Objective: To investigate whether tau accumulation is higher in late life depression (LLD) compared to non-depressed cognitively unimpaired (CU) older adults. To situate these findings in the neurodegeneration model of LLD by assessing group differences in tau and grey matter volume (GMV) between LLD, non-depressed CU and mild cognitive impairment due to Alzheimer's Disease (MCI).
Design: Monocentric, cross-sectional study.
Late-life depression has been consistently associated with lower gray matter volume, the origin of which remains largely unexplained. Recent in-vivo PET findings in early-onset depression and Alzheimer's Disease suggest that synaptic deficits contribute to the pathophysiology of these disorders and may therefore contribute to lower gray matter volume in late-life depression. Here, we investigate synaptic density in vivo for the first time in late-life depression using the synaptic vesicle glycoprotein 2A receptor radioligand C-UCB-J.
View Article and Find Full Text PDFObjective: To investigate whether mild motor signs (MMS) in old age correlate with synaptic density in the brain.
Background: Normal aging is associated with a decline in movement quality and quantity, commonly termed "mild parkinsonian signs" or more recently MMS. Whether MMS stem from global brain aging or pathology within motor circuits remains unresolved.
Background: Major depressive disorders rank in the top ten causes of ill health in all but four countries worldwide and are the leading cause of years lived with disability in Europe (WHO). Recent research suggests that neurodegenerative pathology may contribute to the development of late-life depression (LLD) in a sub-group of patients and represent a target for prevention and early diagnosis. In parallel, electroconvulsive therapy (ECT), which is the most effective treatment for severe LLD, has been associated with significant brain structural changes.
View Article and Find Full Text PDFObjective: To study the diagnostic value of volume perfusion CT (VPCT) in patients with transient focal neurologic deficits following and during epileptic seizures, that mimic symptoms of stroke.
Methods: A retrospective case-control study was performed on 159 patients who presented with a seizure and received an emergency VPCT within the first 3.5 hours of admission, after being misjudged to have an acute stroke.