Title: Vascular neuropathology in geriatric psychiatry - depression, cognitive disturbance, and dementia
Abstract
A growing body of evidence supports an association between cerebrovascular disease and geriatric depression. The term “vascular depression” has been used to describe a subtype occurring later in life and characterized by brain changes that may be related to depression onset.
Over previous decades, several generations of hypotheses have linked depression to the etiology or pathophysiology of dementia.
The likely biological mechanisms linking depression to dementia include vascular disease, alterations in glucocorticoid steroid levels and hippocampal atrophy, increased deposition of amyloid-β plaques, inflammatory changes, and deficits of nerve growth factors.
The relationship between depression and both dementia and cerebrovascular pathology has, for good reason, received much attention from researchers and clinicians alike.
This presentation focused on relevant findings of neuroanatomical pathways and associated monoaminergic abnormality in vascular depression, apathy, cognitive dysfunction, and pathway linking depression, apathy to cognitive dysfunction, and dementia.
We examined the relationships between post-stroke depression (PSD), functional recovery, cognitive functioning, and lesion location, after separating PSD into two core symptom dimensions: Affective (depressive) and apathetic (loss of interest). These two core symptom dimensions appear to have different underlying neuroanatomical mechanisms, and appear to exert different effects on cognitive functioning and functional recovery: Among the patients with higher depressive scores, the lesion overlap centered on the brainstem, left basal ganglia, and left frontal cortex. Among the patients with higher apathy scores, the lesion overlap centered on the brainstem and bilateral striatum. And apathy was a better predictor of poor functional recovery after a stroke than depression although apathy and depression both affect negatively on cognitive functioning. It is therefore important that studies of PSD consider the two symptoms dimensions separately.
Next, we investigated relationship between abnormality of neuroanatomical pathways, and monoaminergic abnormality in PSD patients. Findings indicated that depression and apathy scores did not correlate with monoamine, and or metabolite values. However, the decrease of NA&DA and the increase of NA&DA turnover were related to lesions in the brainstem, whereas the increase in NA&DA and the decrease in NA&DA turnover were related to cortical and/or striatum lesions. The data on 5-HT turnover showed an opposite tendency to NA&DA turnover. Results of our studies on vascular depression and apathy may indicate catecholamine (NA&DA) and serotonin, both of which are anatomically and functionally interconnected and could respectively influence apathetic, and affective symptoms of depression after stroke.