Cognitive Rehabilitation Improves Ischemic Stroke-Induced Cognitive Impairment: Role of Growth Factors

Farokhi-Sisakht, Fatemeh; Farhoudi, Mehdi; Sadigh‐Eteghad, Saeed; Mahmoudi, Javad; Mohaddes, Gisou

doi:10.1016/j.jstrokecerebrovasdis.2019.07.015

Cited by 51 publications

(29 citation statements)

References 133 publications

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“…The upregulation of Srf directly controls the immediate early gene response and is an essential regulator of neuronal‐activity‐induced gene expression (Knoll & Nordheim, 2009). Of note, most of the direct neuronal effects of VEGF‐A—such as neuronal survival in cell culture models of stroke involving oxygen and glucose deprivation (Maiese, 2015) or excitotoxicity (Matsuzaki et al., 2001), hypoxic preconditioning in vitro (Wick et al., 2002), and protection in MCA occlusion models of stroke in vivo (Hayashi, Abe, & Itoyama, 1998)—have been ascribed to activation of Vegfr2 (Farokhi‐Sisakht, Farhoudi, Sadigh‐Eteghad, Mahmoudi, & Mohaddes, 2019; Greenberg & Jin, 2013; Moriyama, Takagi, Hashimura, Itokawa, & Tanonaka, 2013).…”

Section: Discussionmentioning

confidence: 99%

The effect of pentadecapeptide BPC 157 on hippocampal ischemia/reperfusion injuries in rats

et al. 2020

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Background and purpose We focused on the, yet undescribed, therapy effect of the stable gastric pentadecapeptide BPC 157 in hippocampal ischemia/reperfusion injuries, after bilateral clamping of the common carotid arteries in rats. The background is the proven therapy effect of BPC 157 in ischemia/reperfusion injuries in different tissues. Furthermore, there is the subsequent oxidative stress counteraction, particularly when given during reperfusion. The recovering effect it has on occluded vessels, results with activation of the alternative pathways, bypassing the occlusion in deep vein thrombosis. Finally, the BPC 157 therapy benefits with its proposed role as a novel mediator of Roberts’ cytoprotection and bidirectional effects in the gut‐brain axis. Materials and Methods Male Wistar rats underwent bilateral clamping of the common carotid arteries for a 20‐min period. At 30 s thereafter, we applied medication (BPC 157 10 µg/kg; or saline) as a 1 ml bath directly to the operated area, that is, trigonum caroticum. We documented, in reperfusion, the resolution of the neuronal damages sustained in the brain, resolution of the damages reflected in memory, locomotion, and coordination disturbances, with the presentation of the particular genes expression in hippocampal tissues. Results In the operated rats, at 24 and 72 hr of the reperfusion, the therapy counteracted both early and delayed neural hippocampal damage, achieving full functional recovery (Morris water maze test, inclined beam‐walking test, lateral push test). mRNA expression studies at 1 and 24 hr, provided strongly elevated ( Egr1, Akt1, Kras, Src, Foxo, Srf, Vegfr2, Nos3, and Nos1 ) and decreased ( Nos2, Nfkb ) gene expression ( Mapk1 not activated), as a way how BPC 157 may act. Conclusion Together, these findings suggest that these beneficial BPC 157 effects may provide a novel therapeutic solution for stroke.

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Section: Discussionmentioning

confidence: 99%

The effect of pentadecapeptide BPC 157 on hippocampal ischemia/reperfusion injuries in rats

et al. 2020

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“…This complex concept has been the subject of extensive research in recent years, which has resulted in finding that physical exercise [4], environment, cognitive stimulation [5], social interaction and previous pathological conditions all substantially influence the final outcome of this process [3][4][5]. These findings suggest that the process of neuroplasticity is the result of multiple factors, and that its course is personalised, and therefore highly unpredictable.…”

Section: To the Editorsmentioning

confidence: 99%

Neuroplasticity vs. cognitive prediction models in acute ischaemic stroke: limitations must be remembered

Tibocha-Gordon

Morales-Ospina

Lozada-Martínez

et al. 2022

Neurol Neurochir Pol.

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“…Studies performed in recent years point to common points of AD and cerebral ischemia. Cognitive impairment is often found in patients after cerebral ischemic incidents [ 96 ]. The same cognitive deficits have also been shown in animal models of cerebral ischemia [ 97 , 98 ].…”

Section: Neuroinflammation In Admentioning

confidence: 99%

Some Candidate Drugs for Pharmacotherapy of Alzheimer’s Disease

Miziak

Błaszczyk²,

Czuczwar

2021

Pharmaceuticals

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Alzheimer’s disease (AD; progressive neurodegenerative disorder) is associated with cognitive and functional impairment with accompanying neuropsychiatric symptoms. The available pharmacological treatment is of a symptomatic nature and, as such, it does not modify the cause of AD. The currently used drugs to enhance cognition include an N-methyl-d-aspartate receptor antagonist (memantine) and cholinesterase inhibitors. The PUBMED, Medical Subject Heading and Clinical Trials databases were used for searching relevant data. Novel treatments are focused on already approved drugs for other conditions and also searching for innovative drugs encompassing investigational compounds. Among the approved drugs, we investigated, are intranasal insulin (and other antidiabetic drugs: liraglitude, pioglitazone and metformin), bexarotene (an anti-cancer drug and a retinoid X receptor agonist) or antidepressant drugs (citalopram, escitalopram, sertraline, mirtazapine). The latter, especially when combined with antipsychotics (for instance quetiapine or risperidone), were shown to reduce neuropsychiatric symptoms in AD patients. The former enhanced cognition. Procognitive effects may be also expected with dietary antioxidative and anti-inflammatory supplements—curcumin, myricetin, and resveratrol. Considering a close relationship between brain ischemia and AD, they may also reduce post-brain ischemia neurodegeneration. An investigational compound, CN-105 (a lipoprotein E agonist), has a very good profile in AD preclinical studies, and its clinical trial for postoperative dementia is starting soon.

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Cognitive Rehabilitation Improves Ischemic Stroke-Induced Cognitive Impairment: Role of Growth Factors

Cited by 51 publications

References 133 publications

The effect of pentadecapeptide BPC 157 on hippocampal ischemia/reperfusion injuries in rats

The effect of pentadecapeptide BPC 157 on hippocampal ischemia/reperfusion injuries in rats

Neuroplasticity vs. cognitive prediction models in acute ischaemic stroke: limitations must be remembered

Some Candidate Drugs for Pharmacotherapy of Alzheimer’s Disease

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