Treadmill exercise sex-dependently alters susceptibility to depression-like behaviour, cytokines and BDNF in the hippocampus and prefrontal cortex of rats with sporadic Alzheimer-like disease

2021 ◽  
pp. 113595
Author(s):  
Saeed Naghibi ◽  
Mohammad Shariatzadeh ◽  
Ali Barzegari ◽  
Azam Davoodabadi ◽  
Amirhossein Ebrahimi ◽  
...  
2016 ◽  
Vol 313 ◽  
pp. 82-87 ◽  
Author(s):  
Laura Reck Cechinel ◽  
Carla Giovana Basso ◽  
Karine Bertoldi ◽  
Bruna Schallenberger ◽  
Louisiana Carolina Ferreira de Meireles ◽  
...  

2012 ◽  
Vol 516 (2) ◽  
pp. 221-225 ◽  
Author(s):  
Ilkay Aksu ◽  
Basak Baykara ◽  
Seda Ozbal ◽  
Ferihan Cetin ◽  
Ali Riza Sisman ◽  
...  

Cells ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 244
Author(s):  
Lianwei Mu ◽  
Jiajia Cai ◽  
Boya Gu ◽  
Laikang Yu ◽  
Cui Li ◽  
...  

Alzheimer’s disease (AD) is characterized by deficits in learning and memory. A pathological feature of AD is the alterations in the number and size of synapses, axon length, dendritic complexity, and dendritic spine numbers in the hippocampus and prefrontal cortex. Treadmill exercise can enhance synaptic plasticity in mouse or rat models of stroke, ischemia, and dementia. The aim of this study was to examine the effects of treadmill exercise on learning and memory, and structural synaptic plasticity in 3×Tg-AD mice, a mouse model of AD. Here, we show that 12 weeks treadmill exercise beginning in three-month-old mice improves spatial working memory in six-month-old 3×Tg-AD mice, while non-exercise six-month-old 3×Tg-AD mice exhibited impaired spatial working memory. To investigate potential mechanisms for the treadmill exercise-induced improvement of spatial learning and memory, we examined structural synaptic plasticity in the hippocampus and prefrontal cortex of six-month-old 3×Tg-AD mice that had undergone 12 weeks of treadmill exercise. We found that treadmill exercise led to increases in synapse numbers, synaptic structural parameters, the expression of synaptophysin (Syn, a presynaptic marker), the axon length, dendritic complexity, and the number of dendritic spines in 3×Tg-AD mice and restored these parameters to similar levels of non-Tg control mice without treadmill exercise. In addition, treadmill exercise also improved these parameters in non-Tg control mice. Strengthening structural synaptic plasticity may represent a potential mechanism by which treadmill exercise prevents decline in spatial learning and memory and synapse loss in 3×Tg-AD mice.


Author(s):  
Saeed Dabagh Nikukheslat ◽  
Pouran Karimi ◽  
Iraj Sadri

Background: According to the experimental studies, the levels of heat shock protein 27 (HSP27) and brain-derived neurotrophic factor (BDNF) are decreased in diabetes which is associated with impaired cognitive function in the brain. Therefore, the increased expression of these two proteins in some brain regions associated with learning and memory can be one of the positive effects of aerobic training on cognition improvement at diabetes. The aim of the present study was to evaluate the effects of aerobic treadmill exercise training (ATET) on HSP27 and BDNF proteins in the prefrontal cortex and hippocampus of streptozotocin (STZ)-induced diabetes in rats. Methods: Twenty healthy adult male Wistar rats approximately 3-month old, weighing 250 ± 25gr were used in this study. Experimental diabetes was induced by a high-fat diet (HFD) for 4 weeks and a low dose of STZ (35 mg/kg, intraperitoneally). Then diabetic animals were divided into two groups (n=10 per each group): control group (C) and aerobic training group (E). The exercise program was treadmill running at 13 m/min, 25 min/day, for 5 days/week at 0˚ slope for the first week, with a gradual increase to 27 m/min for 60 min/day in week 8. Un-paired t-test was used to compare two groups with the considered significant at p<0.05. Results: The results showed that ATET significantly increased protein expression of HSP27 and BDNF in the hippocampus and prefrontal cortex as compared to C group. Conclusion: Our findings showed that aerobic treadmill exercise program can increase the protein expression of HSP27 and BDNF associated with cognition and synaptic plas­ticity and thus counteract the neurodegenerative diseases of the nervous system.


2020 ◽  
Author(s):  
Feng Xu ◽  
Munenori Ono ◽  
Tetsufumi Ito ◽  
Osamu Uchiumi ◽  
Furong Wang ◽  
...  

2001 ◽  
Vol 12 (1) ◽  
pp. 8-14
Author(s):  
Gertraud Teuchert-Noodt ◽  
Ralf R. Dawirs

Abstract: Neuroplasticity research in connection with mental disorders has recently bridged the gap between basic neurobiology and applied neuropsychology. A non-invasive method in the gerbil (Meriones unguiculus) - the restricted versus enriched breading and the systemically applied single methamphetamine dose - offers an experimental approach to investigate psychoses. Acts of intervening affirm an activity dependent malfunctional reorganization in the prefrontal cortex and in the hippocampal dentate gyrus and reveal the dopamine position as being critical for the disruption of interactions between the areas concerned. From the extent of plasticity effects the probability and risk of psycho-cognitive development may be derived. Advance may be expected from insights into regulatory mechanisms of neurogenesis in the hippocampal dentate gyrus which is obviously to meet the necessary requirements to promote psycho-cognitive functions/malfunctions via the limbo-prefrontal circuit.


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