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Life
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Alpha-Synuclein and Non-Motor Symptoms of Parkinson’s Disease
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Alpha-Synuclein and Non-Motor Symptoms of Parkinson’s Disease

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Proteins and Proteomics".

Deadline for manuscript submissions: closed (25 June 2021) | Viewed by 21528

Special Issue Editors

Dr. Emanuela Colla

E-Mail Website
Guest Editor
Bio@SNS Laboratory, Scuola Normale Superiore, 56126 Pisa, Italy
Interests: Parkinson's disease; alpha-Synuclein; ER stress; neurodegeneration; protein misfolding; gut-brain axis; molecular biology
Dr. Jessica Grigoletto

E-Mail Website
Guest Editor
Last affiliation-German Center for Neurodegenerative Diseases (DZNE), Venusberg-Campus 1, Gebäude 99, 53127 Bonn, Germany
Interests: alpha-synuclein; protein aggregation; neurodegenerative diseases; Parkinson's disease; alpha-synucleinopathy; neurodegeneration; axonal degeneration; striatal matrix vs striatal striosomes; biomarkers

Special Issue Information

Dear Colleagues,

Parkinson’s disease (PD) patients are afflicted by a variety of conditions, including motor and non-motor symptoms that do not necessarily fit the criteria of the dopaminergic nigral pathway degeneration. Non-motor symptoms include not only gastrointestinal dysfunction and anosmia but also anxiety, dementia, hallucinations, insomnia, deficit in working memory, low blood pressure, excessive sweating, and urinary problems. This Special Issue focuses its attention on the link between alpha-synuclein and the occurrence of non-motor symptoms in PD. Our aim is to build a paper collection that highlights the latest findings on this topic, from biomarker validation to the identification of new mechanisms that can tie together alpha-synuclein pathology to the onset of non-conventional, extranigral symptoms in PD. Articles about drugs that can improve such conditions are also welcome.

Dr. Emanuela Colla
Dr. Jessica Grigoletto
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Life is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • alpha-synuclein non-conventional function
  • non-motor symptoms
  • biomarkers for early diagnosis
  • PNS
  • extranigral pathways

Published Papers (5 papers)

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Editorial

Jump to: Research, Review

2 pages, 191 KiB  
Editorial
Alpha-Synuclein and Parkinson’s Disease Motor and Non-Motor Symptoms: What Is New?
by Jessica Grigoletto and Emanuela Colla
Life 2022, 12(6), 904; https://doi.org/10.3390/life12060904 - 16 Jun 2022
Viewed by 1420
Abstract
Although it was discovered about 25 years ago, alpha-synuclein (αS) misfolding and accumulation in neuronal tissues is still recognized as one of the most crucial aspects in Parkinson’s disease (PD) pathology [...] Full article
(This article belongs to the Special Issue Alpha-Synuclein and Non-Motor Symptoms of Parkinson’s Disease)

Research

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14 pages, 1814 KiB  
Article
Loss of Corticostriatal Mu-Opioid Receptors in α-Synuclein Transgenic Mouse Brains
by Jessica Grigoletto, Meir Schechter and Ronit Sharon
Life 2022, 12(1), 63; https://doi.org/10.3390/life12010063 - 03 Jan 2022
Cited by 3 | Viewed by 1663
Abstract
Ultrastructural, neurochemical, and molecular alterations within the striatum are associated with the onset and progression of Parkinson’s disease (PD). In PD, the dopamine-containing neurons in the substantia nigra pars compacta (SNc) degenerate and reduce dopamine-containing innervations to the striatum. The loss of striatal [...] Read more.
Ultrastructural, neurochemical, and molecular alterations within the striatum are associated with the onset and progression of Parkinson’s disease (PD). In PD, the dopamine-containing neurons in the substantia nigra pars compacta (SNc) degenerate and reduce dopamine-containing innervations to the striatum. The loss of striatal dopamine is associated with enhanced corticostriatal glutamatergic plasticity at the early stages of PD. However, with disease progression, the glutamatergic corticostriatal white matter tracts (WMTs) also degenerate. We analyzed the levels of Mu opioid receptors (MORs) in the corticostriatal WMTs, as a function of α-Synuclein (α-Syn) toxicity in transgenic mouse brains. Our data show an age-dependent loss of MOR expression levels in the striatum and specifically, within the caudal striatal WMTs in α-Syn tg mouse brains. The loss of MOR expression is associated with degeneration of the myelinated axons that are localized within the corticostriatal WMTs. In brains affected with late stages of PD, we detect evidence confirming the degeneration of myelinated axons within the corticostriatal WMTs. We conclude that loss of corticostriatal MOR expression is associated with degeneration of corticostriatal WMT in α-Syn tg mice, modeling PD. Full article
(This article belongs to the Special Issue Alpha-Synuclein and Non-Motor Symptoms of Parkinson’s Disease)
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Review

