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Project

Neurobiologie van psychomotore symptomen bij depressie op latere leeftijd

Depression is the most common cause of years lived with disability in Europe and ranked in the top ten causes of impaired health worldwide. Primary a disorder of mood, depression is also associated with cognitive and motor disturbances. Psychomotor disturbance (PMD), a collective term for both slowing (retardation) and increased motor activity (agitation), is  encountered in 20 - 60% of patients with major depressive disorder (MDD). It  involves the quantity and quality of gross and fine motor function, eye movement, facial expression, gait and posture. Its prevalence increases with age and impairs activities of daily life. The pathophysiology of PMD is the subject of ongoing scientific study. Previous research has identified a cognitive (intention, planning, preparation) and a 'pure motor' (execution, speed, fluency) deficit in PMD, noting a similarity with bradykinesia in movement disorders like Parkinson's disease and some dementias. Brain imaging (MRI, PET) in MDD patients with PMD has shown metabolic and structural changes in fronto-striatal areas, the supplementary-motor cortex and the basal ganglia, such as subcortical white matter lesions (WML)  and cortical atrophy.

Our research project aims to unravel the neurobiology of psychomotor retardation, by using late life depression (LLD) as a disease model for a dysfunctional brain network that controls execution of movement and is impaired in common psychiatric and neurodegenerative diseases. We aim to transcend to a symptom based, instead of a disease based, model that increases our understanding of impaired movement. Applying a set of clinical measures of movement and advanced structural and biochemical imaging, we hope to identify these impaired brain regions within the frontostriatal and nigro-meso-striatal loops, and characterize the biochemistry of structural deficits observed in previous studies.  We hypothesize that pathological brain aging, such as neurotoxic protein accumulation or vascular damage, leads to structural and functional changes in cortico-subcortical circuits, and lowers the threshold to develop psychomotor retardation in LLD. Furthermore, we believe that psychomotor retardation in LLD is a heterogeneous syndrome with important between-subject variability in terms of relative weight of affective, cognitive and motor involvement, as well as impairment of distinct sub-circuits and the nature of age-related pathology.

The biochemical research strategy should provide insight in the pathophysiology of psychomotor retardation and possible lifestyle contributors, which could open a new door to both better prevention and new ways of treatment of psychomotor retardation on a symptom-based level.

Datum:1 dec 2018 →  Heden
Trefwoorden:PET, MRI, psychomotor symptoms, late life depression, aging
Disciplines:Neurologische en neuromusculaire ziekten, Gedragsneurowetenschappen, Cognitieve neurowetenschappen
Project type:PhD project