Abstract
Parkinson's disease (PD) is a neurodegenerative disorder accompanied by a series of pathological mechanisms which contribute to a variety of motor and non-motor symptoms. Recently, there has been an increasing interest in structural diffusion tensor imaging (DTI) in PD which has shed light on our understanding of structural abnormalities underlying PD symptoms or its associations with pathological mechanisms. One of the white matter tracts shown to be disrupted in PD with a possible contribution to some PD symptoms is the inferior longitudinal fasciculus (ILF). On the whole, lower ILF integrity contributes to thought disorders, impaired visual emotions, cognitive impairments such as semantic fluency deficits, and mood disorders. This review outlines the microstructural changes in ILF associated with systemic inflammation and various PD symptoms like cognitive decline, facial emotion recognition deficit, depression, color discrimination deficit, olfactory dysfunction, and tremor genesis. However, few studies have investigated DTI correlates of each symptom and larger studies with standardized imaging protocols are required to extend these preliminary findings and lead to more promising results.
Highlights
Parkinson’s disease (PD), the second most prevalent neurodegenerative disorder, is accompanied by several motor [1, 2] and nonmotor symptoms [3]
This study suggests the possible role of inflammation in demyelination and axonal damage in ILF in PD patients
Diffusion tensor imaging has been widely used to study the putative relationship between white matter microstructural (WM) disruptions and PD symptoms
Summary
Parkinson’s disease (PD), the second most prevalent neurodegenerative disorder, is accompanied by several motor (including muscular rigidity, bradykinesia, and resting tremor) [1, 2] and nonmotor symptoms [3]. Accumulation of proteins such as α-synuclein has been recognized as the main pathological mechanism in PD, which adversely affects synaptic function [4]. Concomitant Alzheimer’s disease pathology, i.e., neurofibrillary tangles (NFT) which consist of tau proteins, and plaques of beta-amyloid is a common observation in patients who have developed PD with dementia. NFTs, especially, can lead to axonal damage and contribute to white matter microstructural (WM) changes in different brain regions and tracts, which are consistently reported in patients with PD [7,8,9,10].
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