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Modulation of microRNAs through Lifestyle Changes in Alzheimer’s Disease

Pinto-Hernandez, Paola, Castilla-Silgado, Juan, Coto-Vilcapoma, Almudena, Fernández-Sanjurjo, Manuel, Fernández-García, Benjamín, Tomás-Zapico, Cristina, Iglesias-Gutiérrez, Eduardo·2023·Nutrients
DOI 10.3390/nu15173688PMC PMC10490103
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Abstract

Lifestyle factors, including diet and physical activity (PA), are known beneficial strategies to prevent and delay Alzheimer’s disease (AD) development. Recently, microRNAs have emerged as potential biomarkers in multiple diseases, including AD. The aim of this review was to analyze the available information on the modulatory effect of lifestyle on microRNA expression in AD. Few studies have addressed this question, leaving important gaps and limitations: (1) in human studies, only circulating microRNAs were analyzed; (2) in mice studies, microRNA expression was only analyzed in brain tissue; (3) a limited number of microRNAs was analyzed; (4) no human nutritional intervention studies were conducted; and (5) PA interventions in humans and mice were poorly detailed and only included aerobic training. Despite this, some conclusions could be drawn. Circulating levels of let-7g-5p, miR-107, and miR-144-3p were associated with overall diet quality in mild cognitive impairment patients. In silico analysis showed that these microRNAs are implicated in synapse formation, microglia activation, amyloid beta accumulation, and pro-inflammatory pathways, the latter also being targeted by miR-129-5p and miR-192-5p, whose circulating levels are modified by PA in AD patients. PA also modifies miR-132, miR-15b-5p, miR-148b-3p, and miR-130a-5p expression in mice brains, which targets are related to the regulation of neuronal activity, ageing, and pro-inflammatory pathways. This supports the need to further explore lifestyle-related miRNA changes in AD, both as biomarkers and therapeutic targets.

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Figure 1 Progressive stages in the development of AD.
Figure 1 Progressive stages in the development of AD.CC BY · PubMed Central
Figure 2 Lifestyle interventions such as food and nutrient intake and physical activity in early pre-symptomatic AD can regulate the expression of both circulating microRNAs (c-miRNAs) and brain-derived miRNAs. In the case of c-miRNAs, they could be used as early biomarkers of disease risk or could create an inter-tissular crosstalk by regulating the expression of distant genes in different tissues, such as the brain. Regarding brain miRNAs, some of them are involved in modulating dysregulated pathways in AD pathophysiology, increasing brain-derived neurotrophic factor (BDNF) levels and hippocampal volume, and reducing Aβ aggregation, neuroinflammation, and brain atrophy, which ultimately could delay the development of the disease.
Figure 2 Lifestyle interventions such as food and nutrient intake and physical activity in early pre-symptomatic AD can regulate the expression of both circulating microRNAs (c-miRNAs) and brain-derived miRNAs. In the case of c-miRNAs, they could be used as early biomarkers of disease risk or could create an inter-tissular crosstalk by regulating the expression of distant genes in different tissues, such as the brain. Regarding brain miRNAs, some of them are involved in modulating dysregulated pathways in AD pathophysiology, increasing brain-derived neurotrophic factor (BDNF) levels and hippocampal volume, and reducing Aβ aggregation, neuroinflammation, and brain atrophy, which ultimately could delay the development of the disease.CC BY · PubMed Central
Figure 3 In silico analysis of let-7g-5p, miR-107, and miR-144-3p common targets. KEGG analysis based on TargetScan predicted targets on miRpath v4. Data are presented as -log10 of p-value.
Figure 3 In silico analysis of let-7g-5p, miR-107, and miR-144-3p common targets. KEGG analysis based on TargetScan predicted targets on miRpath v4. Data are presented as -log10 of p-value.CC BY · PubMed Central
Figure 4 In silico analysis of miR-129-5p targets. KEGG analysis based on TargetScan predicted targets on miRpath v4. Data are presented as -log10 of p-value.
Figure 4 In silico analysis of miR-129-5p targets. KEGG analysis based on TargetScan predicted targets on miRpath v4. Data are presented as -log10 of p-value.CC BY · PubMed Central
Figure 5 Lifestyle interventions effect on the modulation of miRNAs involved in the pathophysiology of AD. In relation to β-amyloid production, the healthy lifestyle will promote the non-amyloidogenic pathway, favoring the release of P3 peptide, which has neuroprotective effects. In relation to neuroinflammation, activation of microglia and astrocytes will be reduced, releasing fewer pro-inflammatory cytokines that preserve a healthy state for neurons. In this metabolic pathway, exercise can reduce miR-192-5p expression and increase miR-129-5p and miR-130a-3p expression, reducing neuroinflammation. In terms of β-amyloid clearance, lifestyle interventions can enhance autophagic activity and effectively clear the neuronal β-amyloid burden. Furthermore, they can increase phagocytosis of Aβ by microglia into soluble forms and promote outward transport of Aβ into the peripheral system at an increased rate due to increased expression of LRP1 transporters at the blood–brain barrier.
Figure 5 Lifestyle interventions effect on the modulation of miRNAs involved in the pathophysiology of AD. In relation to β-amyloid production, the healthy lifestyle will promote the non-amyloidogenic pathway, favoring the release of P3 peptide, which has neuroprotective effects. In relation to neuroinflammation, activation of microglia and astrocytes will be reduced, releasing fewer pro-inflammatory cytokines that preserve a healthy state for neurons. In this metabolic pathway, exercise can reduce miR-192-5p expression and increase miR-129-5p and miR-130a-3p expression, reducing neuroinflammation. In terms of β-amyloid clearance, lifestyle interventions can enhance autophagic activity and effectively clear the neuronal β-amyloid burden. Furthermore, they can increase phagocytosis of Aβ by microglia into soluble forms and promote outward transport of Aβ into the peripheral system at an increased rate due to increased expression of LRP1 transporters at the blood–brain barrier.CC BY · PubMed Central

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Metadata

Authors
Pinto-Hernandez, P., Castilla-Silgado, J., Coto-Vilcapoma, A., Fernández-Sanjurjo, M., Fernández-García, B., Tomás-Zapico, C., & Iglesias-Gutiérrez, E.
Affiliations
  • Department of Functional Biology, Physiology, University of Oviedo, 33006 Asturias, Spain
  • Health Research Institute of the Principality of Asturias (ISPA), 33011 Asturias, Spain
ORCID
Venue
Nutrients
Publisher
MDPI AG
Published
2023-08-23
Volume
15
Issue
17
Pages
3688
ISSN
2072-6643
DOI
10.3390/nu15173688
PMC
PMC10490103
Cited by
22
References
12
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
Fundación Tatiana Pérez de Guzmán el Bueno

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CoChat. (2026). Citation check: Modulation of microRNAs through Lifestyle Changes in Alzheimer’s Disease. https://app.cochat.ai/papers/10.3390/nu15173688
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Pinto-Hernandez, P., Castilla-Silgado, J., Coto-Vilcapoma, A., Fernández-Sanjurjo, M., Fernández-García, B., Tomás-Zapico, C., & Iglesias-Gutiérrez, E. (2023). Modulation of microRNAs through Lifestyle Changes in Alzheimer’s Disease. Nutrients. https://doi.org/10.3390/nu15173688