Physical Exercise Training Improves Judgment and Problem-Solving and Modulates Serum Biomarkers in Patients with Alzheimer’s Disease

Farias, Joni Marcio de; Tramontin, Natalia dos Santos; Pereira, Eduarda Valim; Moraes, Geiziane Laurindo de; Furtado, Beatriz Giusti; Tietbohl, Lariani Tamires Witt; Pereira, Bárbara da Costa; Simon, Kellen Ugioni; Müller, Alexandre Pastoris

doi:10.1007/s12035-021-02411-z

Cited by 19 publications

(18 citation statements)

References 71 publications

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“…Furthermore, longitudinal studies demonstrated that low levels of physical activity were associated with a higher risk of dementia in older individuals ( Tan et al, 2017 ), whereas regular physical activity could reduce the risk or delay the onset of dementia and AD, especially among genetically susceptible individuals ( Rovio et al, 2005 ). Nowadays, physical activity and exercise have been widely acknowledged as effective strategies for improving AD pathology and AD-associated cognitive impairment ( Northey et al, 2018 ; Jia et al, 2019 ; de Farias et al, 2021 ). From a mechanistic perspective, macroscopically, regular exercise has been shown to alleviate some abnormalities of brain structure and function and to increase cerebral blood flow in subjects with mild cognitive impairment (MCI) and AD ( Broadhouse et al, 2020 ; Tomoto et al, 2021 ; Yu et al, 2021 ); microscopically, exercise training not only increases levels of exerkines (e.g., irisin, Lourenco et al, 2019 ; Islam et al, 2021 ) and metabolic factors (e.g., lactate, El Hayek et al, 2019 ) in the peripheral circulation, which act on the AD brain indirectly, but also exert direct neuroprotective effects by increasing levels of brain-derived neurotrophic factor (BDNF) ( Wang and Holsinger, 2018 ) and promoting adult hippocampal neurogenesis ( Choi et al, 2018 ), enhancing synaptic plasticity ( Mu et al, 2022 ), reducing neuroinflammation and oxidative stress ( Zhang et al, 2019 ), and ameliorating Aβ deposition and tau hyperphosphorylation ( Brown et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

Understanding How Physical Exercise Improves Alzheimer’s Disease: Cholinergic and Monoaminergic Systems

Zong

Zhang

et al. 2022

Front. Aging Neurosci.

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Alzheimer’s disease (AD) is an age-related neurodegenerative disorder, characterized by the accumulation of proteinaceous aggregates and neurofibrillary lesions composed of β-amyloid (Aβ) peptide and hyperphosphorylated microtubule-associated protein tau, respectively. It has long been known that dysregulation of cholinergic and monoaminergic (i.e., dopaminergic, serotoninergic, and noradrenergic) systems is involved in the pathogenesis of AD. Abnormalities in neuronal activity, neurotransmitter signaling input, and receptor function exaggerate Aβ deposition and tau hyperphosphorylation. Maintenance of normal neurotransmission is essential to halt AD progression. Most neurotransmitters and neurotransmitter-related drugs modulate the pathology of AD and improve cognitive function through G protein-coupled receptors (GPCRs). Exercise therapies provide an important alternative or adjunctive intervention for AD. Cumulative evidence indicates that exercise can prevent multiple pathological features found in AD and improve cognitive function through delaying the degeneration of cholinergic and monoaminergic neurons; increasing levels of acetylcholine, norepinephrine, serotonin, and dopamine; and modulating the activity of certain neurotransmitter-related GPCRs. Emerging insights into the mechanistic links among exercise, the neurotransmitter system, and AD highlight the potential of this intervention as a therapeutic approach for AD.

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Section: Introductionmentioning

confidence: 99%

Understanding How Physical Exercise Improves Alzheimer’s Disease: Cholinergic and Monoaminergic Systems

Zong

Zhang

et al. 2022

Front. Aging Neurosci.

