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      Biomarkers for Alzheimer’s Disease Diagnosis

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          Abstract

          Objective:

          The dramatic increase in the population with dementia expected in the next decades is accompanied by the establishment of novel and innovated methods that will offer accurate and efficient detection of the disease in its early stages. While Alzheimer’s disease is the most common cause of dementia, by the time it is typically diagnosed, substantial neuronal loss and neuropathological lesions can damage many brain regions. The aim of this study is to investigate the main risk factors that affect and increase Alzheimer’s disease progression over time even in cases with no significant memory impairment present. Several potential markers are discussed such as oxidative stress, metal ions, vascular disorders, protein dysfunctions and alterations in the mitochondrial populations.

          Conclusion:

          A multiparametric model of Alzheimer’s biomarkers is presented according to the latest classification of the disease.

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          Most cited references42

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          Impaired balance of mitochondrial fission and fusion in Alzheimer's disease.

          Xinglong Wang, Bo Su, Hyoung-gon Lee … (2009)
          Mitochondrial dysfunction is a prominent feature of Alzheimer's disease (AD) neurons. In this study, we explored the involvement of an abnormal mitochondrial dynamics by investigating the changes in the expression of mitochondrial fission and fusion proteins in AD brain and the potential cause and consequence of these changes in neuronal cells. We found that mitochondria were redistributed away from axons in the pyramidal neurons of AD brain. Immunoblot analysis revealed that levels of DLP1 (also referred to as Drp1), OPA1, Mfn1, and Mfn2 were significantly reduced whereas levels of Fis1 were significantly increased in AD. Despite their differential effects on mitochondrial morphology, manipulations of these mitochondrial fission and fusion proteins in neuronal cells to mimic their expressional changes in AD caused a similar abnormal mitochondrial distribution pattern, such that mitochondrial density was reduced in the cell periphery of M17 cells or neuronal process of primary neurons and correlated with reduced spine density in the neurite. Interestingly, oligomeric amyloid-beta-derived diffusible ligands (ADDLs) caused mitochondrial fragmentation and reduced mitochondrial density in neuronal processes. More importantly, ADDL-induced synaptic change (i.e., loss of dendritic spine and postsynaptic density protein 95 puncta) correlated with abnormal mitochondrial distribution. DLP1 overexpression, likely through repopulation of neuronal processes with mitochondria, prevented ADDL-induced synaptic loss, suggesting that abnormal mitochondrial dynamics plays an important role in ADDL-induced synaptic abnormalities. Based on these findings, we suggest that an altered balance in mitochondrial fission and fusion is likely an important mechanism leading to mitochondrial and neuronal dysfunction in AD brain.
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            Tau protein isoforms, phosphorylation and role in neurodegenerative disorders.

            L Buée, T Bussière, V Buée-Scherrer … (2000)
            Tau proteins belong to the family of microtubule-associated proteins. They are mainly expressed in neurons where they play an important role in the assembly of tubulin monomers into microtubules to constitute the neuronal microtubules network. Microtubules are involved in maintaining the cell shape and serve as tracks for axonal transport. Tau proteins also establish some links between microtubules and other cytoskeletal elements or proteins. Tau proteins are translated from a single gene located on chromosome 17. Their expression is developmentally regulated by an alternative splicing mechanism and six different isoforms exist in the human adult brain. Tau proteins are the major constituents of intraneuronal and glial fibrillar lesions described in Alzheimer's disease and numerous neurodegenerative disorders referred to as 'tauopathies'. Molecular analysis has revealed that an abnormal phosphorylation might be one of the important events in the process leading to their aggregation. Moreover, a specific set of pathological tau proteins exhibiting a typical biochemical pattern, and a different regional and laminar distribution could characterize each of these disorders. Finally, a direct correlation has been established between the progressive involvement of the neocortical areas and the increasing severity of dementia, suggesting that pathological tau proteins are reliable marker of the neurodegenerative process. The recent discovery of tau gene mutations in frontotemporal dementia with parkinsonism linked to chromosome 17 has reinforced the predominant role attributed to tau proteins in the pathogenesis of neurodegenerative disorders, and underlined the fact that distinct sets of tau isoforms expressed in different neuronal populations could lead to different pathologies.
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              Mitochondrial abnormalities in Alzheimer's disease.

              H Fujioka, Farkhad G. Aliev, Robert Atwood … (2001)
              The finding that oxidative damage, including that to nucleic acids, in Alzheimer's disease is primarily limited to the cytoplasm of susceptible neuronal populations suggests that mitochondrial abnormalities might be part of the spectrum of chronic oxidative stress of Alzheimer's disease. In this study, we used in situ hybridization to mitochondrial DNA (mtDNA), immunocytochemistry of cytochrome oxidase, and morphometry of electron micrographs of biopsy specimens to determine whether there are mitochondrial abnormalities in Alzheimer's disease and their relationship to oxidative damage marked by 8-hydroxyguanosine and nitrotyrosine. We found that the same neurons showing increased oxidative damage in Alzheimer's disease have a striking and significant increase in mtDNA and cytochrome oxidase. Surprisingly, much of the mtDNA and cytochrome oxidase is found in the neuronal cytoplasm and in the case of mtDNA, the vacuoles associated with lipofuscin. Morphometric analysis showed that mitochondria are significantly reduced in Alzheimer's disease. The relationship shown here between the site and extent of mitochondrial abnormalities and oxidative damage suggests an intimate and early association between these features in Alzheimer's disease.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Curr Alzheimer Res
                Journal ID (iso-abbrev): Curr Alzheimer Res
                Journal ID (publisher-id): CAR
                Title: Current Alzheimer Research
                Publisher: Bentham Science Publishers
                ISSN (Print): 1567-2050
                ISSN (Electronic): 1875-5828
                Publication date (Print): November 2017
                Publication date (Electronic): November 2017
                Volume: 14
                Issue: 11
                Pages: 1149-1154
                Affiliations
                [1 ]Novel Global Community Educational Foundational, Australia;
                [2 ]Department of Computer Science and Biomedical Informatics, University of Thessaly , 35100, Lamia , Greece
                Author notes
                [* ]Address correspondence to this author at the Novel Global Community Educational Foundation, Australia; Tel:/Fax: +306987467249,, E-mail: alexiou@ 123456ngcef.net
                Article
                Publisher ID: CAR-14-1149
                DOI: 10.2174/1567205014666170203125942
                PMC ID: 5684784
                PubMed ID: 28164766
                SO-VID: 1af4dc9e-9bea-4d5d-9eea-47acdec136b3
                Copyright © © 2017 Bentham Science Publishers
                License:

                This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                Date received : 05 November 2016
                Date revision received : 07 December 2016
                Date accepted : 30 January 2017
                Categories
                Subject: Article

                ScienceOpen disciplines: Neurology
                Keywords: alzheimer’s disease biomarkers,oxidative stress,metal ions,vascular disorders,protein dysfunctions,mitochondrial dynamics,mild cognitive impairment
                Data availability:
                ScienceOpen disciplines: Neurology
                Keywords: alzheimer’s disease biomarkers, oxidative stress, metal ions, vascular disorders, protein dysfunctions, mitochondrial dynamics, mild cognitive impairment

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