Peptides isolated from animal venom as a platform for new therapeutics for the treatment of Alzheimer's disease

Camargo, Luana Cristina; Campos, Gabriel Avohay Alves; Galante, Priscilla; Biolchi, Andréia Mayer; Gonçalves, Jacqueline Coimbra; Lopes, Kamila Soares; Mortari, Márcia Renata

doi:10.1016/j.npep.2017.11.010

Cited by 14 publications

(8 citation statements)

References 121 publications

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“…An interesting solution for new AD therapeutics was recently proposed. Camargo et al [121] suggested that peptides isolated from animal venoms could be new weapons in a battle against Alzheimer’s disease. Suggested venoms are from animals like for example Daboia russelli russelli , a subspecies of Russell’s viper found in eastern India [122], Buthus martensii Karsch scorpion [123], Eastern Green Mamba ( Dendroaspis angusticeps ) [124] and Taiwan banded krait ( Bungarus multicinctus ) [125].…”

Section: Treatment Strategiesmentioning

confidence: 99%

Bridging the Gap between Alzheimer’s Disease and Alzheimer’s-like Diseases in Animals

Gołaszewska

Bik

Motyl

et al. 2019

IJMS

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The average life span steadily grows in humans and in animals kept as pets or left in sanctuaries making the issue of elderly-associated cognitive impairment a hot-spot for scientists. Alzheimer’s disease (AD) is the most prevalent cause of progressive mental deterioration in aging humans, and there is a growing body of evidence that similar disorders (Alzheimer’s-like diseases, ALD) are observed in animals, more than ever found in senescent individuals. This review reveals up to date knowledge in pathogenesis, hallmarks, diagnostic approaches and modalities in AD faced up with ALD related to different animal species. If found at necropsy, there are striking similarities between senile plaques (SP) and neurofibrillary tangles (NFT) in human and animal brains. Also, the set of clinical symptoms in ALD resembles that observed in AD. At molecular and microscopic levels, the human and animal brain histopathology in AD and ALD shows a great resemblance. AD is fatal, and the etiology is still unknown, although the myriad of efforts and techniques were employed in order to decipher the molecular mechanisms of disease onset and its progression. Nowadays, according to an increasing number of cases reported in animals, apparently, biochemistry of AD and ALD has a lot in common. Described observations point to the importance of extensive in vivo models and extensive pre-clinical studies on aging animals as a suitable model for AD disease.

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Section: Treatment Strategiesmentioning

confidence: 99%

Bridging the Gap between Alzheimer’s Disease and Alzheimer’s-like Diseases in Animals

Gołaszewska

Bik

Motyl

et al. 2019

IJMS

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“…Some reports asserted that the amyloid precursor protein (transmembrane protein) isoforms were expressed in peripheral tissues (almost all body cells) and also have mitogenic, motogenic and cell-cell adhesion function in keratinocytes. Thus, different body cells contributed to the production of the circulating Aβ [12,33,45] . T3DM sections displayed statistically significant different results comparing to control groups.…”

Section: Group IV (Zingiber)mentioning

confidence: 99%

“…In some sections, diffuse strong membranous and intracellular fluorescence was detected in basal and some suprabasal epithelial cell layers as well as in the palatine acinar cells. In explanation of these findings, the cerebral amyloid deposits in a neurodegenerative condition like T3DM were evidenced to be associated with increased Aβ levels shown in peripheral tissues such as skin, skeletal muscle, heart, liver and thyroid secondary to the abnormal calcium fluxes and overexpression of pathogenic APP form resulting in defective oxidative metabolism [12,33,46] . The mitochondrial alterations along with reduced ATP levels were associated with intracellular A-aggregates which preceded the extracellular Aβ deposition [47] .…”

Section: Group IV (Zingiber)mentioning

confidence: 99%

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The influence of Zingiber officinale Roscoe on the histological changes of soft palatal mucosa in streptozotocin-induced type 3 diabetes rat model

