scholarly journals PPARs in Alzheimer's Disease

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-8 ◽  
Author(s):  
Markus P. Kummer ◽  
Michael T. Heneka
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Peptide ◽  
Peroxisome Proliferator ◽  
Attractive Therapeutic Target ◽  
Ppar Agonists ◽  
The Central Nervous System ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Peroxisome Proliferator Activated Receptors

Peroxisome proliferator-activated receptors (PPARs) are well studied for their peripheral physiological and pathological impact, but they also play an important role for the pathogenesis of various disorders of the central nervous system (CNS) like multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer's, and Parkinson's disease. The observation that PPARs are able to suppress the inflammatory response in peripheral macrophages and in several models of human autoimmune diseases lead to the idea that PPARs might be beneficial for CNS disorders possessing an inflammatory component. The neuroinflammatory response during the course of Alzheimer's disease (AD) is triggered by the neurodegeneration and the deposition of the -amyloid peptide in extracellular plaques. Nonsteroidal anti-inflammatory drugs (NSAIDs) have been considered to delay the onset and reduce the risk to develop Alzheimer's disease, while they also directly activate PPAR. This led to the hypothesis that NSAID protection in AD may be partly mediated by PPAR. Several lines of evidence have supported this hypothesis, using AD-related transgenic cellular and animal models. Stimulation of PPAR receptors by synthetic agonist (thiazolidinediones) inducing anti-inflammatory, anti-amyloidogenic, and insulin sensitising effects may account for the observed effects. Several clinical trials already revealed promising results using PPAR agonists, therefore PPARs represent an attractive therapeutic target for the treatment of AD.

scholarly journals Peroxisome Proliferator-Activated Receptors: A New Ray Of Hope For Parkinson’s Disease

2021 ◽  
Vol 9 (9) ◽  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Peroxisome Proliferator ◽  
Neuroprotective Effects ◽  
In Vivo Models ◽  
Ppar Agonists ◽  
Peroxisome Proliferator Activated Receptors

PD (PD) is a debilitating progressive age-related neurodegenerative disorder that negatively impacts bodily movement. It is the second most common type of neurodegenerative disease after Alzheimer's disease. Although the etiology and pathogenesis of PD remain unknown, a vast body of evidence indicates that oxidative stress, inflammation, apoptosis, mitochondrial dysfunction, and proteasomal dysfunction all play a role in the disease's pathogenesis. Because of the multifactorial nature of the disease, current drug treatment can only offer symptomatic relief and cannot stop or delay the disease progression. The Peroxisome proliferator-activated receptors (PPARs) are the member of the receptor’s superfamily called, nuclear receptors, regulates the growth, differentiation of the tissues, inflammation, mitochondrial function, wound healing, lipid metabolism, and glucose metabolism. Several PPAR agonists have recently been shown to protect neurons from oxidative damage, inflammation, and apoptosis in Alzheimer's disease, PD, Huntington's disease, amyotrophic lateral sclerosis, and multiple sclerosis. We review the research on the neuroprotective effects of PPAR agonists in in-vitro and in-vivo models of PD in this paper. Similarly, the pharmacological mechanism of PPAR agonists' neuroprotective effects is examined. Finally, PPAR agonists exert neuroprotective effects by controlling the expression of a set of genes involved in cell survival processes, suggesting that they may be a potential therapeutic target in crippling neurodegenerative diseases like PD. Keywords: Parkinson’s disease, neuroprotective, neuro inflammatory, oxidative stress, PPAR agonist

Immune modulations and immunotherapies for Alzheimer’s disease: a comprehensive review

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Sara Mahdiabadi ◽  
Sara Momtazmanesh ◽  
George Perry ◽  
Nima Rezaei
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Cognitive Outcomes ◽  
Tau Proteins ◽  
Causal Role ◽  
Wide Range ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Immune Related Genes

