Effects of a physical exercise or motor activity protocol on cognitive function, lipid profile, and BDNF levels in older adults with mild cognitive impairment

Sá, Clodoaldo Antônio De; Saretto, Chrystianne Barros; Cardoso, Andréia Machado; Remor, Aline Pertile; Breda, Christian Ouriques; Córralo, Vanessa da Silva

doi:10.1007/s11010-023-04733-z

Cited by 6 publications

(3 citation statements)

References 83 publications

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“…Caspase-3 is transformed into an active form (Cleaved Caspase-3) through clipping to perform its functions [62][63][64]. BDNF, a crucial member of the neurotrophic factor family with vital effects on the development of the nervous system, affects the growth, development, differentiation, and survival of neurons via multiple signaling pathways [65,66]. The results of the present study elaborated that GF could further lower the Bcl-2/Bax ratio but increase the Cleaved Caspase-3 level in the hippocampus of diabetic rats, hinting that GF is capable of worsening the apoptosis of hippocampal neurons in diabetic rats, in agreement with the changes observed by TEM.…”

Section: Discussionmentioning

confidence: 99%

Glucose Fluctuation Inhibits Nrf2 Signaling Pathway in Hippocampal Tissues and Exacerbates Cognitive Impairment in Streptozotocin-Induced Diabetic Rats

Chi,

Sun,

Lin

et al. 2024

Journal of Diabetes Research

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Background. This research investigated whether glucose fluctuation (GF) can exacerbate cognitive impairment in streptozotocin-induced diabetic rats and explored the related mechanism. Methods. After 4 weeks of feeding with diets containing high fats plus sugar, the rat model of diabetes mellitus (DM) was established by intraperitoneal injection of streptozotocin (STZ). Then, GF was triggered by means of alternating satiety and starvation for 24 h. The weight, blood glucose level, and water intake of the rats were recorded. The Morris water maze (MWM) test was carried out to appraise the cognitive function at the end of week 12. Moreover, the morphological structure of hippocampal neurons was viewed through HE and Nissl staining, and transmission electron microscopy (TEM) was performed for ultrastructure observation. The protein expression levels of Nrf2, HO-1, NQO-1, Bax, Bcl-2, and Caspase-3 in the hippocampal tissues of rats were measured via Western blotting, and the mRNA expressions of Nrf2, HO-1, and NQO-1 were examined using qRT-PCR. Finally, Western blotting and immunohistochemistry were conducted to detect BDNF levels. Results. It was manifested that GF not only aggravated the impairment of spatial memory in rats with STZ-induced type 2 DM but also stimulated the loss, shrinkage, and apoptosis of hippocampal neurons. Regarding the expressions in murine hippocampal tissues, GF depressed Nrf2, HO-1, NQO-1, Bcl-2, and BDNF but boosted Caspase-3 and Bax. Conclusions. GF aggravates cognitive impairment by inhibiting the Nrf2 signaling pathway and inducing oxidative stress and apoptosis in the hippocampal tissues.

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Section: Discussionmentioning

confidence: 99%

Glucose Fluctuation Inhibits Nrf2 Signaling Pathway in Hippocampal Tissues and Exacerbates Cognitive Impairment in Streptozotocin-Induced Diabetic Rats

Chi,

Sun,

Lin

et al. 2024

Journal of Diabetes Research

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“…The progression to dementia is often preceded by subtle difficulties in performing everyday activities [5] and can include diagnoses of subjective cognitive impairment [6], mild behavioral impairment [7,8], and psychiatric disturbances including anxiety [9,10], depression [11][12][13], and posttraumatic stress disorder [14,15]. Amidst ongoing challenges in developing disease-modifying drugs, nonpharmacological interventions including exercise are recommended as part of the overall MCI management [16] based on the positive effects of exercise on cognitive performance [17][18][19][20][21][22][23].…”

Section: Introductionmentioning

confidence: 99%

“…Further, physical exercise may present challenges related to mobility and movement that limit the accessibility of the intervention to all individuals. Nonetheless, physical exercise is an affordable and alternative approach to alleviate symptoms of cognitive decline [17][18][19][20][21][22]38,39].…”

Section: Introductionmentioning

confidence: 99%

The Effects of Exercise on Synaptic Plasticity in Individuals With Mild Cognitive Impairment: Protocol for a Pilot Intervention Study (Preprint)

Ramdeo¹,

Fahnestock²,

Gibala³

et al. 2023

Preprint

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BACKGROUND Mild cognitive impairment (MCI) is a syndrome before more severe impairment characterized by dementia. MCI affects an estimated 15% to 20% of people over age 65. Non-pharmacological interventions including exercise are recommended as part of overall MCI management based on the positive effects of exercise on cognitive performance. Interval training involves brief intermittent bouts of exercise interspersed with short recovery periods. This type of exercise promotes cognitive improvement and can be performed in individuals with MCI. Synaptic plasticity can be assessed in-vivo by the neurophysiological response to repetitive transcranial magnetic stimulation. It is unknown whether interval training causes changes in synaptic plasticity in individuals living with MCI. OBJECTIVE This research will determine whether interval training performed using a cycle ergometer enhances synaptic plasticity in older individuals with MCI. The two aims are: (1) to quantify synaptic plasticity after interval training performed at a self-selected intensity in aging and in individuals with MCI, and (2) to determine whether changes in synaptic plasticity correlate with changes in serum brain-derived neurotrophic factor, osteocalcin, and cognition. METHODS Thirty-six individuals will be recruited for assignment to one of three equally sized groups: exercise in MCI, no exercise in MCI and exercise non-MCI. The Exercise MCI group and the exercise non-MCI will perform thrice weekly exercise sessions for four weeks. Synaptic plasticity will be measured before the exercise intervention and following the four-week intervention. At these time points, synaptic plasticity will be measured as the response to single pulse TMS. before and after an rTMS protocol used to induce synaptic plasticity. RESULTS The study began as of March 2023. CONCLUSIONS The proposed research is the first to assess whether synaptic plasticity is enhanced after exercise training in individuals with MCI. If exercise does, indeed, modify synaptic plasticity, this will create a new avenue by which we can study and manipulate the neural plasticity in these individuals. CLINICALTRIAL clinicaltrials.gov Trial number: NCT05663918

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Biosensors, Recent Advances in Determination of BDNF and NfL

Mobed,

Charsouei,

Yazdani

et al. 2023

Cell Mol Neurobiol

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Effects of a physical exercise or motor activity protocol on cognitive function, lipid profile, and BDNF levels in older adults with mild cognitive impairment

Cited by 6 publications

References 83 publications

Glucose Fluctuation Inhibits Nrf2 Signaling Pathway in Hippocampal Tissues and Exacerbates Cognitive Impairment in Streptozotocin-Induced Diabetic Rats

Glucose Fluctuation Inhibits Nrf2 Signaling Pathway in Hippocampal Tissues and Exacerbates Cognitive Impairment in Streptozotocin-Induced Diabetic Rats

The Effects of Exercise on Synaptic Plasticity in Individuals With Mild Cognitive Impairment: Protocol for a Pilot Intervention Study (Preprint)

Biosensors, Recent Advances in Determination of BDNF and NfL

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