Neurodegeneration in Cognitive Impairment and Mood Disorders for Experimental, Clinical, and Translational Neuropsychiatry—Second Edition

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

Deadline for manuscript submissions: 31 December 2024 | Viewed by 9759

Special Issue Editors


E-Mail Website1 Website2
Guest Editor
1. Department of Psychology, University of Turin, Turin, Italy
2. Center for Studies and Research in Cognitive Neuroscience, Department of Psychology, University of Bologna, Bologna, Italy
Interests: NIBS techniques; TMS; skin conductance; heart rate variability; fear conditioning; fear learning; learning; neuropsychology; prefrontal cortex; amygdala; hippocampus; anxiety; depression; working memory; PTSD; skin conductance responses; psychophysiology; error-related negativity; EEG; tDCS; Alzheimer’s disease; PIT; stress-related disorders; Parkinson’s disease; resilience; memory; neurologic patients; cognitive decisions; fMRI; translational and molecular psychiatry
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Guest Editor
Danube Neuroscience Research Laboratory, HUN-REN-SZTE Neuroscience Research Group, Hungarian Research Network, University of Szeged (HUN-REN-SZTE), Tisza Lajos krt. 113, H-6725 Szeged, Hungary
Interests: depression; anxiety; dementia pain; their comorbidities nature; translational research in neurological diseases and psychiatric disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegeneration is the progressive atrophy and subsequent functional loss of neurons responsible for the pathogenesis of neurodegenerative diseases and psychiatric disorders. This degenerative change of neurons may take place on molecular, cellular, histological, functional, and organizational levels; may initiate in the prodromal stage during the early gestational period in neurodevelopmental disorders; and may progress to the progression and exacerbation of neuropsychiatric symptoms in mental illnesses. It is particularly important to understand degenerative changes in the neural correlates of consciousness and pay attention to the cognitive and emotional domains in the development of neuropsychiatric disorders. Thus, probing neurodegenerative changes is of great importance for susceptibility detection, understanding pathogenesis and progression, and discovering novel therapeutic targets. Moreover, many branches of neuroscience can help us understand the underlying biological factors and neural computations behind brain impairments, neurodegeneration, and psychiatric disorders, as well as determine where and how to focus on research and treatment. Currently, most neurodegenerative diseases lack effective disease-modifying treatments, highlighting the urgent need for new and effective therapeutic strategies. In recent years, noninvasive brain stimulation (NIBS) techniques, such as transcranial magnetic stimulation (TMS) and transcranial electric current stimulation (TES), have been developed for both diagnostic and therapeutic purposes in patients with neurodegenerative disorders. These techniques have been shown to have meaningful cognitive outcomes in various neurodegenerative diseases, and their mechanistic approach aims to modulate local and spread-out effects via structural connectivity to rebalance the abnormal activity levels between different brain regions. Importantly, NIBS has been linked to the induction of neuroplasticity, which refers to the ability of the brain to reorganize by forming new neural connections throughout life. By stimulating the brain and promoting the formation of new neural connections, NIBS may help improve the symptoms and functional outcomes in conditions such as neurodegenerative diseases.

This Special Issue highlights the most recent advances in experimental, clinical, and translational research in the field of neuropsychiatry, focusing on neurodegeneration and neural correlates of the development of cognitive impairment and psychiatric emotional disturbance. We invite authors to contribute comprehensive review and original research articles focusing on (but not limited to) the following:

  • Etiology, pathogenesis, and mechanisms of progression;
  • Early diagnosis, including biomarkers, bioimaging, and biosensors;
  • Prophylactic, disease-modifying, and therapeutic strategies and novel targets;
  • Novel drug discovery and development, naturally driven biomedicines, natural bioactive molecules, and vaccines;
  • Preclinical in vitro and animal models;
  • Bench-to-bedside translational research;
  • Bedside-to-bench translational research;
  • Noninvasive brain stimulation (NIBS) to diagnosis and treatment of neurodegenerative and psychiatric disorders.

