Special Issue "Proteomics in Neurodegenerative Diseases"

A special issue of Proteomes (ISSN 2227-7382).

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 3678

Special Issue Editor

Dr. Eleanor Drummond
E-Mail Website
Guest Editor
1. Faculty of Medicine and Health, University of Sydney, Sydney 2050, Australia
2. New York University School of Medicine, New York, NY 10016, USA
Interests: Alzheimer’s disease; frontotemporal dementia; proteomics; neuropathology; protein-protein interactions

Special Issue Information

Dear Colleagues, 

Proteomics provides an incredibly exciting path forward for our understanding of neurodegenerative diseases. The causes of major neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and frontotemporal dementia are still unknown and studies suggest that complex, intersecting disease mechanisms are involved. Proteomics is an ideal method to understand the complex pathogenesis of neurodegenerative diseases and to identify new biomarkers and therapeutic targets. It also provides an excellent opportunity to explore the pathological role that particular post-translational modifications and protein–protein interactions have in neurodegenerative diseases. Exciting recent methodological advances have allowed the examination of disease-associated protein differences with unprecedented sensitivity, and have permitted the examination of highly localized disease-associated protein changes in specific cell types, subcellular fractions or in neuropathological lesions. 

This Special Issue welcomes submissions of original research, method papers, and review articles that focus on the use of proteomics approaches to study neurodegenerative disease. We are especially interested in articles that use proteomics to profile disease-associated protein interactions or post-translational modifications, and that use proteomics approaches to profile localized protein differences present in particular regions, fractions, cell types, or neuropathological lesions. We are also particularly interested in studies that use proteomics to identify novel biomarkers for neurodegenerative disease and studies that discuss new bioinformatics approaches to study this rapidly expanding field of neurodegenerative disease proteomics.

Dr. Eleanor Drummond
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. Proteomes is an international peer-reviewed open access quarterly 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 1600 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

  • Neurodegenerative disease
  • Neuroproteomics
  • Mass spectrometry
  • Quantitative proteomics
  • Protein-protein interaction
  • Neuropathology
  • Post-translational modifications
  • Biomarkers

Published Papers (1 paper)

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Research

Article
CSF Proteomic Alzheimer’s Disease-Predictive Subtypes in Cognitively Intact Amyloid Negative Individuals
Proteomes 2021, 9(3), 36; https://doi.org/10.3390/proteomes9030036 - 02 Aug 2021
Cited by 1 | Viewed by 2870
Abstract
We recently discovered three distinct pathophysiological subtypes in Alzheimer’s disease (AD) using cerebrospinal fluid (CSF) proteomics: one with neuronal hyperplasticity, a second with innate immune system activation, and a third subtype with blood–brain barrier dysfunction. It remains unclear whether AD proteomic subtype profiles [...] Read more.
We recently discovered three distinct pathophysiological subtypes in Alzheimer’s disease (AD) using cerebrospinal fluid (CSF) proteomics: one with neuronal hyperplasticity, a second with innate immune system activation, and a third subtype with blood–brain barrier dysfunction. It remains unclear whether AD proteomic subtype profiles are a consequence of amyloid aggregation, or might exist upstream from aggregated amyloid. We studied this question in 127 older individuals with intact cognition and normal AD biomarkers in two independent cohorts (EMIF-AD MBD and ADNI). We clustered 705 proteins measured in CSF that were previously related to AD. We identified in these cognitively intact individuals without AD pathology three subtypes: two subtypes were seen in both cohorts (n = 49 with neuronal hyperplasticity and n = 44 with blood–brain barrier dysfunction), and one only in ADNI (n = 12 with innate immune activation). The proteins specific for these subtypes strongly overlapped with AD subtype protein profiles (overlap coefficients 92%–71%). Longitudinal p181-tau and amyloid β 1–42 (Aβ42) CSF analysis showed that in the hyperplasticity subtype p181-tau increased (β = 2.6 pg/mL per year, p = 0.01) and Aβ42 decreased over time (β = −4.4 pg/mL per year, p = 0.03), in the innate immune activation subtype p181-tau increased (β = 3.1 pg/mL per year, p = 0.01) while in the blood–brain barrier dysfunction subtype Aβ42 decreased (β = −3.7 pg/mL per year, p = 0.009). These findings suggest that AD proteomic subtypes might already manifest in cognitively normal individuals and may predispose for AD before amyloid has reached abnormal levels. Full article
(This article belongs to the Special Issue Proteomics in Neurodegenerative Diseases)
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