bims-empneu Biomed News
on Exercise and Molecular Pathways Involved in Neuroprotection
Issue of 2021‒03‒28
two papers selected by
Navabeh Zare-Kookandeh
Victoria University

  1. Brain Res. 2021 Mar 19. pii: S0006-8993(21)00296-1. [Epub ahead of print] 147439
      Previously, we demonstrated that one single physical exercise session could positively modulate recognition memory persistence by D1/D5 activation. Here, we aim to investigate whether the effect of physical exercise on memory occurs due to the activation of both receptors, D1 and D5, or only one of them. Adult male Wistar rats were habituated on a treadmill one week before experiments. After learning session in the object recognition task, some animals received intrahippocampal infusions of the vehicle or a D1/D5 agonist (SKF 38393, 12.5 μg/μL/side), whereas others performed a single session of physical exercise on a treadmill (30 min at an intensity of 60-70% of indirect VO2 max.). Immediately after physical exercise, some animals received intrahippocampal infusions of vehicle or D1/D5 antagonist (SCH 23390, 1 μg/μL/side). Signaling pathways of D1 and D5 receptors in the hippocampus were evaluated by pharmacological activation or inactivation of protein kinases A (PKA) and C (PKC), respectively. According to previous findings, D1/D5 agonist and a single physical exercise session after learning promoted memory persistence, and D1/D5 block impaired physical exercise effect. Importantly, here we demonstrated for the first time that PKA inhibition, but not PKC, impairs the effect of acute physical exercise on memory persistence. Besides, PKA stimulation can promote its effects on memory. Therefore, we provide evidence that corroborates the idea that D1-like dopaminergic receptors, by activation of the PKA pathway, are involved in the effects of acute physical exercise on memory.
    Keywords:  acute physical exercise; dopaminergic system; long-term memory; single bout exercise; treadmill running
  2. Life Sci. 2021 Mar 18. pii: S0024-3205(21)00357-X. [Epub ahead of print] 119372
      AIMS: Alzheimer's disease (AD) is the most common irreversible chronic neurodegenerative disease. It is characterized by the abnormal accumulation of β-amyloid protein (Aβ), which triggers homeostatic breakage in several physiological systems. However, the effect of chronic exercise on the formation of Aβ as an alternative therapy has been investigated. This systematic review examines the antiamyloid effect of different types and intensities of exercise, seeking to elucidate its neuroprotective mechanisms.MAIN METHODS: The research was conducted in the electronic databases Pubmed, Embase, Scopus and Web of Science, using the following descriptors: "amyloid beta" (OR senile plaque OR amyloid plaque) and "exercise" (OR physical activity OR training). The risk of bias was evaluated through SYRCLE's Risk of Bias for experimental studies.
    KEY FINDINGS: 2268 articles were found, being 36 included in the study. A higher frequency of use of mice with genetic alterations was identified for the Alzheimer's disease (AD) model (n = 29). It was used as chronic training: treadmill running (n = 24), voluntary running wheel (n = 7), swimming (n = 4) and climbing (n = 2). The hippocampus and the cortex were the most investigated regions. However, physiological changes accompanied by the reduction of Aβ and associated with AD progression were verified. It is concluded that exercise reduces the production of Aβ in models of animals with AD.
    SIGNIFICANCE: Nevertheless, this effect contributes to the improvement of several physiological aspects related to Aβ and that contribute to neurological impairment in AD.
    Keywords:  Alzheimer's disease; Amyloid plaque; Beta-amyloid protein; Dementia; Neurodegenerative disease; Physical activity; Regular exercise