Dr. Simone Battaglia
Dr. Masaru Tanaka
Guest Editors

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Keywords

  • Alzheimer’s disease
  • Parkinson’s disease
  • aging decline
  • mild cognitive impairment
  • multiple sclerosis
  • stroke
  • psychiatric disorders
  • depressive disorder
  • bipolar disorder
  • post-traumatic stress disorder
  • anxiety disorder
  • schizophrenia
  • somatic symptom disorder
  • autism spectrum disorder
  • hyperactive attention deficit disorder
  • learning disabilities
  • acquired brain damage
  • altered cognitive processes
  • brain functional impairment
  • neurocognitive disorders
  • cognitive, behavioral, and functional disorders
  • acquired trauma
  • brain plasticity and connectivity
  • non-invasive brain stimulation
  • diagnosis and treatment
  • functional evidence of altered cognition and connectivity

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Related Special Issue

Published Papers (5 papers)

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Research

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12 pages, 648 KiB  
Article
Exploring Cognitive Impairments Associated with Primary Open-Angle Glaucoma and Exfoliation Glaucoma
by Yoichi Kadoh, Suguru Kubota, Soichiro Shimomine and Masaki Tanito
Biomedicines 2024, 12(8), 1706; https://doi.org/10.3390/biomedicines12081706 - 1 Aug 2024
Cited by 1 | Viewed by 890
Abstract
This study explored the link between different types of glaucoma and cognitive function in a cohort of 620 Japanese patients. Participants were categorized into primary open-angle glaucoma (PG), exfoliation glaucoma (EG), and non-glaucomatous control groups. The findings revealed a significant decline in cognitive [...] Read more.
This study explored the link between different types of glaucoma and cognitive function in a cohort of 620 Japanese patients. Participants were categorized into primary open-angle glaucoma (PG), exfoliation glaucoma (EG), and non-glaucomatous control groups. The findings revealed a significant decline in cognitive function as indicated by the Mini-Cog test in the EG group (mean ± SD: 4.0 ± 1, 95% CI: 3.9 to 4.2) compared to the PG group (4.4 ± 0.1, 4.3 to 4.5, p < 0.0001). Levels of fingertip measured advanced glycation end-products (AGEs) were significantly higher in the EG group (mean ± SD: 0.45 ± 0.006, 95% CI: 0.44 to 0.46) compared to the PG group (0.43 ± 0.004, 0.42 to 0.44, p = 0.0014). Although the multivariate analysis initially showed no direct association between glaucoma types and Mini-Cog scores, the EG group exhibited higher age and intraocular pressure (IOP) compared to the PG group. Further analysis revealed that high levels of AGEs were associated with cognitive decline and decreased mean visual fields in the EG group. Age was identified as a cofounding factor in these associations. An inverse correlation was observed between the accumulation of AGEs and skin carotenoid levels. Early detection of cognitive decline in glaucoma patients could enable timely intervention to preserve visual fields. Fingertip measurements of skin carotenoids and AGEs offer promising potential as non-invasive, straightforward diagnostic tools that could be widely adopted for monitoring ophthalmic and cognitive health in glaucoma patients. Full article
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15 pages, 319 KiB  
Article
Platelet Levels of Brain-Derived Neurotrophic Factor in Adults with Autism Spectrum Disorder: Is There a Specific Association with Autism Spectrum Psychopathology?
by Barbara Carpita, Benedetta Nardi, Chiara Bonelli, Lavinia Pascariello, Gabriele Massimetti, Ivan Mirko Cremone, Stefano Pini, Lionella Palego, Laura Betti, Gino Giannaccini and Liliana Dell’Osso
Biomedicines 2024, 12(7), 1529; https://doi.org/10.3390/biomedicines12071529 - 10 Jul 2024
Viewed by 994
Abstract
To date, although several studies have investigated the circulating levels of brain-derived neurotrophic factor (BDNF) in children with autism spectrum disorder (ASD), only a few authors have addressed their evaluation in adults. Furthermore, an important limitation of these studies lies in the fact [...] Read more.
To date, although several studies have investigated the circulating levels of brain-derived neurotrophic factor (BDNF) in children with autism spectrum disorder (ASD), only a few authors have addressed their evaluation in adults. Furthermore, an important limitation of these studies lies in the fact that circulating BDNF is stored in platelets and released into the circulation when needed. To the best of our knowledge, a very limited number of studies have related peripheral BDNF values to platelet counts, and yet no study has evaluated intra-platelet BDNF levels in adults with ASD. In this framework, the aim of the present work is to pave the way in this field and evaluate platelet BNDF levels in adult ASD patients, as well as their correlation with autistic symptoms and related psychopathological dimensions. We recruited 22 ASD and 22 healthy controls, evaluated with the Adult autism subthreshold spectrum (AdAS Spectrum), the Social Anxiety Spectrum—self report (SHY-SR), the Trauma and loss spectrum—self report (TALS-SR), the Work and Social Adjustment Scale (WSAS), and the Mood Spectrum—self report for suicidality. Intra-platelet BDNF levels were also assessed. The results highlighted lower BDNF levels in the ASD group; moreover, AdAS Spectrum and WSAS total score as well as AdAS Spectrum Restricted interest and rumination, WSAS Private leisure activities, TALS-SR Arousal, and SHY-SR Childhood domains were significant negative predictors of platelet BDNF levels. Full article

