Miguel Á. Labrador-Espinosa (Spain)
Instituto de Biomedicina de Sevilla (IBiS)
Movement Disorders Group
Miguel Á. Labrador-Espinosa was formally trained in Health Engineering at the University of Seville, Spain. Looking for an interdisciplinary profile, he intensified his technical training and clinical neuroscience knowledge through MSc studies in Data Science and Big Data as well as in Biomedical Research at the University of Seville. Currently, he is developing his PhD at the Neuroimaging section of the Movement Disorders Group at the Instituto de Biomedicina de Sevilla (IBiS), Spain, with a competitive PhD fellowship from the Department of Medicine of the University of Seville. His research focuses on the use of multimodal neuroimaging techniques to better understand the pathophysiology of Parkinson's disease, and to find clinically useful neuroimaging biomarkers that may help early diagnosis and more accurate prognosis of the disease.

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 Conference Calendar

LONGITUDINAL CHOLINERGIC BASAL FOREBRAIN DEGENERATION IN EARLY-STAGE PD LINKS WITH PARALLEL ATROPHY OF COGNITION-RELEVANT CORTICAL AREAS.

Session Name
0630 - CHOLINERGIC MECHANISMS IN AD AND PD (ID 30)
Session Type
SYMPOSIUM
Date
Thu, 17.03.2022
Session Time
09:10 AM - 11:10 AM
Room
ONSITE: 114
Lecture Time
09:40 AM - 09:55 AM
Presenter

Abstract

Aims

Degeneration of the cortically-projecting cholinergic basal forebrain (cBF) is an early pathologic feature of both Alzheimer’s disease (AD) and Parkinson’s disease (PD). In AD, in-vivo cBF degeneration on MRI was shown to be associated with parallel atrophy of its cortical projection areas. We examined whether longitudinal cBF degeneration in early-stage PD is linked with regional cortical atrophy, and whether this link depends on the presence of AD co-pathology as assessed by a CSF amyloid-β biomarker.

Methods

The study included a total of 167 de novo PD patients that underwent serial 3T MRI scanning within the Parkinson’s Progression Markers Initiative (average follow-up: 2.3±1.5 years). Gray matter volumes of the cBF and 34 cortical regions per hemisphere were automatically extracted using established procedures within SPM12. Individual slopes of regional volume changes were estimated from the serial measurements using linear-mixed models, controlled for intracranial volume, age, and sex. Associations between longitudinal cBF degeneration and cortical atrophy were assessed using Pearson correlations. Complementary analyses assessed these correlations separately for amyloid-β-positive (N=58) and –negative (N=105) patient groups.

Results

Longitudinal cBF degeneration was highly correlated with longitudinal degeneration of specific cortical limbic and association areas, most notably the insular, medial temporal, and posterior medial cortices (Fig-1a). Interestingly, significant associations were observed independent of amyloid-β status (Fig-1b,c), although associations with posterior cortical areas were significantly more pronounced in amyloid-β-positive patients.

figure1.jpg

Conclusions

These findings establish a link between longitudinal atrophy of the cBF and cognition-relevant cortical areas in early-stage PD, which is enhanced by AD co-pathology.

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