Dataset Information

Imaging the Limbic System in Parkinson's Disease-A Review of Limbic Pathology and Clinical Symptoms.

ABSTRACT: The limbic system describes a complex of brain structures central for memory, learning, as well as goal directed and emotional behavior. In addition to pathological studies, recent findings using in vivo structural and functional imaging of the brain pinpoint the vulnerability of limbic structures to neurodegeneration in Parkinson's disease (PD) throughout the disease course. Accordingly, dysfunction of the limbic system is critically related to the symptom complex which characterizes PD, including neuropsychiatric, vegetative, and motor symptoms, and their heterogeneity in patients with PD. The aim of this systematic review was to put the spotlight on neuroimaging of the limbic system in PD and to give an overview of the most important structures affected by the disease, their function, disease related alterations, and corresponding clinical manifestations. PubMed was searched in order to identify the most recent studies that investigate the limbic system in PD with the help of neuroimaging methods. First, PD related neuropathological changes and corresponding clinical symptoms of each limbic system region are reviewed, and, finally, a network integration of the limbic system within the complex of PD pathology is discussed.

SUBMITTER: Banwinkler M

PROVIDER: S-EPMC9496800 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Imaging the Limbic System in Parkinson's Disease-A Review of Limbic Pathology and Clinical Symptoms.

Banwinkler Magdalena M Theis Hendrik H Prange Stéphane S van Eimeren Thilo T

Brain sciences 20220915 9

The limbic system describes a complex of brain structures central for memory, learning, as well as goal directed and emotional behavior. In addition to pathological studies, recent findings using in vivo structural and functional imaging of the brain pinpoint the vulnerability of limbic structures to neurodegeneration in Parkinson's disease (PD) throughout the disease course. Accordingly, dysfunction of the limbic system is critically related to the symptom complex which characterizes PD, includ ...[more]

PMID: 36138984

Similar Datasets

Project description:BackgroundBoth Parkinson's disease (PD) and multiple system atrophy (MSA) exhibit degeneration of brainstem serotoninergic nuclei, affecting multiple subcortical and cortical serotoninergic projections. In MSA, medullary serotoninergic neuron pathology is well documented, but serotonin system changes throughout the rest of the brain are less well characterized.ObjectivesTo use serotonin transporter [11 C]3-amino-4-(2-dimethylaminomethyl-phenylsulfaryl)-benzonitrile positron emission tomography (PET) to compare serotoninergic innervation in patients with MSA and PD.MethodsWe performed serotonin transporter PET imaging in 18 patients with MSA, 23 patients with PD, and 16 healthy controls to explore differences in brainstem, subcortical, and cortical regions of interest.ResultsPatients with MSA showed lower serotonin transporter distribution volume ratios compared with patients with PD in the medulla, raphe pontis, ventral striatum, limbic cortex, and thalamic regions, but no differences in the dorsal striatal, ventral anterior cingulate, or total cortical regions. Controls showed greater cortical serotonin transporter binding compared with PD or MSA groups but lower serotonin transporter binding in the striatum and other relevant basal ganglia regions. There were no regional differences in binding between patients with MSA-parkinsonian subtype (n = 8) and patients with MSA-cerebellar subtype (n = 10). Serotonin transporter distribution volume ratios in multiple different regions of interest showed an inverse correlation with the severity of Movement Disorders Society Unified Parkinson's Disease Rating Scale motor score in patients with MSA but not patients with PD.ConclusionsBrainstem and some forebrain subcortical region serotoninergic deficits are more severe in MSA compared with PD and show an MSA-specific correlation with the severity of motor impairments. © 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Project description:Parkinson's disease is delayed in clinical onset, asymmetric in initial appearance, and slow in progression. One explanation for these characteristics may be a boost in natural defenses after early exposure to mild cellular stress. As the patient ages and resilience recedes, however, stress levels may become sufficiently high that toxic cellular responses can no longer be curbed, culminating in inverted U-shaped stress-response curves as a function of disease duration. If dopaminergic systems are indeed capable of responding to mild stress with effective natural defenses, experimental models of Parkinson's disease should adhere to the principles of preconditioning, whereby stress exposure fortifies cells and tempers the toxic sequelae of subsequent stressors. Here, I review evidence favoring the efficacy of preconditioning in dopaminergic systems. Recent animal work also raises the possibility that cross-hemispheric preconditioning may arrest the spread of asymmetric Parkinson's pathology to the other side of the brain. Indeed, compensatory homeostatic systems have long been hypothesized to maintain neurological function until a threshold of cell loss is exceeded and are often displayed as inverted U-shaped curves. However, some stress responses assume an exponential or sigmoidal profile as a function of disease severity, suggesting end-stage deceleration of disease processes. Thus, surviving dopaminergic neurons may become progressively harder to kill, with the dorsal nigral tier dying slower due to superior baseline defenses, inducible conditioning capacity, or delayed dorsomedial nigral spread of disease. In addition, compensatory processes may be useful as biomarkers to distinguish "responder patients" from "nonresponders" before clinical trials. However, another possibility is that defenses are already maximally conditioned in most patients and no further boost is possible. A third alternative is that genuinely diseased human cells cannot be conditioned, in contrast to preclinical models, none of which faithfully recapitulate age-related human conditions. Disease-related "conditioning deficiencies" would then explain how Parkinson's pathology takes root, progressively shrinks defenses, and eventually kills the patient.

Dataset Information

Imaging the Limbic System in Parkinson's Disease-A Review of Limbic Pathology and Clinical Symptoms.

Publications

Imaging the Limbic System in Parkinson's Disease-A Review of Limbic Pathology and Clinical Symptoms.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets