in humans/corticosterone in rodents) from the adrenal cortex