Review

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37 pages, 2898 KiB  
Review
Vascular Impairment, Muscle Atrophy, and Cognitive Decline: Critical Age-Related Conditions
by Enzo Pereira de Lima, Masaru Tanaka, Caroline Barbalho Lamas, Karina Quesada, Claudia Rucco P. Detregiachi, Adriano Cressoni Araújo, Elen Landgraf Guiguer, Virgínia Maria Cavallari Strozze Catharin, Marcela Vialogo Marques de Castro, Edgar Baldi Junior, Marcelo Dib Bechara, Bruna Fidencio Rahal Ferraz, Vitor Cavallari Strozze Catharin, Lucas Fornari Laurindo and Sandra Maria Barbalho
Biomedicines 2024, 12(9), 2096; https://doi.org/10.3390/biomedicines12092096 - 13 Sep 2024
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Abstract
The triad of vascular impairment, muscle atrophy, and cognitive decline represents critical age-related conditions that significantly impact health. Vascular impairment disrupts blood flow, precipitating the muscle mass reduction seen in sarcopenia and the decline in neuronal function characteristic of neurodegeneration. Our limited understanding [...] Read more.
The triad of vascular impairment, muscle atrophy, and cognitive decline represents critical age-related conditions that significantly impact health. Vascular impairment disrupts blood flow, precipitating the muscle mass reduction seen in sarcopenia and the decline in neuronal function characteristic of neurodegeneration. Our limited understanding of the intricate relationships within this triad hinders accurate diagnosis and effective treatment strategies. This review analyzes the interrelated mechanisms that contribute to these conditions, with a specific focus on oxidative stress, chronic inflammation, and impaired nutrient delivery. The aim is to understand the common pathways involved and to suggest comprehensive therapeutic approaches. Vascular dysfunctions hinder the circulation of blood and the transportation of nutrients, resulting in sarcopenia characterized by muscle atrophy and weakness. Vascular dysfunction and sarcopenia have a negative impact on physical function and quality of life. Neurodegenerative diseases exhibit comparable pathophysiological mechanisms that affect cognitive and motor functions. Preventive and therapeutic approaches encompass lifestyle adjustments, addressing oxidative stress, inflammation, and integrated therapies that focus on improving vascular and muscular well-being. Better understanding of these links can refine therapeutic strategies and yield better patient outcomes. This study emphasizes the complex interplay between vascular dysfunction, muscle degeneration, and cognitive decline, highlighting the necessity for multidisciplinary treatment approaches. Advances in this domain promise improved diagnostic accuracy, more effective therapeutic options, and enhanced preventive measures, all contributing to a higher quality of life for the elderly population. Full article
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16 pages, 1156 KiB  
Review
P-tau217 as a Reliable Blood-Based Marker of Alzheimer’s Disease
by Roy Lai, Brenden Li and Ram Bishnoi
Biomedicines 2024, 12(8), 1836; https://doi.org/10.3390/biomedicines12081836 - 13 Aug 2024
Viewed by 2393
Abstract
Amyloid plaques and tau tangles are the hallmark pathologic features of Alzheimer’s disease (AD). Traditionally, these changes are identified in vivo via cerebrospinal fluid (CSF) analysis or positron emission tomography (PET) scans. However, these methods are invasive, expensive, and resource-intensive. To address these [...] Read more.
