Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
2.7
3.2
Journals
Life
Special Issues
Advances in Neuroprotein Research: Functions, Pathologies and Treatments
share announcement

Advances in Neuroprotein Research: Functions, Pathologies and Treatments

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

Deadline for manuscript submissions: closed (19 April 2024) | Viewed by 1578

Special Issue Editors

Dr. Santosh Jadhav

E-Mail Website
Guest Editor
Department of Immunochemistry of Glycoconjugates, Institute of Chemistry, Slovak Academy of Sciences, 84510 Bratislava, Slovakia
Interests: Alzheimer's disease; tauopathies; synaptic impairment; macrophages; peripheral immune system; dendritic cells; aging
Dr. Ondrej Cehlár

E-Mail Website
Guest Editor
Institute of Neuroimmunology, Slovak Academy of Sciences, Dubravska Cesta 9, 84510 Bratislava, Slovakia
Interests: structural biology and biophysics of IDPs; protein-protein interactions; antibodies and immune system; molecular dynamics and docking

Special Issue Information

Dear Colleagues,

Neuroproteins, including key molecules such as Tau, α-synuclein and amyloid-β, play critical roles in both neural function and pathology. Dysregulation of these proteins is often a crucial factor in neurodegenerative conditions. New discoveries from fields such as transcriptomics, biological imaging and proteomics, among others, have enhanced our understanding. These advances show us the varied roles of neuroproteins in cellular signaling, immune responses, environmental factors, and potential treatments.

For this Special Issue, we invite contributions that expand our understanding of neuroproteins from a functional and/or pathological perspective. Topics of interest include, but are not limited to, the following:

  • Neuroprotein aggregation and pathogenesis;
  • Neuro–immune interactions;
  • Neuroproteins in neuropsychiatric conditions;
  • Experimental therapeutics targeting neuroproteins;
  • Biomarker discovery related to neuroproteins;
  • Environmental factors in neuroprotein function;
  • Calcium signaling related to neuroproteins;
  • Neuroprotein structure and function;
  • Post-translational modifications.

Dr. Santosh Jadhav
Dr. Ondrej Cehlár
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

  • neuroproteins
  • tau protein
  • α-synuclein
  • amyloid
  • biomarker discovery
  • brain function
  • neurodegeneration

Published Papers (1 paper)

Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

26 pages, 10128 KiB  
Article
Behavioral and Neuropathological Phenotyping of the Tau58/2 and Tau58/4 Transgenic Mouse Models for FTDP-17
by Debby Van Dam, Femke Valkenburg, Kristof Van Kolen, Isabel Pintelon, Jean-Pierre Timmermans and Peter Paul De Deyn
Life 2023, 13(10), 2088; https://doi.org/10.3390/life13102088 - 20 Oct 2023
Cited by 1 | Viewed by 1208
Abstract
Background: The Tau58/2 and Tau58/4 mouse lines expressing 0N4R tau with a P301S mutation mimic aspects of frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). In a side-by-side comparison, we report the age-dependent development of cognitive, motor, and behavioral deficits in comparison [...] Read more.
Background: The Tau58/2 and Tau58/4 mouse lines expressing 0N4R tau with a P301S mutation mimic aspects of frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). In a side-by-side comparison, we report the age-dependent development of cognitive, motor, and behavioral deficits in comparison with the spatial-temporal evolution of cellular tau pathology in both models. Methods: We applied the SHIRPA primary screen and specific neuromotor, behavioral, and cognitive paradigms. The spatiotemporal development of tau pathology was investigated immunohistochemically. Levels of sarkosyl-insoluble paired helical filaments were determined via a MesoScale Discovery biomarker assay. Results: Neuromotor impairments developed from age 3 months in both models. On electron microscopy, spinal cord neurofibrillary pathology was visible in mice aged 3 months; however, AT8 immunoreactivity was not yet observed in Tau58/4 mice. Behavioral abnormalities and memory deficits occurred at a later stage (>9 months) when tau pathology was fully disseminated throughout the brain. Spatiotemporally, tau pathology spread from the spinal cord via the midbrain to the frontal cortex, while the hippocampus was relatively spared, thus explaining the late onset of cognitive deficits. Conclusions: Our findings indicate the face and construct validity of both Tau58 models, which may provide new, valuable insights into the pathologic effects of tau species in vivo and may consequently facilitate the development of new therapeutic targets to delay or halt neurodegenerative processes occurring in tauopathies. Full article
(This article belongs to the Special Issue Advances in Neuroprotein Research: Functions, Pathologies and Treatments)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-1
Back to TopTop