Saad

2019

Egyptian Journal of Histology

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Background: Zingiber officinale Roscoe presents valuable outcomes in some neurodegenerative diseases. Objective: This study aimed to evaluate Zingiber oil extract efficacy in the regression of Type3 diabetes mellitus (T3DM) induced in rat model. Methodology: 28 adult male albino rats were divided into four equal groups: Control-ve group received no injections; Control+ve group received a single bilateral intra-cerebroventricular (ICV) injection of sterile 0.9% saline, T3DM group received a single bilateral ICV injection of streptozotocin (3 mg/kg) dissolved in sterile 0.9% saline; Zingiber treated group five weeks after ICV-STZ, received orally 100 mg/kg/day Zingiber oil extract for two months. Soft palate oral mucosal sections were processed for H&E, fluorescence staining (using thioflavin-T dye) and immunohistochemical (using anticaspase-3 and anti-VEGF antibodies) examination. Results: Both control groups were almost identical. Some T3DM sections histopathologically displayed inflammatory signs represented by cloudy swelling of keratinocytes, nuclear degenerative signs, apparently increased apoptotic keratinocytes, subepithelial degeneration, chronic inflammatory infiltrates, congested dilated blood vessels, hyperplasia and dilatation of palatal glandular acini and excretory duct. Irregular and decreased palatal fungiform papillae with few vacuolated taste cells were illustrated. Comparing to control groups, significant strong diffuse thioflavin-T fluorescence in oral epithelium, palatal acini, endothelium of blood vessels along with subepithelial amyloid deposits in some T3DM specimens were detected. Likewise, caspase-3 immunoreactivity in oral epithelial and connective tissue cells significantly increased in T3DM group. Similarly, significant positivity to VEGF in oral epithelium and in the significantly increased blood vessels in wall thickness and distribution were exhibited in T3DM sections. All T3DM results were significantly restored in Zingiber group except for the low significant decrease of caspase-3 reactivity in this group. Conclusions: It was concluded that Zingiber oil extract was an appropriate selected approach to ameliorate the possible T3DM associated peripheral tissue insults but most probably in a higher dose or prolonged supplementation.

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“…Current therapies for AD offer discrete benefits for clinical symptoms; however, they do not prevent the continued degeneration of neuronal cells. Therefore, novel therapeutic strategies need to be further investigated (Camargo et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Genome-wide RNA sequencing analysis reveals that IGF-2 attenuates memory decline, oxidative stress and amyloid plaques in an Alzheimer’s disease mouse model (AD) by activating the PI3K/AKT/CREB signaling pathway

Xia

Zhu

Zhao

et al. 2019

Int. Psychogeriatr.

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Objectives:Alzheimer’s Disease (AD), characterized by deficits in memory and cognition and by behavioral impairment, is a progressive neurodegenerative disorder that influences more than 47 million people worldwide. Currently, no available drug is able to stop AD progression. Therefore, novel therapeutic strategies need to be investigated.Measurements:We analyzed the RNA sequencing data (RNA-seq) derived from the Gene Expression Omnibus (GEO) database to identify the differentially expressed mRNAs in AD. The AD mouse model Tg2576 was used to verify the effects of IGF-2. The Morris Water Maze was administered to test the role of IGF-2 in memory consolidation. In addition, we quantified cell apoptosis by the TUNEL assay. The levels of amyloid plaques and the levels of Aβ40 and Aβ42 in the hippocampus were also determined by immunohistochemistry and ELISA, respectively.Results:RNA-seq analysis revealed that IGF-2 was remarkably reduced in AD. The expression of the upstream genes PI3K and AKT and the downstream gene CREB in the PI3K signaling pathway was significantly increased in the hippocampus of Tg2576 mice cells treated with IGF-2. The Morris water maze test showed that IGF-2 improved memory consolidation in Tg2576 mice. The activity of caspase-3 was decreased in Tg2576 mice treated with IGF-2. Amyloid plaques in the hippocampus were reduced, and the levels of Aβ40 and Aβ42 were decreased. The above effects of IGF-2 on AD were blocked when the PI3K signaling pathway inhibitor wortmannin was added.Conclusions:IGF-2 attenuates memory decline, oxidative stress, cell apoptosis and amyloid plaques in the AD mouse model Tg2576 by activating the PI3K/AKT/CREB signaling pathway.

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Peptides isolated from animal venom as a platform for new therapeutics for the treatment of Alzheimer's disease

Cited by 14 publications

References 121 publications

Bridging the Gap between Alzheimer’s Disease and Alzheimer’s-like Diseases in Animals

Bridging the Gap between Alzheimer’s Disease and Alzheimer’s-like Diseases in Animals

The influence of Zingiber officinale Roscoe on the histological changes of soft palatal mucosa in streptozotocin-induced type 3 diabetes rat model

Genome-wide RNA sequencing analysis reveals that IGF-2 attenuates memory decline, oxidative stress and amyloid plaques in an Alzheimer’s disease mouse model (AD) by activating the PI3K/AKT/CREB signaling pathway

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