scholarly journals Treadmill exercise improves memory and increases hippocampal BDNF in a rat model of Alzheimer's Disease

2020 ◽  
Vol 24 (4) ◽  
pp. 250-256
Author(s):  
Rokhsareh Abshenas ◽  
◽  
Tayebe Artimani ◽  
Iraj Amiri ◽  
Siamak Shahidi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Avoidance Learning ◽  
Memory Impairment ◽  
Treadmill Exercise ◽  
Amyloid Β ◽  
Male Rats ◽  
Bdnf Expression ◽  
Learning Tasks ◽  
Model Of Alzheimer’S Disease

Introduction: Alzheimer’s disease is strongly correlated with learning and memory impairments. As exercise can enhance memory and learning, in this study, we have investigated the effects of treadmill exercise on memory impairment in amyloid β (Aβ)- treated rats focusing on brain-derived neurotrophic factor (BDNF) expression. Methods: Wistar male rats received intracerebroventricular (ICV) injection of Aβ and exercised on a treadmill for one month. Memory function was assessed using Morris water maze (MWM) and avoidance learning tasks. The level of BDNF was examined by the ELISA test. Results: The results of MWM and avoidance learning tasks showed that treadmill exercise could improve Aβ- induced memory impairment significantly. Moreover, BDNF expression increased following exercise in the Aβ- treated rats. Conclusion: The present results suggested that treadmill exercise may improve memory in Alzheimer’s disease by increasing BDNF level in the hippocampus.

scholarly journals Effects of GrandFusion Diet on Cognitive Impairment in Transgenic Mouse Model of Alzheimer’s Disease

Nutrients ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 117 ◽  
Author(s):  
Jin Yu ◽  
Hong Zhu ◽  
Saeid Taheri ◽  
William Mondy ◽  
Stephen Perry ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Cathepsin B ◽  
Memory Impairment ◽  
Chronic Traumatic Encephalopathy ◽  
Disease Process ◽  
Amyloid Β ◽  
Aβ Peptide ◽  
Model Of Alzheimer’S Disease

Alzheimer’s disease (AD) is the result of the deposition of amyloid β (Aβ) peptide into amyloid fibrils and tau into neurofibrillary tangles. At the present time, there are no possible treatments for the disease. We have recently shown that diets enriched in phytonutrients show protection or limit the extent of damage in a number of neurological disorders. GrandFusion (GF) diets have attenuated the outcomes in animal models of traumatic brain injury, cerebral ischemia, and chronic traumatic encephalopathy. In this study, we investigated the effect of GF diets in a mouse model of AD prior to the development of amyloid plaques to show how this treatment paradigm would alter the accumulation of Aβ peptide and related pathologic changes (i.e., inflammation, cathepsin B, and memory impairment). Administration of GF diets (2–4%) over a period of four months in APP/ΔPS1 double-transgenic mice resulted in attenuation in Aβ peptide levels, reduction of amyloid load, and inflammation, increased cathepsin B expression, and improved spatial orientation. Additionally, treatment with GF diets increased nerve growth factor (NGF) levels in the brain and tempered the memory impairment in the animal model. These data suggest that GF diets may alter the development and progression of the mechanisms associated with the disease process to effectively modify AD pathogenesis.

scholarly journals The Effect of Spironolactone on β-amyloid-Induced Memory Impairment in Male Rats: The Role of Microglial Inhibition

2021 ◽  
Author(s):  
Mohammad Mehdipour ◽  
Masoumeh Emamghoreishi ◽  
Majid Reza Farrokhi ◽  
Elahe Amirinezhadfard ◽  
Mojtaba Keshavarz
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rat Model ◽  
Memory Impairment ◽  
Microglial Activation ◽  
Memory Loss ◽  
Inhibitory Avoidance ◽  
Male Rats ◽  
Model Of Alzheimer’S Disease ◽  
Β Amyloid

Purpose: Neuroinflammation was indicated in the pathophysiology of Alzheimer’s disease. Previous reports have also signified that spironolactone has anti-inflammatory effects. Therefore, the aim of this study was to assess the modulatory effects of spironolactone on neuroinflammation and memory loss in a rat model of Alzheimer’s disease. Methods: The β-amyloid protein fragment 25-35 (Aβ) was injected in the dorsal hippocampus (5μg/2.5μl each side) of male Sprague-Dawley rats for four consecutive days to induce memory impairment. Animals have intraperitoneally received spironolactone (10, 25, or 50 mg/kg, N=6/group) or vehicle for 14 days. The passive inhibitory avoidance and the novel recognition tests were used for memory evaluation. Neuroinflammation was assessed by measuring the level of Iba1 protein, a marker of microglial activation, using western immunoblotting. Results: Different doses of spironolactone showed no significant changes in latency times and discriminations ratios in passive inhibitory avoidance and novel recognition tests, respectively, as compared to vehicle. However, spironolactone-treated groups showed significantly lower Iba1 protein levels in comparison to the vehicle-treated group (p<0.01). Conclusion: Spironolactone had a modulatory effect on neuroinflammation through a repressive effect on microglial activation with no valuable effect on memory improvement in a rat model of Alzheimer’s disease. The findings of this study suggest that Ab-induced memory loss may not be directly linked to microglial activation. Spironolactone may be a potential candidate to be examined in other neuroinflammatory disorders.

Clioquinol Decreases Amyloid-β Burden and Reduces Working Memory Impairment in a Transgenic Mouse Model of Alzheimer's Disease

2009 ◽  
Vol 17 (2) ◽  
pp. 423-440 ◽  
Author(s):  
Cristina Grossi ◽  
Simona Francese ◽  
Angela Casini ◽  
Maria Cristina Rosi ◽  
Ilaria Luccarini ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Working Memory ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Memory Impairment ◽  
Amyloid Β ◽  
Transgenic Mouse Model ◽  
Model Of Alzheimer’S Disease
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