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      Current understanding of Alzheimer’s disease diagnosis and treatment

      review-article
      Author(s): a , 1 , 2 , 1 , 2
      Publication date (Electronic):
      Journal: F1000Research
      Publisher: F1000 Research Limited
      Keywords: Alzheimer's disease, dementia, amyloid, tau

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          Abstract

          Alzheimer’s disease is the most common cause of dementia worldwide, with the prevalence continuing to grow in part because of the aging world population. This neurodegenerative disease process is characterized classically by two hallmark pathologies: β-amyloid plaque deposition and neurofibrillary tangles of hyperphosphorylated tau. Diagnosis is based upon clinical presentation fulfilling several criteria as well as fluid and imaging biomarkers. Treatment is currently targeted toward symptomatic therapy, although trials are underway that aim to reduce the production and overall burden of pathology within the brain. Here, we discuss recent advances in our understanding of the clinical evaluation and treatment of Alzheimer’s disease, with updates regarding clinical trials still in progress.

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          Mechanisms of gamma oscillations.

          György Buzsáki, Xiao-Jing Wang (2012)
          Gamma rhythms are commonly observed in many brain regions during both waking and sleep states, yet their functions and mechanisms remain a matter of debate. Here we review the cellular and synaptic mechanisms underlying gamma oscillations and outline empirical questions and controversial conceptual issues. Our main points are as follows: First, gamma-band rhythmogenesis is inextricably tied to perisomatic inhibition. Second, gamma oscillations are short-lived and typically emerge from the coordinated interaction of excitation and inhibition, which can be detected as local field potentials. Third, gamma rhythm typically concurs with irregular firing of single neurons, and the network frequency of gamma oscillations varies extensively depending on the underlying mechanism. To document gamma oscillations, efforts should be made to distinguish them from mere increases of gamma-band power and/or increased spiking activity. Fourth, the magnitude of gamma oscillation is modulated by slower rhythms. Such cross-frequency coupling may serve to couple active patches of cortical circuits. Because of their ubiquitous nature and strong correlation with the "operational modes" of local circuits, gamma oscillations continue to provide important clues about neuronal population dynamics in health and disease.
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            Gamma frequency entrainment attenuates amyloid load and modifies microglia.

            Hannah F Iaccarino, Annabelle Singer, Anthony Martorell … (2016)
            Changes in gamma oscillations (20-50 Hz) have been observed in several neurological disorders. However, the relationship between gamma oscillations and cellular pathologies is unclear. Here we show reduced, behaviourally driven gamma oscillations before the onset of plaque formation or cognitive decline in a mouse model of Alzheimer's disease. Optogenetically driving fast-spiking parvalbumin-positive (FS-PV)-interneurons at gamma (40 Hz), but not other frequencies, reduces levels of amyloid-β (Aβ)1-40 and Aβ 1-42 isoforms. Gene expression profiling revealed induction of genes associated with morphological transformation of microglia, and histological analysis confirmed increased microglia co-localization with Aβ. Subsequently, we designed a non-invasive 40 Hz light-flickering regime that reduced Aβ1-40 and Aβ1-42 levels in the visual cortex of pre-depositing mice and mitigated plaque load in aged, depositing mice. Our findings uncover a previously unappreciated function of gamma rhythms in recruiting both neuronal and glial responses to attenuate Alzheimer's-disease-associated pathology.
            Article 0 comments Cited 455 times – based on 0 reviews     Review now
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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.
              Article 0 comments Cited 416 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Jason Weller: Role: ConceptualizationRole: Data CurationRole: Formal AnalysisRole: InvestigationRole: MethodologyRole: Project AdministrationRole: ResourcesRole: SoftwareRole: ValidationRole: VisualizationRole: Writing – Original Draft PreparationRole: Writing – Review & Editing
                ORCID: https://orcid.org/0000-0003-0387-5542
                Andrew Budson: Role: Formal AnalysisRole: Project AdministrationRole: ResourcesRole: SupervisionRole: Writing – Review & Editing
                Journal
                Journal ID (nlm-ta): F1000Res
                Journal ID (iso-abbrev): F1000Res
                Journal ID (pmc): F1000Research
                Title: F1000Research
                Publisher: F1000 Research Limited (London, UK )
                ISSN (Electronic): 2046-1402
                Publication date (Electronic): 31 July 2018
                Publication date Collection: 2018
                Volume: 7
                Electronic Location Identifier: F1000 Faculty Rev-1161
                Affiliations
                [1 ]Department of Neurology, Boston VA Hospital, 150 South Huntington Street, Jamaica Plain, MA, 02130, USA
                [2 ]Department of Neurology, Boston University School of Medicine, 72 East Concord Street C-309, Boston, MA, USA
                Author notes

                Competing interests: Jason Weller has no competing interests to declare. Andrew Budson is a consultant and speaker for General Electric, Lilly, and Axovant and is a clinical trial investigator for Biogen, Lilly, vTv therapeutics, and Axovant.

                Author information
                https://orcid.org/0000-0003-0387-5542
                Article
                DOI: 10.12688/f1000research.14506.1
                PMC ID: 6073093
                PubMed ID: 30135715
                SO-VID: 8f4de38b-1ceb-415d-8aeb-792d1f287eee
                Copyright © Copyright: © 2018 Weller J and Budson A
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution Licence, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date accepted : 24 July 2018
                Funding
                The author(s) declared that no grants were involved in supporting this work.
                Categories
                Subject: Review
                Subject: Articles

                Keywords: alzheimer's disease,dementia,amyloid,tau
                Data availability:
                Keywords: alzheimer's disease, dementia, amyloid, tau

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