Involvement of glucose related energy crisis and endoplasmic reticulum stress: Insinuation of streptozotocin induced Alzheimer's like pathology

Biswas, Joyshree; Gupta, Sonam; Verma, Dinesh; Gupta, Parul; Singh, A. K.; Tiwari, Shubhangini; Goswami, Poonam; Sharma, Sharad; Singh, Sarika

doi:10.1016/j.cellsig.2017.10.018

Cited by 44 publications

(44 citation statements)

References 55 publications

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“…FDG-PET studies in rats detected glucose hypometabolism starting from 3 weeks following STZ-icv treatment onward (Chen et al 2018a, b;Knezovic et al 2018;Babic Perhoc et al 2019), which was observed also in STZ-icv treated monkeys after 6 and 12 weeks . Regarding the alterations of GLUTs, consistent findings on decreased levels of GLUT1 and GLUT3 were detected in the brain of the STZ-icv rat model starting from 1 week following treatment (Table 1) Biswas et al 2018). GLUT3 was found additionally decreased 1 month after STZ treatment (Table 1) .…”

Section: Time Course Of the Appearance Of Insulin Signalling Dysfunctsupporting

confidence: 71%

Shared cerebral metabolic pathology in non-transgenic animal models of Alzheimer's and Parkinson's disease

et al. 2020

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Parkinson's disease (PD) and Alzheimer's disease (AD) are the most common chronic neurodegenerative disorders, characterized by motoric dysfunction or cognitive decline in the early stage, respectively, but often by both symptoms in the advanced stage. Among underlying molecular pathologies that PD and AD patients have in common, more attention is recently paid to the central metabolic dysfunction presented as insulin resistant brain state (IRBS) and altered cerebral glucose metabolism, both also explored in animal models of these diseases. This review aims to compare IRBS and alterations in cerebral glucose metabolism in representative non-transgenic animal PD and AD models. The comparison is based on the selectivity of the neurotoxins which cause experimental PD and AD, towards the cellular membrane and intracellular molecular targets as well as towards the selective neurons/non-neuronal cells, and the particular brain regions. Mitochondrial damage and coexpression of insulin receptors, glucose transporter-2 and dopamine transporter on the membrane of particular neurons as well as astrocytes seem to be the key points which are further discussed in a context of alterations in insulin signalling in the brain and its interaction with dopaminergic transmission, particularly regarding the time frame of the experimental AD/ PD pathology appearance and the correlation with cognitive and motor symptoms. Such a perspective provides evidence on IRBS being a common underlying metabolic pathology and a contributor to neurodegenerative processes in representative non-transgenic animal PD and AD models, instead of being a direct cause of a particular neurodegenerative disorder.Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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Section: Time Course Of the Appearance Of Insulin Signalling Dysfunctsupporting

confidence: 71%

Shared cerebral metabolic pathology in non-transgenic animal models of Alzheimer's and Parkinson's disease

et al. 2020

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“…CHOP is a key molecule in the downstream of PERK, and ER stress can be mediated by the PERK-CHOP pathway [11]. Caspase-12 is another marker of ER stress which is cleaved into active fragment on ER stress [22].The augment of these ER stress markers is considered to correlate with increased calcium level and directly destroys the balance of calcium homeostasis which is another important characteristic of AD [5,12,16]. Results in our study showed the decrease in the expression of GRP78, CHOP and cleaved caspase-12 after treatment of schisandrin which indicated the positive effect of schisandrin on ER stress.…”

Section: Discussionmentioning

confidence: 99%

“…Alzheimer's disease (AD) is a typical neurodegenerative disorder that mainly occurs among the older people [4,5]. According to the latest report, approximately 44 million people are suffering from the AD which leads to an increasingly economic burden for society [4].…”

