Amsterdam UMC, location VUmc
Anatomy and Neurosciences
I'm a PhD-candidate and a core member of the ENIGMA-Parkinson's consortium, focused on identifying markers for alpha-synucleinopathies and subtypes using neuroimaging. I believe strongly that worldwide collaborations in research will play a crucial role in raising our understanding of the pathophysiology of neurological diseases and to enhance effective personalised treatment. Our first collaborative study showed, in a sample of 2367 patients and 1183 healthy controls, distinct patterns of brain structure abnormalities across the clinical stages of Parkinson's disease (https://movementdisorders.onlinelibrary.wiley.com/doi/10.1002/mds.28706). In the following study we will investigate the morphology of the cerebellum and its relation to clinical symptoms.

Presenter of 1 Presentation

REGIONAL ABNORMALITIES IN CEREBELLAR STRUCTURE ASSOCIATED WITH PARKINSON’S DISEASE: A MULTICOHORT CASE-CONTROL STUDY

Session Type
SYMPOSIUM
Date
Sat, 19.03.2022
Session Time
09:10 AM - 11:10 AM
Room
ONSITE: 133-134
Lecture Time
10:25 AM - 10:40 AM

Abstract

Aims

The cerebellum is a crucial structure for both motor and cognitive functions, yet studies on cerebellar abnormalities in Parkinson’s disease (PD) are limited and findings lack consistency. With a multi-cohort approach and state-of-the-art analysis methods, we attempted to better understand how cerebellar structure is affected in PD.

Methods

T1-weighted MR images of 670 PD patients (mean age 65.1y, 41% female, mean illness duration 4.1y) and 275 healthy controls (mean age 63.6y, 51% female) were collected from eight cohorts, and processed using the ACAPULCO segmentation toolbox (http://iacl.jhu.edu/index.php?title=Cerebellum_CNN). Linear mixed-effect models, including age, sex, ICV, and cohort as covariates, were used for group comparison of volumes of 14 cerebellar lobules in each hemisphere. P-values were FDR-corrected.

Results

Compared to controls, PD patients showed a higher total volume (t = 2.55, puncorrected = 0.011) and regional volume in 7 of 28 lobules (tmin = 2.19, tmax = 3.80, puncorrected < 0.029), before FDR-correction. After correction, the right lobule V (t = 3.26, pFDR = 0.014) and right lobule VI (t = 3.80, pFDR < 0.001) remained significantly different.

Conclusions

The larger lobules in PD are intriguing in the context of neurodenegeration. Lobule V and VI have previously been linked to motor function; possibly the enlargement is the result of (temporary) hypertrophy due to constant motor activation in patients. This is supported by literature showing that greater intensity of tremor is related to an enlargement of lobule V. Follow-up research will need to focus on the relation between motor and cognitive symptoms and cerebellar morphology in PD.

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