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“…The TGF-β can induce both regulatory/inhibitory and proinflammatory T cells, depending on proinflammatory cytokines [ 44 ]. Many research reports show that the protective effect of regular exercise may be due to reduced inflammatory immune profiles, characterized by reduced proinflammatory levels and raised IL-6 and anti-inflammatory levels in aged or at-risk populations [ 42 , 45 , 46 ]. Similarly, we found that the SIT stimulated increases in the IL-6 concentration and the IL-10/TNF-α ratio.…”

Section: Discussionmentioning

confidence: 99%

Targeted Lipidomics and Inflammation Response to Six Weeks of Sprint Interval Training in Male Adolescents

Wang

Zhang

Liu

et al. 2023

IJERPH

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Lipids play an important role in coordinating and regulating metabolic and inflammatory processes. Sprint interval training (SIT) is widely used to improve sports performance and health outcomes, but the current understanding of SIT-induced lipid metabolism and the corresponding systemic inflammatory status modification remains controversial and limited, especially in male adolescents. To answer these questions, twelve untrained male adolescents were recruited and underwent 6 weeks of SIT. The pre- and post-training testing included analyses of peak oxygen consumption (VO2peak), biometric data (weight and body composition), serum biochemical parameters (fasting blood glucose, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triacylglycerol, testosterone, and cortisol), inflammatory markers, and targeted lipidomics. After the 6-week SIT, the serum C-reactive protein (CRP), interleukin (IL)-1β, IL-2, IL-4, IL-10, tumor necrosis factor (TNF)-α, and transforming growth factor (TGF)-β significantly decreased (p < 0.05), whereas IL-6 and IL-10/TNF-α significantly increased (p < 0.05). In addition, the targeted lipidomics revealed changes in 296 lipids, of which 33 changed significantly (p < 0.05, fold change > 1.2 or <1/1.2). The correlation analysis revealed that the changes in the inflammatory markers were closely correlated with the changes in some of the lipids, such as LPC, HexCer, and FFA. In conclusion, the 6-week SIT induced significant changes in the inflammatory markers and circulating lipid composition, offering health benefits to the population.

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“…Nevertheless, physical activity and a healthy lifestyle can restore neurotrophins and cytokine levels. Crucial questions therefore include which are the specific molecules that are modulated by physical activity in AD [ 124 ]. It is also of great relevance to investigate the concentrations or the temporal dynamics of such molecules, or what is their role in the amelioration of clinical symptomatology.…”

Section: Discussionmentioning

confidence: 99%

Adult Hippocampal Neurogenesis in Alzheimer’s Disease: An Overview of Human and Animal Studies with Implications for Therapeutic Perspectives Aimed at Memory Recovery

Farioli-Vecchioli

Ricci

2022

Neural Plasticity

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The mammalian hippocampal dentate gyrus is a niche for adult neurogenesis from neural stem cells. Newborn neurons integrate into existing neuronal networks, where they play a key role in hippocampal functions, including learning and memory. In the ageing brain, neurogenic capability progressively declines while in parallel increases the risk for developing Alzheimer’s disease (AD), the main neurodegenerative disorder associated with memory loss. Numerous studies have investigated whether impaired adult neurogenesis contributes to memory decline in AD. Here, we review the literature on adult hippocampal neurogenesis (AHN) and AD by focusing on both human and mouse model studies. First, we describe key steps of AHN, report recent evidence of this phenomenon in humans, and describe the specific contribution of newborn neurons to memory, as evinced by animal studies. Next, we review articles investigating AHN in AD patients and critically examine the discrepancies among different studies over the last two decades. Also, we summarize researches investigating AHN in AD mouse models, and from these studies, we extrapolate the contribution of molecular factors linking AD-related changes to impaired neurogenesis. Lastly, we examine animal studies that link impaired neurogenesis to specific memory dysfunctions in AD and review treatments that have the potential to rescue memory capacities in AD by stimulating AHN.

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Physical Exercise Training Improves Judgment and Problem-Solving and Modulates Serum Biomarkers in Patients with Alzheimer’s Disease

Cited by 19 publications

References 71 publications

Understanding How Physical Exercise Improves Alzheimer’s Disease: Cholinergic and Monoaminergic Systems

Understanding How Physical Exercise Improves Alzheimer’s Disease: Cholinergic and Monoaminergic Systems

Targeted Lipidomics and Inflammation Response to Six Weeks of Sprint Interval Training in Male Adolescents

Adult Hippocampal Neurogenesis in Alzheimer’s Disease: An Overview of Human and Animal Studies with Implications for Therapeutic Perspectives Aimed at Memory Recovery

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