6
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Deep brain stimulation: potential for neuroprotection

      review-article

      Read this article at

      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

          Over the last two decades there has been an exponential rise in the number of patients receiving deep brain stimulation ( DBS) to manage debilitating neurological symptoms in conditions such as Parkinson's disease, essential tremor, and dystonia. Novel applications of DBS continue to emerge including treatment of various psychiatric conditions (e.g. obsessive‐compulsive disorder, major depression) and cognitive disorders such as Alzheimer's disease. Despite widening therapeutic applications, our understanding of the mechanisms underlying DBS remains limited. In addition to modulation of local and network‐wide neuronal activity, growing evidence suggests that DBS may also have important neuroprotective effects in the brain by limiting synaptic dysfunction and neuronal loss in neurodegenerative disorders. In this review, we consider evidence from preclinical and clinical studies of DBS in Parkinson's disease, Alzheimer's disease, and epilepsy that suggest chronic stimulation has the potential to mitigate neuronal loss and disease progression.

          Related collections

          Most cited references78

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

          A phase I trial of deep brain stimulation of memory circuits in Alzheimer's disease.

          Alzheimer disease (AD) is characterized by functional impairment in the neural elements and circuits underlying cognitive and memory functions. We hypothesized that fornix/hypothalamus deep brain stimulation (DBS) could modulate neurophysiological activity in these pathological circuits and possibly produce clinical benefits. We conducted a phase I trial in 6 patients with mild AD receiving ongoing medication treatment. Patients received continuous stimulation for 12 months. Three main lines of investigation were pursued including: (1) mapping the brain areas whose physiological function was modulated by stimulation using standardized low-resolution electromagnetic tomography, (2) assessing whether DBS could correct the regional alterations in cerebral glucose metabolism in AD using positron emission tomography (PET), and 3) measuring the effects of DBS on cognitive function over time using clinical scales and instruments. DBS drove neural activity in the memory circuit, including the entorhinal, and hippocampal areas and activated the brain's default mode network. PET scans showed an early and striking reversal of the impaired glucose utilization in the temporal and parietal lobes that was maintained after 12 months of continuous stimulation. Evaluation of the Alzheimer's Disease Assessment Scale cognitive subscale and the Mini Mental State Examination suggested possible improvements and/or slowing in the rate of cognitive decline at 6 and 12 months in some patients. There were no serious adverse events. There is an urgent need for novel therapeutic approaches for AD. Modulating pathological brain activity in this illness with DBS merits further investigation.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The road to restoring neural circuits for the treatment of Alzheimer's disease.

            Alzheimer's disease is a progressive loss of memory and cognition, for which there is no cure. Although genetic studies initially suggested a primary role for amyloid-in Alzheimer's disease, treatment strategies targeted at reducing amyloid-have failed to reverse cognitive symptoms. These clinical findings suggest that cognitive decline is the result of a complex pathophysiology and that targeting amyloid-alone may not be sufficient to treat Alzheimer's disease. Instead, a broad outlook on neural-circuit-damaging processes may yield insights into new therapeutic strategies for curing memory loss in the disease.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Cortical map reorganization enabled by nucleus basalis activity.

              Little is known about the mechanisms that allow the cortex to selectively improve the neural representations of behaviorally important stimuli while ignoring irrelevant stimuli. Diffuse neuromodulatory systems may facilitate cortical plasticity by acting as teachers to mark important stimuli. This study demonstrates that episodic electrical stimulation of the nucleus basalis, paired with an auditory stimulus, results in a massive progressive reorganization of the primary auditory cortex in the adult rat. Receptive field sizes can be narrowed, broadened, or left unaltered depending on specific parameters of the acoustic stimulus paired with nucleus basalis activation. This differential plasticity parallels the receptive field remodeling that results from different types of behavioral training. This result suggests that input characteristics may be able to drive appropriate alterations of receptive fields independently of explicit knowledge of the task. These findings also suggest that the basal forebrain plays an active instructional role in representational plasticity.
                Bookmark

                Author and article information

                Contributors
                suneil.kalia@utoronto.ca
                Journal
                Ann Clin Transl Neurol
                Ann Clin Transl Neurol
                10.1002/(ISSN)2328-9503
                ACN3
                Annals of Clinical and Translational Neurology
                John Wiley and Sons Inc. (Hoboken )
                2328-9503
                08 November 2018
                January 2019
                : 6
                : 1 ( doiID: 10.1002/acn3.2019.6.issue-1 )
                : 174-185
                Affiliations
                [ 1 ] Krembil Research Institute University Health Network Toronto Western Hospital Toronto Ontario Canada
                [ 2 ] Division of Neurology Toronto Western Hospital University of Toronto Toronto Ontario Canada
                [ 3 ] Division of Neurosurgery Toronto Western Hospital University of Toronto Toronto Ontario Canada
                [ 4 ] Harquail Centre for Neuromodulation Division of Neurosurgery Sunnybrook Health Sciences Centre University of Toronto Toronto Ontario Canada
                [ 5 ] Tanz Centre for Research in Neurodegenerative Diseases University of Toronto Toronto Ontario Canada
                Author notes
                [*] [* ] Correspondence

                Suneil K. Kalia, Krembil Research Institute, University Health Network, Toronto Western Hospital, Toronto, Ontario M5T 2S8, Canada.

                E‐mail: suneil.kalia@ 123456utoronto.ca

                [†]

                These authors contributed equally to this work.

                Author information
                http://orcid.org/0000-0002-1932-318X
                http://orcid.org/0000-0002-9384-1305
                http://orcid.org/0000-0003-2054-1915
                Article
                ACN3682
                10.1002/acn3.682
                6331208
                30656196
                e6cce065-7874-4c57-91af-71f793b9d7b0
                © 2018 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 03 June 2018
                : 12 September 2018
                : 28 September 2018
                Page count
                Figures: 1, Tables: 0, Pages: 12, Words: 8246
                Categories
                Review Article
                Review Articles
                Custom metadata
                2.0
                acn3682
                January 2019
                Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.5.4 mode:remove_FC converted:14.01.2019

                Comments

                Comment on this article