PPARγ and Cognitive Performance

Castelli, Vanessa; Catanesi, Mariano; Antonosante, Andrea; Dominguez-Benot, Reyes; Ippoliti, Roberto; Benedetti, Elisabetta; Cimini, Annamaria

doi:10.3390/ijms20205068

Cited by 38 publications

(31 citation statements)

References 170 publications

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“…A study demonstrated that among antipsychotics-treated patients with schizophrenia, there was a significant association of PPAR γ gene in altered glucose levels and psychosis profile( Liu et al, 2014 ). Arulmozhi suggested a possible role of PPAR agonists in antipsychotic-induced insulin resistance rodents( Arulmozhi et al, 2006 ), and such medications were related with BDNF levels in schizophrenia, which might play a part in the management of this illness( d'Angelo et al, 2019 ). In a small pilot clinical trial, rosiglitazone treatment for 8 weeks failed to show the potential cognitive benefit in schizophrenia patients treated with clozapine( Yi et al, 2012 ).…”

Section: Repurposing Of Anti-diabetic Agents As a Potential Treatmentmentioning

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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Section: Repurposing Of Anti-diabetic Agents As a Potential Treatmentmentioning

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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“…The mechanisms underlying neurodegeneration are still unclear, but it would be relevant for developing new therapeutic approaches. Mitochondria are critical regulators of neuronal cell death and survival, especially during aging; mitochondrial energy impairment induces decreased ATP production, altered calcium buffering, and improved reactive ROS production [ 4 , 5 , 6 ]. Low ROS concentrations are essential for normal cellular signaling, whereas higher levels and long-time exposure cause damage to cellular macromolecules such as DNA, lipids and proteins, and accelerates the mutation rate of mitochondrial DNA (mtDNA) [ 1 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

MicroRNAs Dysregulation and Mitochondrial Dysfunction in Neurodegenerative Diseases

Catanesi

d’Angelo

Tupone

et al. 2020

IJMS

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Neurodegenerative diseases are debilitating and currently incurable conditions causing severe cognitive and motor impairments, defined by the progressive deterioration of neuronal structure and function, eventually causing neuronal loss. Understand the molecular and cellular mechanisms underlying these disorders are essential to develop therapeutic approaches. MicroRNAs (miRNAs) are short non-coding RNAs implicated in gene expression regulation at the post-transcriptional level. Moreover, miRNAs are crucial for different processes, including cell growth, signal transmission, apoptosis, cancer and aging-related neurodegenerative diseases. Altered miRNAs levels have been associated with the formation of reactive oxygen species (ROS) and mitochondrial dysfunction. Mitochondrial dysfunction and ROS formation occur in many neurodegenerative diseases such as Alzheimer’s, Parkinson’s and Huntington’s diseases. The crosstalk existing among oxidative stress, mitochondrial dysfunction and miRNAs dysregulation plays a pivotal role in the onset and progression of neurodegenerative diseases. Based on this evidence, in this review, with a focus on miRNAs and their role in mitochondrial dysfunction in aging-related neurodegenerative diseases, with a focus on their potential as diagnostic biomarkers and therapeutic targets.

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“…Beyond synaptic pruning, Aβ is associated with a loss of synaptic integrity, where the neurotransmitters, such as glutamate, can leak out of the synapse and activate extra-synaptic receptors (Hardingham and Bading, 2010;Parsons and Raymond, 2014). It has been hypothesized that the high level of glutamate release by astrocytes leads to an increase in extra-synaptic glutamate signaling and excitotoxicity (Sattler et al, 2000;Hardingham and Bading, 2010;Parsons and Raymond, 2014;Wang and Reddy, 2016), which is hypothesized to both induce ER stress (Sokka et al, 2007;Concannon et al, 2008) and activate pro-apoptotic pathways (Hardingham et al, 2002), while antagonizing prosurvival pathways, particularly brain-derived neurotrophic factor (BDNF) signaling, leading to neuron death (Hardingham et al, 2002;Hardingham and Bading, 2010;Parsons and Raymond, 2014;Wang and Reddy, 2016). Thus, the accumulation of Aβ Genes in bold have been previously found in AD GWAS.…”

Section: Discussionmentioning

confidence: 99%

System-Level Analysis of Alzheimer’s Disease Prioritizes Candidate Genes for Neurodegeneration

et al. 2021

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Alzheimer’s disease (AD) is a debilitating neurodegenerative disorder. Since the advent of the genome-wide association study (GWAS) we have come to understand much about the genes involved in AD heritability and pathophysiology. Large case-control meta-GWAS studies have increased our ability to prioritize weaker effect alleles, while the recent development of network-based functional prediction has provided a mechanism by which we can use machine learning to reprioritize GWAS hits in the functional context of relevant brain tissues like the hippocampus and amygdala. In parallel with these developments, groups like the Alzheimer’s Disease Neuroimaging Initiative (ADNI) have compiled rich compendia of AD patient data including genotype and biomarker information, including derived volume measures for relevant structures like the hippocampus and the amygdala. In this study we wanted to identify genes involved in AD-related atrophy of these two structures, which are often critically impaired over the course of the disease. To do this we developed a combined score prioritization method which uses the cumulative distribution function of a gene’s functional and positional score, to prioritize top genes that not only segregate with disease status, but also with hippocampal and amygdalar atrophy. Our method identified a mix of genes that had previously been identified in AD GWAS including APOE, TOMM40, and NECTIN2(PVRL2) and several others that have not been identified in AD genetic studies, but play integral roles in AD-effected functional pathways including IQSEC1, PFN1, and PAK2. Our findings support the viability of our novel combined score as a method for prioritizing region- and even cell-specific AD risk genes.

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PPARγ and Cognitive Performance

Cited by 38 publications

References 170 publications

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

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

MicroRNAs Dysregulation and Mitochondrial Dysfunction in Neurodegenerative Diseases

System-Level Analysis of Alzheimer’s Disease Prioritizes Candidate Genes for Neurodegeneration

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