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doi:10.13040/ijpsr.0975-8232.7(8).3233-42

Cited by 2 publications

(2 citation statements)

References 37 publications

(51 reference statements)

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“…Contrary to their results indicating no degeneration in CA3, our results showed neurodegeneration in the CA3 and hilus areas of the hippocampus. Many previous studies have also demonstrated the same results following the ICV injection of Aβ 25-35 (Asha & Sumathi, 2016;Mazzola, Micale, & Drago, 2003). CA1 and hilus areas are the most vulnerable areas of the hippocampus in AD.…”

Section: Discussionsupporting

confidence: 68%

Protective Role Of Apigenin Against Aβ25-35 Toxicity Via Inhibition Of Mitochondrial Cytochrome C Release

Nikbakht

Khadem

Haghani

et al. 2019

Basic Clin. Neurosci. J.

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Cognitive dysfunction is the most common problem of patients with Alzheimer Disease (AD). The pathological mechanism of cognitive impairment in AD may contribute to neuronal loss, synaptic dysfunction, and alteration in neurotransmitters receptors. Mitochondrial synapses dysfunction due to the accumulation of Amyloid Beta (Aβ) is one of the earliest pathological features of AD. The flavone apigenin has been reported to play some protective roles in AD through the anti-oxidative and anti-inflammatory properties. This study aimed at investigating the effects of apigenin on spatial working memory and neural protection by restoring mitochondrial dysfunction and inhibition of caspase 9. Methods: Intracerebroventricular (ICV) microinjection of Aβ 25-35 was used for AD modeling. Working memory was assessed 21 days later using the Y maze test. Neuronal loss was detected in the hilar area of the hippocampus using Nissl and Fluoro-jade B staining, whereas immunohistochemistry was used to illustrate cytochrome c positive cells and caspase 9. Results: The results revealed that apigenin significantly ameliorated spatial working memory. It also significantly reduced the number of degenerative neurons in the hilus area. Apigenin almost completely blocked the release of cytochrome c and caspase 9 in hilus. Conclusion: Apigenin may improve the spatial working memory deficits and neuronal degeneration through the amelioration of the mitochondrial dysfunction.

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Section: Discussionsupporting

confidence: 68%

Protective Role Of Apigenin Against Aβ25-35 Toxicity Via Inhibition Of Mitochondrial Cytochrome C Release

Nikbakht

Khadem

Haghani

et al. 2019

Basic Clin. Neurosci. J.

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“…The naturally occurring flavonoids including curcumin and EGCG are reported to restrain Aβ-mediated BACE1 upregulation in the neuronal cultures (Shimmyo et al, 2008). Isorhamnetin has shown a neuroprotective effect against Aβ-induced memory impairment (Asha and Sumathi, 2016). It enhances cognition and memory by uplifting antioxidant defense system, cholinergic signaling, and synaptic plasticity (Ishola et al, 2019).…”

Section: Pathological Aspects and Drug Targetsmentioning

confidence: 99%

Flavonoids as Prospective Neuroprotectants and Their Therapeutic Propensity in Aging Associated Neurological Disorders

Ayaz

Sadiq

Junaid

et al. 2019

Front. Aging Neurosci.

262

184

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Modern research has revealed that dietary consumption of flavonoids and flavonoids-rich foods significantly improve cognitive capabilities, inhibit or delay the senescence process and related neurodegenerative disorders including Alzheimer’s disease (AD). The flavonoids rich foods such as green tea, cocoa, blue berry and other foods improve the various states of cognitive dysfunction, AD and dementia-like pathological alterations in different animal models. The mechanisms of flavonoids have been shown to be mediated through the inhibition of cholinesterases including acetylcholinesterase (AChE), and butyrylcholinesterase (BChE), β-secretase (BACE1), free radicals and modulation of signaling pathways, that are implicated in cognitive and neuroprotective functions. Flavonoids interact with various signaling protein pathways like ERK and PI3-kinase/Akt and modulate their actions, thereby leading to beneficial neuroprotective effects. Moreover, they enhance vascular blood flow and instigate neurogenesis particularly in the hippocampus. Flavonoids also hamper the progression of pathological symptoms of neurodegenerative diseases by inhibiting neuronal apoptosis induced by neurotoxic substances including free radicals and β-amyloid proteins (Aβ). All these protective mechanisms contribute to the maintenance of number, quality of neurons and their synaptic connectivity in the brain. Thus flavonoids can thwart the progression of age-related disorders and can be a potential source for the design and development of new drugs effective in cognitive disorders.

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Cited by 2 publications

References 37 publications

Protective Role Of Apigenin Against Aβ25-35 Toxicity Via Inhibition Of Mitochondrial Cytochrome C Release

Protective Role Of Apigenin Against Aβ25-35 Toxicity Via Inhibition Of Mitochondrial Cytochrome C Release

Flavonoids as Prospective Neuroprotectants and Their Therapeutic Propensity in Aging Associated Neurological Disorders

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