Exendin-4 for Parkinson's disease

Salazar, Felipe Esparza; Toledo, Alma R. Lezama; Rivera-Monroy, Germán; Borlongan, Cesario V.

doi:10.4103/bc.bc_21_21

Cited by 9 publications

(4 citation statements)

References 20 publications

(23 reference statements)

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“…As N-palmitoyl serinol acts as an agonist for GPR119, we aimed to confirm whether it has a similar neuroprotective effect to the GLP-1 family of proteins that has recently attracted attention [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

The Neuroprotective Effect of NEUROMIDE, a Compound Bioidentical to Commensal Bacteria Metabolites

Seo¹,

Tak²,

Park³

et al. 2022

Life

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GPR119 is a novel cannabinoid receptor that is primarily expressed in the pancreas and gastrointestinal tract and has beneficial effects on glucose homeostasis exerted through the stimulation of GLP-1 secretion, as demonstrated in the rodent brain. GLP-1 also has important anti-inflammatory effects in chronic inflammatory diseases, including type 1 and 2 diabetes, asthma, psoriasis, and neurodegenerative disorders. Recently, there has been increasing interest in the effect of the gut microbiota on both the gut and the brain. However, few studies have examined how gut microbes affect brain health through the endocannabinoid system. NEUROMIDE is a compound that shares a bioidentical structure with certain commensal bacterial metabolites, acting as a CB1 and GPR119 agonist. In an in vitro system exposed to reactive oxygen species (ROS), pretreatment with NEUROMIDE resulted in a significant increase in cell viability. The ROS-exposed system also showed decreased acetylcholine and an increase in inflammatory cytokines such as IL-1β, changes that were counteracted in a dose-dependent manner in the NEUROMIDE treatment groups. To measure the effectiveness of NEUROMIDE in an in vivo system, we used scopolamine-treated mice as a neurodegenerative disease model and performed a series of passive avoidance tests to observe and quantify the cognitive impairment of the mice. Mice in the NEUROMIDE treatment group had increased latency time, thus indicating an improvement in their cognitive function. Furthermore, the NEUROMIDE treatment groups showed dose-dependent increases in acetylcholine along with decreases in TNF-α and IL-1β. These experiments demonstrate that NEUROMIDE can potentially be used for neuroprotection and the improvement of cognitive ability.

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Section: Discussionmentioning

confidence: 99%

The Neuroprotective Effect of NEUROMIDE, a Compound Bioidentical to Commensal Bacteria Metabolites

Seo¹,

Tak²,

Park³

et al. 2022

Life

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“…In a Phase II clinical trial, exenatide, an agonist of the GLP-1 receptor, showed great protective effects in PD patients. 572 NLY01, a different GLP-1 receptor agonist that can protect dopaminergic neurons from inflammatory responses elicited by glial cells, 573 has been enrolled recently in a Phase II clinical trial. The GLP-1 analogue semaglutide showed multiple benefits in a MPTP-induced PD mouse model: it reduced the accumulation of α-synuclein, alleviated chronic inflammation, attenuated the peroxidation of lipid, inhibited the mitophagy related signaling and increased the expression of glial cell line-derived neurotrophic factor (GDNF).…”

Section: Immune-directed Therapiesmentioning

confidence: 99%

Role of neuroinflammation in neurodegeneration development

Zhang

Xiao

Mao

et al. 2023

Sig Transduct Target Ther

212

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Studies in neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease and Amyotrophic lateral sclerosis, Huntington’s disease, and so on, have suggested that inflammation is not only a result of neurodegeneration but also a crucial player in this process. Protein aggregates which are very common pathological phenomenon in neurodegeneration can induce neuroinflammation which further aggravates protein aggregation and neurodegeneration. Actually, inflammation even happens earlier than protein aggregation. Neuroinflammation induced by genetic variations in CNS cells or by peripheral immune cells may induce protein deposition in some susceptible population. Numerous signaling pathways and a range of CNS cells have been suggested to be involved in the pathogenesis of neurodegeneration, although they are still far from being completely understood. Due to the limited success of traditional treatment methods, blocking or enhancing inflammatory signaling pathways involved in neurodegeneration are considered to be promising strategies for the therapy of neurodegenerative diseases, and many of them have got exciting results in animal models or clinical trials. Some of them, although very few, have been approved by FDA for clinical usage. Here we comprehensively review the factors affecting neuroinflammation and the major inflammatory signaling pathways involved in the pathogenicity of neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and Amyotrophic lateral sclerosis. We also summarize the current strategies, both in animal models and in the clinic, for the treatment of neurodegenerative diseases.

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“…Embora várias investigações pré-clínicas tenham relatado potencial neuroprotetor dos inibidores de DPP4 em vários distúrbios neurodegenerativos. A ativação de GLP1 mediada por DPP4 tem relação direta com a neurotransmissão monoaminérgica e a síntese de dopamina e, portanto, pode ter um papel importante na patologia da DP (Esparza-Salazar et al, 2021). No entanto, relatórios de ensaios clínicos pré-clínicos e randomizados controlados sugerem que a ativação do receptor GLP1 reduz o risco da DP e melhora as funções motoras.…”

Section: Inibidores Da Dipeptidil Peptidase 4 (Dpp4)unclassified