Special Issue "Pathogenesis and Treatment of Neurodegenerative Diseases"

A special issue of Brain Sciences (ISSN 2076-3425).

Deadline for manuscript submissions: 20 October 2018

Special Issue Editor

Guest Editor
Assoc. Prof. Dr. Basavaraj S. Balapal

Department of Psychiatry, New York University Langone Medical Center, New York City, New York, USA
Faculty at Columbia University Medical Center, Scientist, Division of Analytical Psychopharmacology, Nathan Kline Institute for Psychiatric Research, Orangeburg, New York, USA
Website | E-Mail
Interests: cannabinoid receptors; synaptic plasticity; learning and memory; developmental disorders; neurodegeneration; drugs of abuse and psychiatric disorders

Special Issue Information

Dear Colleagues,

Increasing evidence suggests that brain disorders are becoming the most dangerous public health problems in modern society. More than 600 disorders affect the nervous system. Irrespective of genetic (familial) or environmental (sporadic) cause, many of these disorders become more progressive with age, including Alzheimer’s disease (AD), Parkinson’s disease (PD), stroke, amyotrophic lateral sclerosis (ALS), and many other intellectual disabilities. Most of these disorders are often accompanying atrophy in the structure and function of the central or peripheral nervous systems. Moreover, accumulating evidence also suggests that late-onset neurological disorders might be due to aberrant neural maturation with epigenetic and pathological changes that are set up at early stages of brain maturation, before the appearance of disease symptoms. Thus, evaluating epigenetic, proteins and pathways that are important in neurodegeneration in the developing, as well as adult, brain, together with the characterization of mechanisms necessary during brain development with relevance to brain aging, are of critical importance. The economic and human costs of these neurodegenerative diseases are expected to increase as the population ages. Understanding the underlying brain mechanisms that are affected by these diseases would help to develop potential therapeutic interventions and will form the basis for novel therapeutic treatments for these neurodegenerative disorders.

The current Special Issue is intended to collect a selected number of articles that establish deeper insight in these topics, which bring both broad scientific and public health impact.

Dr. Balapal S. Basavarajappa
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 papers will be 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. Brain Sciences 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 650 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 disorders
  • drugs of abuse
  • alcohol
  • environmental toxicants
  • epigenetics
  • cognitive deficits
  • learning and memory
  • neurodegenerative disorders
  • molecular mechanisms
  • early brain development
  • synaptic plasticity
  • intellectual disability

Published Papers (4 papers)

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Research

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Open AccessArticle Disturbed Glucose Metabolism in Rat Neurons Exposed to Cerebrospinal Fluid Obtained from Multiple Sclerosis Subjects
Brain Sci. 2018, 8(1), 1; https://doi.org/10.3390/brainsci8010001
Received: 14 August 2017 / Revised: 13 December 2017 / Accepted: 15 December 2017 / Published: 21 December 2017
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Abstract
Axonal damage is widely accepted as a major cause of permanent functional disability in Multiple Sclerosis (MS). In relapsing-remitting MS, there is a possibility of remyelination by myelin producing cells and restoration of neurological function. The purpose of this study was to delineate
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Axonal damage is widely accepted as a major cause of permanent functional disability in Multiple Sclerosis (MS). In relapsing-remitting MS, there is a possibility of remyelination by myelin producing cells and restoration of neurological function. The purpose of this study was to delineate the pathophysiological mechanisms underpinning axonal injury through hitherto unknown factors present in cerebrospinal fluid (CSF) that may regulate axonal damage, remyelinate the axon and make functional recovery possible. We employed primary cultures of rat unmyelinated cerebellar granule neurons and treated them with CSF obtained from MS and Neuromyelitis optica (NMO) patients. We performed microarray gene expression profiling to study changes in gene expression in treated neurons as compared to controls. Additionally, we determined the influence of gene-gene interaction upon the whole metabolic network in our experimental conditions using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) program. Our findings revealed the downregulated expression of genes involved in glucose metabolism in MS-derived CSF-treated neurons and upregulated expression of genes in NMO-derived CSF-treated neurons. We conclude that factors in the CSF of these patients caused a perturbation in metabolic gene(s) expression and suggest that MS appears to be linked with metabolic deformity. Full article
(This article belongs to the Special Issue Pathogenesis and Treatment of Neurodegenerative Diseases)
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Open AccessArticle Alzheimer’s Disease Early Diagnosis Using Manifold-Based Semi-Supervised Learning
Brain Sci. 2017, 7(8), 109; https://doi.org/10.3390/brainsci7080109
Received: 18 July 2017 / Revised: 15 August 2017 / Accepted: 16 August 2017 / Published: 20 August 2017
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Abstract
Alzheimer’s disease (AD) is currently ranked as the sixth leading cause of death in the United States and recent estimates indicate that the disorder may rank third, just behind heart disease and cancer, as a cause of death for older people. Clearly, predicting
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Alzheimer’s disease (AD) is currently ranked as the sixth leading cause of death in the United States and recent estimates indicate that the disorder may rank third, just behind heart disease and cancer, as a cause of death for older people. Clearly, predicting this disease in the early stages and preventing it from progressing is of great importance. The diagnosis of Alzheimer’s disease (AD) requires a variety of medical tests, which leads to huge amounts of multivariate heterogeneous data. It can be difficult and exhausting to manually compare, visualize, and analyze this data due to the heterogeneous nature of medical tests; therefore, an efficient approach for accurate prediction of the condition of the brain through the classification of magnetic resonance imaging (MRI) images is greatly beneficial and yet very challenging. In this paper, a novel approach is proposed for the diagnosis of very early stages of AD through an efficient classification of brain MRI images, which uses label propagation in a manifold-based semi-supervised learning framework. We first apply voxel morphometry analysis to extract some of the most critical AD-related features of brain images from the original MRI volumes and also gray matter (GM) segmentation volumes. The features must capture the most discriminative properties that vary between a healthy and Alzheimer-affected brain. Next, we perform a principal component analysis (PCA)-based dimension reduction on the extracted features for faster yet sufficiently accurate analysis. To make the best use of the captured features, we present a hybrid manifold learning framework which embeds the feature vectors in a subspace. Next, using a small set of labeled training data, we apply a label propagation method in the created manifold space to predict the labels of the remaining images and classify them in the two groups of mild Alzheimer’s and normal condition (MCI/NC). The accuracy of the classification using the proposed method is 93.86% for the Open Access Series of Imaging Studies (OASIS) database of MRI brain images, providing, compared to the best existing methods, a 3% lower error rate. Full article
(This article belongs to the Special Issue Pathogenesis and Treatment of Neurodegenerative Diseases)
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Review

