Stress, depression and Parkinson's disease

Abstract

In this review, we focus on the relationship among Parkinson’s disease (PD), stress and depression. Parkinson’s disease patients have a high risk of developing depression, and it is possible that stress contributes to the development of both pathologies. Stress dysfunction may have a role in the etiology of preclinical non-motor symptoms of PD (such as depression) and, later in the course of the disease, may worsen motor symptoms. However, relatively few studies have examined stress or depression and the injured nigrostriatal system. This review discusses the effects of stress on neurodegeneration and depression, and their association with the symptoms and progression of PD.

Depression and Parkinson disease: prevalence, temporal relationship, and determinants

“…A recently published cohort study also showed that having prior depression increases the risk of having a PD diagnosis in the following year by 3.2 times (30). In animal models where depression is modeled by chronic stress paradigms, increased HPA axis and oxidative stress, increased dendritic atrophy, decreased neurogenesis, and increased inflammation are shown (31,32). Each of these neuropathological mechanisms of depression may trigger or effect the onset of PD and should be investigated further in future studies.…”

Early use of oleanolic acid provides protection against 6-hydroxydopamine induced dopamine neurodegeneration

“…The integrity of dopamine neurons in the basal ganglia is imperative for normal functioning of the motor as well as the non-motor systems (reward and motivation) (Hemmerle et al, 2012). Parkinson's disease which affects approximately 1% of people over the age of 65 years is progressive in nature (Redgrave and Vautrelle, 2011).…”

Neuroprotective mechanism of losartan and its interaction with nimesulide against chronic fatigue stress

“…In the present study, RWATS for 21 days treated animals demonstrated a delayed time latency to enter, decreased number of entries and time spent in mirror chamber as compared to naive animals, suggesting anxiety-like behavior which is further strengthened as evidenced by an increased corticosterone level in RWATS treated group. Glucocorticoid hyper-secretion is known to cause dendrite atrophy in hippocampus, an area concerned with learning and memory and dendrite hypertrophy in amygdala, a region positively linked to fear and anxiety in CNS (Hemmerle et al 2012). Increased plasma cortisol is also known to influence the mobilization of stored fat and carbohydrate reserves which in turn increase blood glucose levels (Taché et al 1976) leading to metabolic alterations.…”