Abstract Alzheimer’s disease (AD), the most common cause of dementia, is characterized by progressive cognitive and memory impairment ensued from neuronal dysfunction and eventual death. Intraneuronal deposition of tau proteins and extracellular senile amyloid-β plaques have ruled as the supreme postulations of AD for a relatively long time, and accordingly, a wide range of therapeutics, especially immunotherapies have been implemented. However, none of them resulted in significant positive cognitive outcomes. Especially, the repetitive failure of anti-amyloid therapies proves the inefficiency of the amyloid cascade hypothesis, suggesting that it is time to reconsider this hypothesis. Thus, for the time being, the focus is being shifted to neuroinflammation as a third core pathology in AD. Neuroinflammation was previously considered a result of the two aforementioned phenomena, but new studies suggest that it might play a causal role in the pathogenesis of AD. Neuroinflammation can act as a double-edged sword in the pathogenesis of AD, and the activation of glial cells is indispensable for mediating such attenuating or detrimental effects. The association of immune-related genes polymorphisms with the clinical phenotype of AD as well as the protective effect of anti-inflammatory drugs like nonsteroidal anti-inflammatory drugs supports the possible causal role of neuroinflammation in AD. Here, we comprehensively review immune-based therapeutic approaches toward AD, including monoclonal antibodies and vaccines. We also discuss their efficacy and underlying reasons for shortcomings. Lastly, we highlight the capacity of modulating the neuroimmune interactions and targeting neuroinflammation as a promising opportunity for finding optimal treatments for AD.

scholarly journals Non-Steroidal Anti-Inflammatory Drugs in Alzheimer's Disease and Parkinson's Disease: Reconsidering the Role of Neuroinflammation

2010 ◽  
Vol 3 (6) ◽  
pp. 1812-1841 ◽  
Author(s):  
Amy H. Moore ◽  
Matthew J. Bigbee ◽  
Grace E. Boynton ◽  
Colin M. Wakeham ◽  
Hilary M. Rosenheim ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

A Case-Control Analysis of Nonsteroidal Anti-Inflammatory Drugs and Alzheimer’s Disease: Are They Protective?

2002 ◽  
Vol 21 (2) ◽  
pp. 81-86 ◽  
Author(s):  
C. Wolfson ◽  
A. Perrault ◽  
Y. Moride ◽  
J.M. Esdaile ◽  
L. Abenhaim ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Case Control ◽  
Control Analysis ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Case Control Analysis

scholarly journals Neuroprotective Mechanisms of PPARδ: Modulation of Oxidative Stress and Inflammatory Processes

PPAR Research ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Caroline I. Schnegg ◽  
Mike E. Robbins
Keyword(s):  
Energy Homeostasis ◽  
Peroxisome Proliferator ◽  
Cellular Processes ◽  
Wide Range ◽  
Inflammatory Processes ◽  
The Central Nervous System ◽  
Chronic Injuries ◽  
Neuroprotective Efficacy ◽  
Anti Inflammatory ◽  
Peroxisome Proliferator Activated Receptors

Peroxisome proliferator-activated receptors (PPARα,δ, andγ) are ligand-activated transcription factors that regulate a wide range of cellular processes, including inflammation, proliferation, differentiation, metabolism, and energy homeostasis. All three PPAR subtypes have been identified in the central nervous system (CNS) of rodents. While PPARαand PPARγare expressed in more restricted areas of the CNS, PPARδis ubiquitously expressed and is the predominant subtype. Although data regarding PPARδare limited, studies have demonstrated that administration of PPARδagonists confers neuroprotection following various acute and chronic injuries to the CNS, such as stroke, multiple sclerosis, and Alzheimer's disease. The antioxidant and anti-inflammatory properties of PPARδagonists are thought to underly their neuroprotective efficacy. This review will focus on the putative neuroprotective benefits of therapeutically targeting PPARδin the CNS, and specifically, highlight the antioxidant and anti-inflammatory functions of PPARδagonists.

Anti-Inflammatory Drugs and Risk of Alzheimer's Disease: An Updated Systematic Review and Meta-Analysis

2015 ◽  
Vol 44 (2) ◽  
pp. 385-396 ◽  
Author(s):  
Jun Wang ◽  
Lan Tan ◽  
Hui-Fu Wang ◽  
Chen-Chen Tan ◽  
Xiang-Fei Meng ◽  
...  
Keyword(s):  
Systematic Review ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Meta Analysis ◽  
Inflammatory Drugs ◽  
Anti Inflammatory
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