4.7 Review

Immunotherapy for Parkinson's disease

Journal

NEUROBIOLOGY OF DISEASE
Volume 137, Issue -, Pages -

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2020.104760

Keywords

Immune transformation; Regulatory T cells; Tregs; Effector T cells; Teffs; Granulocyte-macrophage colony stimulating factor; Immune homeostasis; Neurodegeneration; Neuroprotection; Nigrostriatal degeneration; Neuroinflammation; Parkinson's disease; Neurodegenerative disorders; Alzheimer's disease; Ischemic stroke; Traumatic brain injury

Categories

Funding

  1. National Institutes of Health [P01 DA028555, R01 NS36126, P01 NS31492, P01 MH64570, P01 NS43985, P30 MH062261, R01 AG043540, 2R01 NS034239]
  2. Frances and Louie Blumkin Foundation
  3. Harriet Singer Research Foundation
  4. Margaret R. Larson Professorship

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With the increasing prevalence of Parkinson's disease (PD), there is an immediate need to interdict disease signs and symptoms. In recent years this need was met through therapeutic approaches focused on regenerative stem cell replacement and alpha-synuclein clearance. However, neither have shown long-term clinical benefit. A novel therapeutic approach designed to affect disease is focused on transforming the brain's immune microenvironment. As disordered innate and adaptive immune functions are primary components of neurodegenerative disease pathogenesis, this has emerged as a clear opportunity for therapeutic development. Interventions that immunologically restore the brain's homeostatic environment can lead to neuroprotective outcomes. These have recently been demonstrated in both laboratory and early clinical investigations. To these ends, efforts to increase the numbers and function of regulatory T cells over dominant effector cells that exacerbate systemic inflammation and neurodegeneration have emerged as a primary research focus. These therapeutics show broad promise in affecting disease outcomes beyond PD, such as for Alzheimer's disease, stroke and traumatic brain injuries, which share common neurodegenerative disease processes.

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