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23 pages, 1361 KiB  
Review
Alpha-Synuclein and Cognitive Decline in Parkinson Disease
by Tian-Sin Fan, Sam Chi-Hao Liu and Ruey-Meei Wu
Life 2021, 11(11), 1239; https://doi.org/10.3390/life11111239 - 16 Nov 2021
Cited by 21 | Viewed by 5856
Abstract
Parkinson disease (PD) is the second most common neurodegenerative disorder in elderly people. It is characterized by the aggregation of misfolded alpha-synuclein throughout the nervous system. Aside from cardinal motor symptoms, cognitive impairment is one of the most disabling non-motor symptoms that occurs [...] Read more.
Parkinson disease (PD) is the second most common neurodegenerative disorder in elderly people. It is characterized by the aggregation of misfolded alpha-synuclein throughout the nervous system. Aside from cardinal motor symptoms, cognitive impairment is one of the most disabling non-motor symptoms that occurs during the progression of the disease. The accumulation and spreading of alpha-synuclein pathology from the brainstem to limbic and neocortical structures is correlated with emerging cognitive decline in PD. This review summarizes the genetic and pathophysiologic relationship between alpha-synuclein and cognitive impairment in PD, together with potential areas of biomarker advancement. Full article
(This article belongs to the Special Issue Alpha-Synuclein and Non-Motor Symptoms of Parkinson’s Disease)
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17 pages, 664 KiB  
Review
Astrocytes in Neurodegenerative Diseases: A Perspective from Tauopathy and α-Synucleinopathy
by Peng Wang and Yihong Ye
Life 2021, 11(9), 938; https://doi.org/10.3390/life11090938 - 09 Sep 2021
Cited by 12 | Viewed by 4568
Abstract
Neurodegenerative diseases are aging-associated chronic pathological conditions affecting primarily neurons in humans. Inclusion bodies containing misfolded proteins have emerged as a common pathologic feature for these diseases. In many cases, misfolded proteins produced by a neuron can be transmitted to another neuron or [...] Read more.
Neurodegenerative diseases are aging-associated chronic pathological conditions affecting primarily neurons in humans. Inclusion bodies containing misfolded proteins have emerged as a common pathologic feature for these diseases. In many cases, misfolded proteins produced by a neuron can be transmitted to another neuron or a non-neuronal cell, leading to the propagation of disease-associated pathology. While undergoing intercellular transmission, misfolded proteins released from donor cells can often change the physiological state of recipient cells. Accumulating evidence suggests that astrocytes are highly sensitive to neuron-originated proteotoxic insults, which convert them into an active inflammatory state. Conversely, activated astrocytes can release a plethora of factors to impact neuronal functions. This review summarizes our current understanding of the complex molecular interplays between astrocyte and neuron, emphasizing on Tau and α-synuclein (α-syn), the disease-driving proteins for Alzheimer’s and Parkinson’s diseases, respectively. Full article
(This article belongs to the Special Issue Alpha-Synuclein and Non-Motor Symptoms of Parkinson’s Disease)
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14 pages, 508 KiB  
Review
The Impact of SNCA Variations and Its Product Alpha-Synuclein on Non-Motor Features of Parkinson’s Disease
by Luca Magistrelli, Elena Contaldi and Cristoforo Comi
Life 2021, 11(8), 804; https://doi.org/10.3390/life11080804 - 09 Aug 2021
Cited by 13 | Viewed by 6581
Abstract
Parkinson’s disease (PD) is a common and progressive neurodegenerative disease, caused by the loss of dopaminergic neurons in the substantia nigra pars compacta in the midbrain, which is clinically characterized by a constellation of motor and non-motor manifestations. The latter include hyposmia, constipation, [...] Read more.
Parkinson’s disease (PD) is a common and progressive neurodegenerative disease, caused by the loss of dopaminergic neurons in the substantia nigra pars compacta in the midbrain, which is clinically characterized by a constellation of motor and non-motor manifestations. The latter include hyposmia, constipation, depression, pain and, in later stages, cognitive decline and dysautonomia. The main pathological features of PD are neuronal loss and consequent accumulation of Lewy bodies (LB) in the surviving neurons. Alpha-synuclein (α-syn) is the main component of LB, and α-syn aggregation and accumulation perpetuate neuronal degeneration. Mutations in the α-syn gene (SNCA) were the first genetic cause of PD to be identified. Generally, patients carrying SNCA mutations present early-onset parkinsonism with severe and early non-motor symptoms, including cognitive decline. Several SNCA polymorphisms were also identified, and some of them showed association with non-motor manifestations. The functional role of these polymorphisms is only partially understood. In this review we explore the contribution of SNCA and its product, α-syn, in predisposing to the non-motor manifestations of PD. Full article
(This article belongs to the Special Issue Alpha-Synuclein and Non-Motor Symptoms of Parkinson’s Disease)
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