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Open AccessReview Neurodegenerative Diseases: Regenerative Mechanisms and Novel Therapeutic Approaches
Brain Sci. 2018, 8(9), 177; https://doi.org/10.3390/brainsci8090177
Received: 13 July 2018 / Revised: 3 September 2018 / Accepted: 12 September 2018 / Published: 15 September 2018
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Abstract
Regeneration refers to regrowth of tissue in the central nervous system. It includes generation of new neurons, glia, myelin, and synapses, as well as the regaining of essential functions: sensory, motor, emotional and cognitive abilities. Unfortunately, regeneration within the nervous system is very
[...] Read more.
Regeneration refers to regrowth of tissue in the central nervous system. It includes generation of new neurons, glia, myelin, and synapses, as well as the regaining of essential functions: sensory, motor, emotional and cognitive abilities. Unfortunately, regeneration within the nervous system is very slow compared to other body systems. This relative slowness is attributed to increased vulnerability to irreversible cellular insults and the loss of function due to the very long lifespan of neurons, the stretch of cells and cytoplasm over several dozens of inches throughout the body, insufficiency of the tissue-level waste removal system, and minimal neural cell proliferation/self-renewal capacity. In this context, the current review summarized the most common features of major neurodegenerative disorders; their causes and consequences and proposed novel therapeutic approaches. Full article
(This article belongs to the Special Issue Pathogenesis and Treatment of Neurodegenerative Diseases)
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Other

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Open AccessConcept Paper Clearing Extracellular Alpha-Synuclein from Cerebrospinal Fluid: A New Therapeutic Strategy in Parkinson’s Disease
Brain Sci. 2018, 8(4), 52; https://doi.org/10.3390/brainsci8040052
Received: 24 February 2018 / Revised: 17 March 2018 / Accepted: 22 March 2018 / Published: 23 March 2018
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Abstract
This concept article aims to show the rationale of targeting extracellular α-Synuclein (α-Syn) from cerebrospinal fluid (CSF) as a new strategy to remove this protein from the brain in Parkinson’s disease (PD). Misfolding and intracellular aggregation of α-synuclein into Lewy bodies are thought
[...] Read more.
This concept article aims to show the rationale of targeting extracellular α-Synuclein (α-Syn) from cerebrospinal fluid (CSF) as a new strategy to remove this protein from the brain in Parkinson’s disease (PD). Misfolding and intracellular aggregation of α-synuclein into Lewy bodies are thought to be crucial in the pathogenesis of PD. Recent research has shown that small amounts of monomeric and oligomeric α-synuclein are released from neuronal cells by exocytosis and that this extracellular alpha-synuclein contributes to neurodegeneration, progressive spreading of alpha-synuclein pathology, and neuroinflammation. In PD, extracellular oligomeric-α-synuclein moves in constant equilibrium between the interstitial fluid (ISF) and the CSF. Thus, we expect that continuous depletion of oligomeric-α-synuclein in the CSF will produce a steady clearance of the protein in the ISF, preventing transmission and deposition in the brain. Full article
(This article belongs to the Special Issue Pathogenesis and Treatment of Neurodegenerative Diseases)
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