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 2046

Special Issue Editors


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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

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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

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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 (2 papers)

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Research

20 pages, 2268 KiB  
Article
A Clinical Study of Urine Amino Acids in Children with Autism Spectrum Disorder
by Cătălina Mihaela Anastasescu, Veronica Gheorman, Florica Popescu, Mioara Desdemona Stepan, Eugen Cristi Stoicănescu, Victor Gheorman and Ion Udriștoiu
Life 2024, 14(5), 629; https://doi.org/10.3390/life14050629 - 15 May 2024
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Abstract
Amino acids are organic compounds that enter the protein structure, being involved in the proper functioning of the body. The role of amino acids in the onset of autism spectrum disorder (ASD) is yet to be established. Our aim was to identify correlations [...] Read more.
Amino acids are organic compounds that enter the protein structure, being involved in the proper functioning of the body. The role of amino acids in the onset of autism spectrum disorder (ASD) is yet to be established. Our aim was to identify correlations between urine amino acids and their derivatives and ASD. Methods: We designed a case–control study that consisted of 75 boys and girls, aged between 2 and 12 years. For amino acid profile, we used urine samples that were analyzed using liquid chromatography–tandem mass spectrometry (LC-MS/MS). Results: Descriptive analysis showed higher values for glutamine, hydroxyproline, tyrosine, aspartic acid, and tryptophan and lower values for serine in the autism group than in the control group. Also, we found that boys with autism had higher values than the boys in the control group for serine, threonine, and aspartic acid. For girls from both groups, we did not find statistically significant values. In terms of age groups, we found significantly higher values for histidine, threonine, valine, methionine, aspartic acid, glutamic acid, alpha amino-adipic acid, sarcosine, alanine, and beta-alanine and significantly lower values for proline for both the autism and control groups under 5 years. Conclusions: The findings of this study support the assumption that amino acids may have a role in the expression of ASD. Full article
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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 1312
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
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