For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
3
views
93
references
 Top references
cited by
0
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      396
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      An Introspective Approach: A Lifetime of Parkinson’s Disease Research and Not Much to Show for It Yet?

      discussion
      Author(s):
      Editor(s):
      Publication date (Electronic):
      Journal: Cells
      Publisher: MDPI
      Keywords: Parkinson’s disease, alpha-synuclein, genetics, deep brain stimulation, organoids, anatomy

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          I feel part of a massive effort to understand what is wrong with motor systems in the brain relating to Parkinson’s disease. Today, the symptoms of the disease can be modified slightly, but dopamine neurons still die; the disease progression continues inexorably. Maybe the next research phase will bring the power of modern genetics to bear on halting, or better, preventing cell death. The arrival of accessible human neuron assemblies in organoids perhaps will provide a better access to the processes underlying neuronal demise.

          Related collections

          Most cited references93

          • Record: found
          • Abstract: found
          • Article: not found

          Optogenetic stimulation of a hippocampal engram activates fear memory recall

          Xu Liu, Steve Ramirez, Petti T. Pang … (2012)
          A specific memory is thought to be encoded by a sparse population of neurons 1,2 . These neurons can be tagged during learning for subsequent identification 3 and manipulation 4,5,6 . Moreover, their ablation or inactivation results in reduced memory expression, suggesting their necessity in mnemonic processes. However, a critical question of sufficiency remains: can one elicit the behavioral output of a specific memory by directly activating a population of neurons that was active during learning? Here we show that optogenetic reactivation of hippocampal neurons activated during fear conditioning is sufficient to induce freezing behavior. We labeled a population of hippocampal dentate gyrus neurons activated during fear learning with channelrhodopsin-2 (ChR2) 7,8 and later optically reactivated these neurons in a different context. The mice showed increased freezing only upon light stimulation, indicating light-induced fear memory recall. This freezing was not detected in non-fear conditioned mice expressing ChR2 in a similar proportion of cells, nor in fear conditioned mice with cells labeled by EYFP instead of ChR2. Finally, activation of cells labeled in a context not associated with fear did not evoke freezing in mice that were previously fear conditioned in a different context, suggesting that light-induced fear memory recall is context-specific. Together, our findings indicate that activating a sparse but specific ensemble of hippocampal neurons that contribute to a memory engram is sufficient for the recall of that memory. Moreover, our experimental approach offers a general method of mapping cellular populations bearing memory engrams.
          Article 0 comments Cited 473 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The functional anatomy of basal ganglia disorders.

            Roger Albin, Anne B Young, John B Penney (1989)
            Basal ganglia disorders are a heterogeneous group of clinical syndromes with a common anatomic locus within the basal ganglia. To account for the variety of clinical manifestations associated with insults to various parts of the basal ganglia we propose a model in which specific types of basal ganglia disorders are associated with changes in the function of subpopulations of striatal projection neurons. This model is based on a synthesis of experimental animal and post-mortem human anatomic and neurochemical data. Hyperkinetic disorders, which are characterized by an excess of abnormal movements, are postulated to result from the selective impairment of striatal neurons projecting to the lateral globus pallidus. Hypokinetic disorders, such as Parkinson's disease, are hypothesized to result from a complex series of changes in the activity of striatal projection neuron subpopulations resulting in an increase in basal ganglia output. This model suggests that the activity of subpopulations of striatal projection neurons is differentially regulated by striatal afferents and that different striatal projection neuron subpopulations may mediate different aspects of motor control.
            Article 0 comments Cited 331 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              A meta-analysis of genome-wide association studies identifies 17 new Parkinson's disease risk loci

              Diana Chang, Mike A Nalls, Ingileif Hallgrímsdóttir … (2017)
              Robert Graham and colleagues carried out a GWAS meta-analysis for Parkinson's disease (PD) and report 17 new risk loci. Their analyses support a key role for autophagy and lysosomal biology in PD risk.
              Article 0 comments Cited 312 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Wolfgang Jost: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Cells
                Journal ID (iso-abbrev): Cells
                Journal ID (publisher-id): cells
                Title: Cells
                Publisher: MDPI
                ISSN (Electronic): 2073-4409
                Publication date (Electronic): 28 February 2021
                Publication date Collection: March 2021
                Volume: 10
                Issue: 3
                Electronic Location Identifier: 513
                Affiliations
                Brain Mechanisms for Behaviour Unit, Okinawa Institute of Science and Technology, Graduate University, Onna-son, Okinawa 904-0495, Japan; gordon@ 123456oist.jp
                Author information
                https://orcid.org/0000-0002-3386-8362
                Article
                Publisher ID: cells-10-00513
                DOI: 10.3390/cells10030513
                PMC ID: 7997292
                PubMed ID: 33670933
                SO-VID: d6e0196b-d509-4d23-88c1-5d8c98cf3a30
                Copyright © © 2021 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 : 02 February 2021
                Date accepted : 23 February 2021
                Categories
                Subject: Commentary

                Keywords: parkinson’s disease,alpha-synuclein,genetics,deep brain stimulation,organoids,anatomy
                Data availability:
                Keywords: parkinson’s disease, alpha-synuclein, genetics, deep brain stimulation, organoids, anatomy

                Comments

                Comment on this article