Molecular Mechanisms Underlying the Neuroprotection of Environmental Enrichment in Parkinson’s Disease

From a study published in July 2023, in the Journal of Neural Regeneration Research.

Alarcón, Tamara Andrea1,2; Presti-Silva, Sarah Martins2,3; Simões, Ana Paula Toniato1,2; Ribeiro, Fabiola Mara3,; Pires, Rita Gomes Wanderley1,2,. Molecular mechanisms underlying the neuroprotection of environmental enrichment in Parkinson’s disease. Neural Regeneration Research 18(7):p 1450-1456, July 2023. | DOI: 10.4103/1673-5374.360264

According to the Parkinson’s Foundation, Parkinson’s (PD) is the second-most common neurodegenerative disease after Alzheimer’s disease, with nearly 90,000 people in the U.S. diagnosed with PD each year.

Parkinson’s is characterized by tremors, mainly at rest, slowness of movement, limb stiffness and posture instability. It is caused by a degeneration of nerve cells in a small part deep inside the brain that is essential for controlling movements, the substantial nigra. This small part of the brain is also important for regulating dopamine levels, which affects learning, mood, judgment, decision-making and other processes.

Environmental enrichment has been studied as a promising form of treatment for diseases like Parkinson’s because it can prompt the brain to grow new cells (neurogenesis) and new connections (dendritic arborization), and help the brain regulate its dopamine function.

In this study, scientists reviewed the available literature to understand more about the molecular mechanisms involved in Parkinson’s Disease in particuler.

  • EE helps revert the motor impairment induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 6-hydroxydopamine (6-OHDA) in animal models of PD,
  • EE ameliorated motor impairments in an α-synuclein animal model of PD.
  • EE ameliorates hyperactivity and anxiety in a hA53T α-synuclein overexpression mouse
  • EE reduces aggregated α-synuclein levels and the interaction between α-synuclein and vesicle-associated member protein 2 in the nucleus accumbens.
  • EE ameliorates olfactory dysfunction and decreases oxidative stress and levels of nitrated α-synuclein, although the mechanism by which EE impacts the aggregate α-synuclein in animal models of synucleinopathies is still unclear.
  • Long-term enriched environment is capable of preventing α-synuclein-induced disturbances in the hippocampal transcriptome including disturbances in microglia and astrocytes.
  • EE exposure led to an improvement in cognitive and psychological damage, which scientists suppose com from decreased dopaminergic neuronal death in the substantia nigra pars compacta (SNpc), increased dopamine turnover, reduced oxidative stress, and decreased intestinal inflammation due to the modulation of anti-inflammatory gut bacteria, or even through the modulation of neurotrophins.

The paper concludes that while “the neuroprotective effects of EE in neurodegenerative diseases such as PD have been well established by many studies, […] further studies are needed to fully elucidate the effects of EE exposure on the other neurotransmission systems known to be involved in the pathology of PD.”

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