Neuroprotective effect of PPAR alpha and gamma agonists in a mouse model of amyloidogenesis through modulation of the Wnt/beta catenin pathway via targeting alpha- and beta-secretases

Assaf, Naglaa; El-Shamarka, Marwa  EA; Salem, Neveen A.; Khadrawy, Yasser A.; Sayed, Nesrine S El

doi:10.1016/j.pnpbp.2019.109793

Cited by 33 publications

(22 citation statements)

References 80 publications

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“…The efficacy of Pioglitazone can be enhanced by combination therapy, as it was reported that combined treatment in AD model mice with Pioglitazone and Fenofibrate, a fibric acid derivative which is used to treat abnormal blood lipid levels, for 21 days in a mice model of AD showed better results than monotherapy. This included recovering the reduced levels of Wnt, β-catenin and PPARα/ β, and increased levels of α- and β-secretase, and also significantly improving the impaired memory and cognition, as indicated by behavioral tests [ 80 ].…”

Section: Pioglitazonementioning

confidence: 99%

Comparative Analysis of Aducanumab, Zagotenemab and Pioglitazone as Targeted Treatment Strategies for Alzheimer’s Disease

Abyadeh

Gupta

et al. 2021

Aging and disease

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Section: Pioglitazonementioning

confidence: 99%

Comparative Analysis of Aducanumab, Zagotenemab and Pioglitazone as Targeted Treatment Strategies for Alzheimer’s Disease

Abyadeh

Gupta

et al. 2021

Aging and disease

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“…In the same line, a recent report showed that targeting PPAR-α with fenofibrate and PPAR-γ with PIO during 21 days ameliorated memory impairment induced by Aβ 1−40 i.c.v injection. Additionally, authors found the Wnt/β catenin to be enhanced with the treatment, proposing this signaling pathway relevant for neuron plasticity and synaptic remodeling altered in AD and mood disorders to be involved (Assaf et al, 2020).…”

Section: Ppar Agonistsmentioning

confidence: 99%

Inflammation and Insulin Resistance as Risk Factors and Potential Therapeutic Targets for Alzheimer’s Disease

et al. 2021

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Overnutrition and modern diets containing high proportions of saturated fat are among the major factors contributing to a low-grade state of inflammation, hyperglycemia and dyslipidemia. In the last decades, the global rise of type 2 diabetes and obesity prevalence has elicited a great interest in understanding how changes in metabolic function lead to an increased risk for premature brain aging and the development of neurodegenerative disorders such as Alzheimer’s disease (AD). Cognitive impairment and decreased neurogenic capacity could be a consequence of metabolic disturbances. In these scenarios, the interplay between inflammation and insulin resistance could represent a potential therapeutic target to prevent or ameliorate neurodegeneration and cognitive impairment. The present review aims to provide an update on the impact of metabolic stress pathways on AD with a focus on inflammation and insulin resistance as risk factors and therapeutic targets.

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“…Monotherapy or combination of pioglitazone and exenatide improved cognitive function, decreased hippocampal neurodegeneration and reduced microglia overexpression in insulin resistant rats( Gad et al, 2016 ). In a mouse model of AD, pioglitazone and fenofibrate combined treatment ameliorated memory and cognitive impairment via modulation of the Wnt/beta catenin pathway, accompanied with a reduction in neuronal damage( Assaf et al, 2020 ). Pioglitazone could rescue impaired synaptic deficits and spatial memory in AD transgenic mice through inhibiting cyclin-dependent kinase 5 activity and reversing Aβ-induced dendritic spine loss( Chen et al, 2015 ).…”

Section: Repurposing Of Anti-diabetic Agents As a Potential Treatment Targeting Cognitive Function In Ad And Schizophreniamentioning

confidence: 99%

Repurposing of Anti-Diabetic Agents as a New Opportunity to Alleviate Cognitive Impairment in Neurodegenerative and Neuropsychiatric Disorders

Chen

Cao

et al. 2021

Front. Pharmacol.

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Cognitive impairment is a shared abnormality between type 2 diabetes mellitus (T2DM) and many neurodegenerative and neuropsychiatric disorders, such as Alzheimer’s disease (AD) and schizophrenia. Emerging evidence suggests that brain insulin resistance plays a significant role in cognitive deficits, which provides the possibility of anti-diabetic agents repositioning to alleviate cognitive deficits. Both preclinical and clinical studies have evaluated the potential cognitive enhancement effects of anti-diabetic agents targeting the insulin pathway. Repurposing of anti-diabetic agents is considered to be promising for cognitive deficits prevention or control in these neurodegenerative and neuropsychiatric disorders. This article reviewed the possible relationship between brain insulin resistance and cognitive deficits. In addition, promising therapeutic interventions, especially current advances in anti-diabetic agents targeting the insulin pathway to alleviate cognitive impairment in AD and schizophrenia were also summarized.

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Neuroprotective effect of PPAR alpha and gamma agonists in a mouse model of amyloidogenesis through modulation of the Wnt/beta catenin pathway via targeting alpha- and beta-secretases

Cited by 33 publications

References 80 publications

Comparative Analysis of Aducanumab, Zagotenemab and Pioglitazone as Targeted Treatment Strategies for Alzheimer’s Disease

Comparative Analysis of Aducanumab, Zagotenemab and Pioglitazone as Targeted Treatment Strategies for Alzheimer’s Disease

Inflammation and Insulin Resistance as Risk Factors and Potential Therapeutic Targets for Alzheimer’s Disease

Repurposing of Anti-Diabetic Agents as a New Opportunity to Alleviate Cognitive Impairment in Neurodegenerative and Neuropsychiatric Disorders

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