Relationship Between Exercise and Alzheimer’s Disease: A Narrative Literature Review

Meng, Qing Cheng; Lin, Muh-Shi; Tzeng, I‐Shiang

doi:10.3389/fnins.2020.00131

Cited by 132 publications

(105 citation statements)

References 46 publications

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“…Expression of the high affinity binding PAC1 receptor [1] decreased in the testis of AD animals, similar to the CNS [18]. Physical exercise can be protective against Aβ neurotoxicity [34]. In our study, the expression of PAC1 receptor was nearly normalized in TAD animals.…”

Section: Discussionsupporting

confidence: 63%

“…Controlled training postponed the manifestation of AD in human patients [33] and it has been demonstrated that continuous physical exercise affects the concentration of Aβ in plasma [33]. Various studies have been published in the last few years about the advantages of physical activity on AD formation [34] but its peripheral effects have not been discussed in detail, although increased locomotion and training in B6C3-Tg(APPswe, PSEN1dE9)85Dbo/J transgenic mice have yielded promising results to slow down AD formation [35,36]. Therefore, physical activity can be a possible intervention with potential systemic effects and positive consequences on different tissue regeneration in AD [35].…”

Section: Introductionmentioning

confidence: 99%

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Alzheimer’s Disease Mouse as a Model of Testis Degeneration

Szegeczki

Horváth

Perényi

et al. 2020

IJMS

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Pituitary adenylate cyclase activating polypeptide (PACAP) is a neuropeptide with protective functions in the central nervous system and various peripheral organs. PACAP has the highest expression level in the testes, among the peripheral organs, and has a positive regulative role in spermatogenesis and in sperm motility. In the present study, we explored testicular degenerative alterations in a mouse model of Alzheimer’s disease (AD) (B6C3-Tg(APPswe,PSEN1dE9)85Dbo/J) and demonstrated changes in PACAP-regulated signaling pathways. In addition, the effects of increased physical activity of AD (trained AD (TAD)) mice on testis were also followed. Reduced cell number and decreased thickness of basement membrane were detected in AD samples. These changes were compensated by physical activity. Expression of PACAP receptors and canonical signaling elements such as PKA, P-PKA, PP2A significantly decreased in AD mice, and altered Sox transcription factor expression was also detected. Via this signaling mechanism, physical activity compensated the negative effects of AD on the expression of type IV collagen. Our findings suggest that the testes of AD mice can be a good model of testis degeneration. Moreover, it can be an appropriate organ to follow the effects of various interventions such as physical activity on tissue regeneration and signaling alterations.

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Section: Discussionsupporting

confidence: 63%

Section: Introductionmentioning

confidence: 99%

Alzheimer’s Disease Mouse as a Model of Testis Degeneration

Szegeczki

Horváth

Perényi

et al. 2020

IJMS

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“…It is known that a sedentary lifestyle might lead to an earlier AD onset. Recent studies have observed that exercise interventions were capable of attenuating the symptoms of neurodegeneration experienced by AD patients, with comparable observations in rodent models of AD [ 29 , 30 , 31 , 32 , 33 ]. In addition, Liang et al [ 34 ] have shown that physical activity reduces the levels of AD-associated biomarkers (e.g., Pittsburgh compound-B, tau, phosphorylated tau) in the cerebrospinal fluid of cognitively normal older adults…”

Section: Protective Role Of Exercise In Preventing Mood Disorders and Neurodegenerative Diseasesmentioning

confidence: 76%

Molecular Mechanisms Underlying the Beneficial Effects of Exercise on Brain Function and Neurological Disorders

Nay

Smiles

Kaiser

et al. 2021

IJMS

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As life expectancy has increased, particularly in developed countries, due to medical advances and increased prosperity, age-related neurological diseases and mental health disorders have become more prevalent health issues, reducing the well-being and quality of life of sufferers and their families. In recent decades, due to reduced work-related levels of physical activity, and key research insights, prescribing adequate exercise has become an innovative strategy to prevent or delay the onset of these pathologies and has been demonstrated to have therapeutic benefits when used as a sole or combination treatment. Recent evidence suggests that the beneficial effects of exercise on the brain are related to several underlying mechanisms related to muscle–brain, liver–brain and gut–brain crosstalk. Therefore, this review aims to summarize the most relevant current knowledge of the impact of exercise on mood disorders and neurodegenerative diseases, and to highlight the established and potential underlying mechanisms involved in exercise–brain communication and their benefits for physiology and brain function.

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“…For example, a recent study showed that individuals with diabetes and the ɛ4 allele demonstrated a faster functional decline than those without diabetes (Thomas et al, 2020). Other confounding factors like smoking (Durazzo et al, 2014), physical activity (Meng et al, 2020), and education levels (Meng and Arcy, 2012) could introduce some bias into our results. This information was not included in the dataset.…”

Section: Discussionmentioning

confidence: 92%

The link between static and dynamic brain functional network connectivity and genetic risk of Alzheimer’s disease

Zendehrouh

et al. 2021

Preprint

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Apolipoprotein E (APOE) polymorphic alleles are genetic factors associated with Alzheimer's disease (AD) risk. Although previous studies have explored the link between AD genetic risk and static functional network connectivity (sFNC), to the best of our knowledge, no previous studies have evaluated the association between dynamic FNC (dFNC) and AD genetic risk. Here, we examined the link between sFNC, dFNC, and AD genetic risk with a reproducible, data-driven approach. We used rs-fMRI, demographic, and APOE data from cognitively normal individuals (N=894) between 42 to 95 years of age (mean = 70 years). We divided individuals into low, moderate, and high-risk groups. Using Pearson correlation, we calculated sFNC across seven brain networks. We also calculated dFNC with a sliding window and Pearson correlation. The dFNC windows were partitioned into three distinct states with k-means clustering. Next, we calculated the amount of time each subject spent in each state, called occupancy rate or OCR. We compared both sFNC and OCR, estimated from dFNC, across individuals with different genetic risk and found that both sFNC and dFNC are related to AD genetic risk. We found that higher AD risk reduces within-visual sensory network (VSN) sFNC and that individuals with higher AD risk spend more time in a state with lower within-VSN dFNC. Additionally, we found that AD genetic risk affects whole-brain sFNC and dFNC in women but not in men. In conclusion, we presented novel insights into the links between sFNC, dFNC, and AD genetic risk.

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Relationship Between Exercise and Alzheimer’s Disease: A Narrative Literature Review

Cited by 132 publications

References 46 publications

Alzheimer’s Disease Mouse as a Model of Testis Degeneration

Alzheimer’s Disease Mouse as a Model of Testis Degeneration

Molecular Mechanisms Underlying the Beneficial Effects of Exercise on Brain Function and Neurological Disorders

The link between static and dynamic brain functional network connectivity and genetic risk of Alzheimer’s disease

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