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      Neurodegenerative Diseases: Regenerative Mechanisms and Novel Therapeutic Approaches

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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 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.

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          Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse.

          Dale Schenk, Robin Barbour, Whitney Dunn … (1999)
          Amyloid-beta peptide (Abeta) seems to have a central role in the neuropathology of Alzheimer's disease (AD). Familial forms of the disease have been linked to mutations in the amyloid precursor protein (APP) and the presenilin genes. Disease-linked mutations in these genes result in increased production of the 42-amino-acid form of the peptide (Abeta42), which is the predominant form found in the amyloid plaques of Alzheimer's disease. The PDAPP transgenic mouse, which overexpresses mutant human APP (in which the amino acid at position 717 is phenylalanine instead of the normal valine), progressively develops many of the neuropathological hallmarks of Alzheimer's disease in an age- and brain-region-dependent manner. In the present study, transgenic animals were immunized with Abeta42, either before the onset of AD-type neuropathologies (at 6 weeks of age) or at an older age (11 months), when amyloid-beta deposition and several of the subsequent neuropathological changes were well established. We report that immunization of the young animals essentially prevented the development of beta-amyloid-plaque formation, neuritic dystrophy and astrogliosis. Treatment of the older animals also markedly reduced the extent and progression of these AD-like neuropathologies. Our results raise the possibility that immunization with amyloid-beta may be effective in preventing and treating Alzheimer's disease.
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            The relation between inflammation and neurodegeneration in multiple sclerosis brains

            Josa M. Frischer, Stephan Bramow, Assunta Dal-Bianco … (2009)
            Some recent studies suggest that in progressive multiple sclerosis, neurodegeneration may occur independently from inflammation. The aim of our study was to analyse the interdependence of inflammation, neurodegeneration and disease progression in various multiple sclerosis stages in relation to lesional activity and clinical course, with a particular focus on progressive multiple sclerosis. The study is based on detailed quantification of different inflammatory cells in relation to axonal injury in 67 multiple sclerosis autopsies from different disease stages and 28 controls without neurological disease or brain lesions. We found that pronounced inflammation in the brain is not only present in acute and relapsing multiple sclerosis but also in the secondary and primary progressive disease. T- and B-cell infiltrates correlated with the activity of demyelinating lesions, while plasma cell infiltrates were most pronounced in patients with secondary progressive multiple sclerosis (SPMS) and primary progressive multiple sclerosis (PPMS) and even persisted, when T- and B-cell infiltrates declined to levels seen in age matched controls. A highly significant association between inflammation and axonal injury was seen in the global multiple sclerosis population as well as in progressive multiple sclerosis alone. In older patients (median 76 years) with long-disease duration (median 372 months), inflammatory infiltrates declined to levels similar to those found in age-matched controls and the extent of axonal injury, too, was comparable with that in age-matched controls. Ongoing neurodegeneration in these patients, which exceeded the extent found in normal controls, could be attributed to confounding pathologies such as Alzheimer's or vascular disease. Our study suggests a close association between inflammation and neurodegeneration in all lesions and disease stages of multiple sclerosis. It further indicates that the disease processes of multiple sclerosis may die out in aged patients with long-standing disease.
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              Trial of Solanezumab for Mild Dementia Due to Alzheimer’s Disease

              Lawrence S. Honig, Bruno Vellas, Michael Woodward … (2018)
              Alzheimer's disease is characterized by amyloid-beta (Aβ) plaques and neurofibrillary tangles. The humanized monoclonal antibody solanezumab was designed to increase the clearance from the brain of soluble Aβ, peptides that may lead to toxic effects in the synapses and precede the deposition of fibrillary amyloid.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Brain Sci
                Journal ID (iso-abbrev): Brain Sci
                Journal ID (publisher-id): brainsci
                Title: Brain Sciences
                Publisher: MDPI
                ISSN (Electronic): 2076-3425
                Publication date (Electronic): 15 September 2018
                Publication date Collection: September 2018
                Volume: 8
                Issue: 9
                Electronic Location Identifier: 177
                Affiliations
                [1 ]Center for Translational Neuromedicine, University of Rochester, NY 14642, USA; spursel2@ 123456u.rochester.edu
                [2 ]Department of Animal Sciences, Quaid-i-Azam University, Islamabad 45320, Pakistan; hirazubair6@ 123456gmail.com
                Author notes
                [* ]Correspondence: rashad_hussain@ 123456urmc.rochester.edu (R.H.); shahab@ 123456qau.edu.pk (M.S.); Tel.: +1-585-276-6390 (R.H.); +92-51-9064-3014 (M.S.)
                Article
                Publisher ID: brainsci-08-00177
                DOI: 10.3390/brainsci8090177
                PMC ID: 6162719
                PubMed ID: 30223579
                SO-VID: 2a8e330e-6c71-4a19-aff6-99caf14d0dae
                Copyright © © 2018 by the author.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 13 July 2018
                Date accepted : 12 September 2018
                Categories
                Subject: Review

                Keywords: neuroregeneration,mechanisms,therapeutics,neurogenesis,intra-cellular signaling
                Data availability:
                Keywords: neuroregeneration, mechanisms, therapeutics, neurogenesis, intra-cellular signaling

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