Section: Introductionmentioning

confidence: 99%

Schisandrin ameliorates cognitive deficits, endoplasmic reticulum stress and neuroinflammation in streptozotocin (STZ)-induced Alzheimer’s disease rats

et al. 2020

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Schisandrin, an active component extracted from Schisandra chinensis (Turcz.) Baill has been reported to alleviate the cognitive impairment in neurodegenerative disorder like Alzheimer's disease (AD). However, the mechanism by which schisandrin regulates the cognitive decline is still unclear. In our study, intracerebroventricular injection of streptozotocin (STZ) was employed to establish AD model in male Wistar rats, and indicated dose of schisandrin was further administered. The Morris water maze test was performed to evaluate the ability of learning and memory in rats with schisandrin treatment. The results indicated that schisandrin improved the capacity of cognition in STZ-induced rats. The contents of pro-inflammatory cytokines in brain tissue were determined by ELISA, and the expressions of these cytokines were assessed by western-blot and immunohistochemistry. The results showed that treatment of schisandrin significantly reduced the production of inflammation mediators including tumor necrosis factor-α, interleukin-1β and interleukin-6. Further study suggested a remarkable decrease in the expressions of ER stress maker proteins like C/EBP-homologous protein, glucose-regulated protein 78 and cleaved caspase-12 in the presence of schisandrin, meanwhile the up-regulation of sirtuin 1 (SIRT1) was also observed in the same group. Additionally, the results of western-blot and EMSA demonstrated that schisandrin inhibited NF-κB signaling in the brain of STZ-induced rats. In conclusion, schisandrin ameliorated STZ-induced cognitive dysfunction, ER stress and neuroinflammation which may be associated with up-regulation of sirtuin 1 (SIRT1). Our study provides novel mechanisms for the neuroprotective effect of 3 schisandrin in AD treatment.

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“…It has been postulated that there is an interrelationship connexin 43, an increase in calcium levels and induction of ER stress. Indeed, in icv injection of streptozotocin-induced Alzheimer's disease model, a correlation was described between increase in calcium levels, development of ER stress (increase in expression of ER stress markers like GRP78, GADD), activation of astrocytes and increase in the expression of connexin 43 [66,67]. There have been other studies showing the correlation in development of ER stress and increase in the expression of connexin 43 in different diseases [68].…”

Section: Increase In Calcium and Endoplasmic Reticulum Stressmentioning

confidence: 99%

Astroglial connexins and cognition: memory formation or deterioration?

Yang

et al. 2020

Bioscience Reports

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Connexins are the membrane proteins that form high-conductance plasma membrane channels and are the important constituents of gap junctions and hemichannels. Among different types of connexins, connexin 43 is the most widely expressed and studied gap junction proteins in astrocytes. Due to the key involvement of astrocytes in memory impairment and abundant expression of connexins in astrocytes, astroglial connexins have been projected as key therapeutic targets for Alzheimer’s disease. On the other hand, the role of connexin gap junctions and hemichannels in memory formation and consolidation has also been reported. Moreover, deletion of these proteins and loss of gap junction communication result in loss of short-term spatial memory. Accordingly, both memory formation and memory deteriorating functions of astrocytes-located connexins have been documented. Physiologically expressed connexins may be involved in the memory formation, while pathologically increased expression of connexins with consequent excessive activation of astrocytes may induce neuronal injury and cognitive decline. The present review describes the memory formation as well as memory deteriorating functions of astroglial connexins in memory disorders of different etiology with possible mechanisms.

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Involvement of glucose related energy crisis and endoplasmic reticulum stress: Insinuation of streptozotocin induced Alzheimer's like pathology

Cited by 44 publications

References 55 publications

Shared cerebral metabolic pathology in non-transgenic animal models of Alzheimer's and Parkinson's disease

Shared cerebral metabolic pathology in non-transgenic animal models of Alzheimer's and Parkinson's disease

Schisandrin ameliorates cognitive deficits, endoplasmic reticulum stress and neuroinflammation in streptozotocin (STZ)-induced Alzheimer’s disease rats

Astroglial connexins and cognition: memory formation or deterioration?

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