Amyloid plaques and tau tangles are the hallmark pathologic features of Alzheimer’s disease (AD). Traditionally, these changes are identified in vivo via cerebrospinal fluid (CSF) analysis or positron emission tomography (PET) scans. However, these methods are invasive, expensive, and resource-intensive. To address these limitations, there has been ongoing research over the past decade to identify blood-based markers for AD. Despite the challenges posed by their extremely low concentrations, recent advances in mass spectrometry and immunoassay techniques have made it feasible to detect these blood markers of amyloid and tau deposition. Phosphorylated tau (p-tau) has shown greater promise in reflecting amyloid pathology as evidenced by CSF and PET positivity. Various isoforms of p-tau, distinguished by their differential phosphorylation sites, have been recognized for their ability to identify amyloid-positive individuals. Notable examples include p-tau181, p-tau217, and p-tau235. Among these, p-tau217 has emerged as a superior and reliable marker of amyloid positivity and, thus, AD in terms of accuracy of diagnosis and ability for early prognosis. In this narrative review, we aim to elucidate the utility of p-tau217 as an AD marker, exploring its underlying basis, clinical diagnostic potential, and relevance in clinical care and trials. Full article
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19 pages, 772 KiB  
Review
Molecular Changes in the Ischemic Brain as Non-Invasive Brain Stimulation Targets—TMS and tDCS Mechanisms, Therapeutic Challenges, and Combination Therapies
by Aleksandra Markowska and Beata Tarnacka
Biomedicines 2024, 12(7), 1560; https://doi.org/10.3390/biomedicines12071560 - 13 Jul 2024
Viewed by 1367
Abstract
Ischemic stroke is one of the leading causes of death and disability. As the currently used neurorehabilitation methods present several limitations, the ongoing research focuses on the use of non-invasive brain stimulation (NIBS) techniques such as transcranial magnetic stimulation (TMS) and transcranial direct [...] Read more.
Ischemic stroke is one of the leading causes of death and disability. As the currently used neurorehabilitation methods present several limitations, the ongoing research focuses on the use of non-invasive brain stimulation (NIBS) techniques such as transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS). NIBS methods were demonstrated to modulate neural excitability and improve motor and cognitive functioning in neurodegenerative diseases. However, their mechanisms of action are not fully elucidated, and the clinical outcomes are often unpredictable. This review explores the molecular processes underlying the effects of TMS and tDCS in stroke rehabilitation, including oxidative stress reduction, cell death, stimulation of neurogenesis, and neuroprotective phenotypes of glial cells. A highlight is put on the newly emerging therapeutic targets, such as ferroptotic and pyroptotic pathways. In addition, the issue of interindividual variability is discussed, and the role of neuroimaging techniques is investigated to get closer to personalized medicine. Furthermore, translational challenges of NIBS techniques are analyzed, and limitations of current clinical trials are investigated. The paper concludes with suggestions for further neurorehabilitation stroke treatment, putting the focus on combination and personalized therapies, as well as novel protocols of brain stimulation techniques. Full article
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