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Neurodegenerative Diseases: From Molecular Basis to Therapy 2.0

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Dear Colleagues,

Neurodegenerative diseases (NDs) are a heterogeneous group of complex diseases characterized by neuronal loss and the progressive degeneration of different areas of the nervous system. NDs represent a major health problem worldwide, with an increasing incidence rate. Although the exact pathogenesis of NDs remains unclear, a complex interaction between genetic, epigenetic and environmental factors has been proposed. To date, no effective therapeutics have been developed to slow down, halt or prevent any NDs. Therefore, information on the molecular mechanisms underlying the pathogenesis of NDs is strongly sought after.

The aim of the current Special Issue is to describe the advances in the field of NDs, including Alzheimer’s disease, multiple sclerosis, amyotrophic lateral sclerosis and Parkinson’s disease, with a focus on their underlying pathobiological mechanisms.

We would like to invite you to submit original research articles and reviews that focus on, but are not limited to, new findings on molecular key players, pathomechanisms, risk factors, biomarkers and therapeutic targets of NDs.

Dr. Luisa Agnello
Prof. Dr. Marcello Ciaccio
Guest Editors

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Keywords

genetic
biomarkers
Alzheimer’s disease
multiple sclerosis
amyotrophic lateral sclerosis
neurodegenerative diseases

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23 pages, 4128 KiB

Open AccessArticle

PDIA3 Expression Is Altered in the Limbic Brain Regions of Triple-Transgenic Mouse Model of Alzheimer’s Disease

by Tommaso Cassano, Flavia Giamogante, Silvio Calcagnini, Adele Romano, Angelo Michele Lavecchia, Francesca Inglese, Giuliano Paglia, Vidyasagar Naik Bukke, Antonino Davide Romano, Marzia Friuli, Fabio Altieri and Silvana Gaetani

Int. J. Mol. Sci. 2023, 24(3), 3005; https://doi.org/10.3390/ijms24033005 - 03 Feb 2023

Cited by 6 | Viewed by 1915

Abstract

In the present study, we used a mouse model of Alzheimer’s disease (AD) (3×Tg-AD mice) to longitudinally analyse the expression level of PDIA3, a protein disulfide isomerase and endoplasmic reticulum (ER) chaperone, in selected brain limbic areas strongly affected by AD-pathology (amygdala, entorhinal cortex, dorsal and ventral hippocampus). Our results suggest that, while in Non-Tg mice PDIA3 levels gradually reduce with aging in all brain regions analyzed, 3×Tg-AD mice showed an age-dependent increase in PDIA3 levels in the amygdala, entorhinal cortex, and ventral hippocampus. A significant reduction of PDIA3 was observed in 3×Tg-AD mice already at 6 months of age, as compared to age-matched Non-Tg mice. A comparative immunohistochemistry analysis performed on 3×Tg-AD mice at 6 (mild AD-like pathology) and 18 (severe AD-like pathology) months of age showed a direct correlation between the cellular level of Aβ and PDIA3 proteins in all the brain regions analysed, even if with different magnitudes. Additionally, an immunohistochemistry analysis showed the presence of PDIA3 in all post-mitotic neurons and astrocytes. Overall, altered PDIA3 levels appear to be age- and/or pathology-dependent, corroborating the ER chaperone’s involvement in AD pathology, and supporting the PDIA3 protein as a potential novel therapeutic target for the treatment of AD. Full article

(This article belongs to the Special Issue Neurodegenerative Diseases: From Molecular Basis to Therapy 2.0)

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16 pages, 1527 KiB

Open AccessArticle

by Tommaso Piccoli, Valeria Blandino, Laura Maniscalco, Domenica Matranga, Fabiola Graziano, Fabrizio Guajana, Luisa Agnello, Bruna Lo Sasso, Caterina Maria Gambino, Rosaria Vincenza Giglio, Vincenzo La Bella, Marcello Ciaccio and Tiziana Colletti

Int. J. Mol. Sci. 2022, 23(18), 10831; https://doi.org/10.3390/ijms231810831 - 16 Sep 2022

Cited by 1 | Viewed by 1608

Abstract

Recently, the synaptic proteins neurogranin (Ng) and α-synuclein (α-Syn) have attracted scientific interest as potential biomarkers for synaptic dysfunction in neurodegenerative diseases. In this study, we measured the CSF Ng and α-Syn concentrations in patients affected by AD (n = 69), non-AD neurodegenerative disorders (n-AD = 50) and non-degenerative disorders (n-ND, n = 98). The concentrations of CSF Ng and α-Syn were significantly higher in AD than in n-AD and n-ND. Moreover, the Aβ42/Ng and Aβ42/α-Syn ratios showed statistically significant differences between groups and discriminated AD patients from n-AD patients, better than Ng or α-Syn alone. Regression analyses showed an association of higher Ng concentrations with MMSE < 24, pathological Aβ 42/40 ratios, pTau, tTau and the ApoEε4 genotype. Aβ 42/Ng was associated with MMSE < 24, an AD-related FDG-PET pattern, the ApoEε4 genotype, pathological Aβ 42 levels and Aβ 42/40 ratios, pTau, and tTau. Moreover, APO-Eε4 carriers showed higher Ng concentrations than non-carriers. Our results support the idea that the Aβ 42/Ng ratio is a reliable index of synaptic dysfunction/degeneration able to discriminate AD from other neurological conditions. Full article

(This article belongs to the Special Issue Neurodegenerative Diseases: From Molecular Basis to Therapy 2.0)

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