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Biomedicines
Special Issues
Imaging and Neurochemical Biomarkers in Parkinsonian Disorders
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Imaging and Neurochemical Biomarkers in Parkinsonian Disorders

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 1628

Special Issue Editor

Dr. Vasilios C. Constantinides

E-Mail Website
Guest Editor
Department of Neurology, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece
Interests: progressive supranuclear palsy; multiple system atrophy; corticobasal syndrome; CSF biomarkers; MRI
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Parkinson’s disease (PD) is the most common neurodegenerative movement disorder. Its neuropathological hallmarks include Lewy bodies (LBs), which are characterized by an intraneuronal aggregation of abnormally misfolded a-synuclein. Multiple system atrophy (MSA) is also a synucleinopathy characterized by glial cytoplasmic inclusions (GCIs), which refer to the abnormal aggregation of misfolded a-synuclein in oligodendroglial cells. In contrast to these diseases, progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) are tauopathies with hyperphosphorylated tau-protein aggregation, resulting in astrocytic tufts and astrocytic plaques, respectively.

These disorders, in their typical manifestations, present with distinct clinical phenotypes, which assist in their differentiation based on established clinical diagnostic criteria. However, there is considerable phenotypical overlap among these disorders, especially in oligosymptomatic or atypical cases, highlighting the need for a biomarker with molecular specificity to enhance the in vivo recognition of the underlying pathology. Over the past 5 years, a-synuclein seeding assays (SAAs) have emerged as promising biomarkers for PD and other synucleinopathies, resulting in a shift in the conceptual framework of PD. Multiple imaging (MRI, Spect, PET) and neurochemical markers are being developed for tauopathies and synucleinopathies in an effort to establish a pathological diagnosis in vivo in patients with Parkinsonism.

This upcoming Special Issue will highlight the latest advances in fluid and imaging biomarkers for Parkinsonian disorders. Original articles, reviews, and case reports are all welcome.

Dr. Vasilios C. Constantinides
Guest Editor

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. Biomedicines 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

  • progressive supranuclear palsy
  • multiple system atrophy
  • corticobasal syndrome
  • CSF biomarkers
  • MRI
  • PET-CT
  • dopamine transporter imaging

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Published Papers (1 paper)

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21 pages, 2693 KiB  
Systematic Review
Cerebrospinal Fluid Total and Phosphorylated Tau Protein in Behavioral Variant Frontotemporal Dementia, Progressive Supranuclear Palsy, Corticobasal Syndrome and Non-Fluent Agrammatic Primary Progressive Aphasia: A Systematic Review and Meta-Analysis
by Nikolaos Giagkou, Ioanna Kapsali, Maria-Evgenia Brinia and Vasilios C. Constantinides
Biomedicines 2024, 12(8), 1781; https://doi.org/10.3390/biomedicines12081781 - 6 Aug 2024
Cited by 1 | Viewed by 1220
Abstract
(1) Background: Frontotemporal lobar degeneration (FTLD) is a generic term which refers to multiple pathologies, including FTLD-tau. The most common FTLD-tau diseases are Pick’s disease (PiD), progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD). These diseases share four major syndromes: behavioral variant frontotemporal [...] Read more.
(1) Background: Frontotemporal lobar degeneration (FTLD) is a generic term which refers to multiple pathologies, including FTLD-tau. The most common FTLD-tau diseases are Pick’s disease (PiD), progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD). These diseases share four major syndromes: behavioral variant frontotemporal dementia (bvFD), Richardson syndrome (RS), corticobasal syndrome (CBS) and non-fluent agrammatic primary progressive aphasia (nfa-PPA). The primary aim of this meta-analysis was to examine the diagnostic performance of CSF total (t-tau) and phosphorylated (p-tau) protein in bvFTD, RS, CBS, nfa-PPA and pathologically or genetically defined tauopathy. (2) Methods: A systematic review and meta-analysis was performed on all studies with >10 subjects in a bvFTD/RS/CBS/nfa-PPA group and control group and available data on CSF t-tau or p-tau (mean, SD). Cohen’s d was used to quantify the effect size of each study (3) Results: The PSP/tauopathy patients exhibited decreased levels of CSF p-tau compared to the control subjects. The CBS/bvFTD/nfa-PPA cohorts exhibited an increase in t-tau compared to the control groups. (4) Conclusions: Tauopathies may exhibit an inherent decrease in CSF p-tau. The admixture of AD patients in FTD cohorts and high heterogeneity among studies on rare diseases are significant confounding factors in FTLD studies. Full article
(This article belongs to the Special Issue Imaging and Neurochemical Biomarkers in Parkinsonian Disorders)
►▼ Show Figures

Figure 1

Figure 1
<p>Flow chart of study selection according to PRISMA criteria.</p> Full article ">Figure 2
<p>QUADAS-2 tool for risk of bias (<b>a</b>) and concerns on applicability of studies (<b>b</b>), for patient selection, index test, reference standard and flow/timing.</p> Full article ">Figure 3
<p>Forest plots of Cohen’s <span class="html-italic">d</span> of bvFTD studies for CSF total tau protein (<b>a</b>); CSF phosphorylated tau protein (<b>b</b>); funnel plots to illustrate possible publication bias for CSF total tau protein (<b>c</b>); CSF phosphorylated tau protein (<b>d</b>). For citations of studies refer to <a href="#biomedicines-12-01781-t001" class="html-table">Table 1</a>.</p> Full article ">Figure 4
<p>Forest plots of Cohen’s <span class="html-italic">d</span> of PSP studies for CSF total tau protein (<b>a</b>); CSF phosphorylated tau protein (<b>b</b>); funnel plots to illustrate possible publication bias for CSF total tau protein (<b>c</b>); CSF phosphorylated tau protein (<b>d</b>). For citations of studies refer to <a href="#biomedicines-12-01781-t001" class="html-table">Table 1</a>.</p> Full article ">Figure 5
<p>Forest plots of Cohen’s <span class="html-italic">d</span> of CBS studies for CSF total tau protein (<b>a</b>); CSF phosphorylated tau protein (<b>b</b>); funnel plots to illustrate possible publication bias for CSF total tau protein (<b>c</b>); CSF phosphorylated tau protein (<b>d</b>). For citations of studies refer to <a href="#biomedicines-12-01781-t001" class="html-table">Table 1</a>.</p> Full article ">Figure 6
<p>Forest plots of Cohen’s <span class="html-italic">d</span> of nfa-PPA studies for CSF total tau protein (<b>a</b>); CSF phosphorylated tau protein (<b>b</b>); funnel plots to illustrate possible publication bias for CSF total tau protein (<b>c</b>); CSF phosphorylated tau protein (<b>d</b>). For citations of studies refer to <a href="#biomedicines-12-01781-t001" class="html-table">Table 1</a>.</p> Full article ">Figure 7
<p>Forest plots of Cohen’s <span class="html-italic">d</span> of tauopathy studies for CSF total tau protein (<b>a</b>); CSF phosphorylated tau protein (<b>b</b>); funnel plots to illustrate possible publication bias for CSF total tau protein (<b>c</b>); CSF phosphorylated tau protein (<b>d</b>). For citations of studies refer to <a href="#biomedicines-12-01781-t001" class="html-table">Table 1</a>.</p> Full article ">
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