Early cortical atrophy is related to depression in patients with neuropathologically confirmed Parkinson's disease.

OBJECTIVE: Depression is a common comorbidity in Parkinson's disease (PD) and other synucleinopathies. In non-PD geriatric patients, cortical atrophy has previously been connected to depression. Here, we investigated cortical atrophy and vascular white matter hyperintensities (WMHs) in autopsy-confirmed parkinsonism patients with the focus on clinical depression. METHODS: The sample consisted of 50 patients with a postmortem confirmed neuropathological diagnosis (30 Parkinson's disease [PD], 10 progressive supranuclear palsy [PSP] and 10 multiple system atrophy [MSA]). Each patient had been scanned with brain computerized tomography (CT) antemortem (median motor symptom duration at scanning = 3.0 years), and 19 patients were scanned again after a mean interval of 2.7 years. Medial temporal atrophy (MTA), global cortical atrophy (GCA) and WMHs were evaluated computationally from CT scans using an image quantification tool based on convolutional neural networks. Depression and other clinical parameters were recorded from patient files. RESULTS: Depression was associated with increased MTA after controlling for diagnosis, age, symptom duration, and cognition (p = 0.006). A similar finding was observed with GCA (p = 0.017) but not with WMH (p = 0.47). In PD patients alone, the result was confirmed for MTA (p = 0.021) with the same covariates. In the longitudinal analysis, GCA change per year was more severe in depressed patients than in nondepressed patients (p = 0.029). CONCLUSIONS: Early medial temporal and global cortical atrophy, as detected with automated analysis of CT-images using convolutional neural networks, is associated with clinical depression in parkinsonism patients. Global cortical atrophy seems to progress faster in depressed patients.

Height and nigral neuron density in Parkinson's disease.

BACKGROUND: The dopaminergic system modulates growth hormone secretion and previous results have suggested a link between short stature and an increased risk of Parkinson's disease (PD). METHODS: In 36 Lewy body spectrum disease (LBD) cases (PD = 22) and 19 controls, nigral TH-positive neuron densities were measured postmortem from midbrain sections and corrected with the Abercrombie method. Body measurements were collected from autopsies or patient records. Our aim was to investigate the possible relationship between height and the density of neurons in the substantia nigra pars compacta (SNc). RESULTS: SNc neuron density (n/mm2) had an inverse association with height, (R2 = 0.317, p < 0.0001) in patients. The association was not explained by weight, age, sex, brain weight, medication, or disease motor severity. The association was also separately observed in patients with PD (n = 22), but not in subjects who died without diagnosed neurological diseases. CONCLUSIONS: Individual adult height may be connected to nigral neuron numbers in patients with LBDs, including PD.