Memory enhancement by Tamoxifen on amyloidosis mouse model

Pandey, Deepika; Banerjee, Sugato; Basu, Mahua; Mishra, Neha

doi:10.1016/j.yhbeh.2015.09.004

Cited by 32 publications

(20 citation statements)

References 18 publications

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“…Research on the dopaminergic transmission in Aβ models indicates changes in the early post-treatment phase as shown by a study of Mukhin et al (2019) in rats treated icv with Aβ 25-35 fragment in which the ability of neurons in the substantia nigra to secrete dopamine in the anterior dorsomedial striatum was reduced already during the hour following the moment of administration. Similar reduction in dopamine levels was observed in the rat prefrontal cortex 2 and 48 h following the icv injection of Aβ 1-42 (Trabace et al 2007), and in the mice striatum 2 weeks after the Aβ 1-42 treatment (Pandey et al 2016).…”

Section: Indirect Toxicity Towards Dopaminergic Signallingsupporting

confidence: 74%

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: Indirect Toxicity Towards Dopaminergic Signallingsupporting

confidence: 74%

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

et al. 2020

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“…Recently, several studies have reported that TMX improved allocentric memory performance and increased pyramidal neuronal dendritic density (Velazquez-Zamora et al, 2012; Zabihi et al, 2014). It has also been shown that TMX could enhance memory function by reducing dopamine metabolism and increasing acetylcholine levels in an amyloidosis mouse model (Pandey et al, 2015). Human studies have shown the beneficial effect of TMX on reversing cholinergic impairment in postmenopausal women (Ernst et al, 2002; Newhouse et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

The Working Memory and Dorsolateral Prefrontal-Hippocampal Functional Connectivity Changes in Long-Term Survival Breast Cancer Patients Treated with Tamoxifen

Chen

Liu

et al. 2017

International Journal of Neuropsychopharmacology

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Background:Tamoxifen is the most widely used drug for treating patients with estrogen receptor-sensitive breast cancer. There is evidence that breast cancer patients treated with tamoxifen exhibit cognitive dysfunction. However, the underlying neural mechanism remains unclear. The present study aimed to investigate the neural mechanisms underlying working memory deficits in combination with functional connectivity changes in premenopausal women with breast cancer who received long-term tamoxifen treatment.Methods:A total of 31 premenopausal women with breast cancer who received tamoxifen and 32 matched healthy control participants were included. The participants completed n-back tasks and underwent resting-state functional magnetic resonance imaging, which measure working memory performance and brain functional connectivity, respectively. A seed-based functional connectivity analysis within the whole brain was conducted, for which the dorsolateral prefrontal cortex was chosen as the seed region.Results:Our results indicated that the tamoxifen group had significant deficits in working memory and general executive function performance and significantly lower functional connectivity of the right dorsolateral prefrontal cortex with the right hippocampus compared with the healthy controls. There were no significant changes in functional connectivity in the left dorsolateral prefrontal cortex within the whole brain between the tamoxifen group and healthy controls. Moreover, significant correlations were found in the tamoxifen group between the functional connectivity strength of the dorsolateral prefrontal cortex with the right hippocampus and decreased working memory performance.Conclusion:This study demonstrates that the prefrontal cortex and hippocampus may be affected by tamoxifen treatment, supporting an antagonistic role of tamoxifen in the long-term treatment of breast cancer patients.

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“…On the other hand, estrogen prevents Aβ-induced neuronal death, which is mediated through ERα since agonists of ERα produce the same neuroprotective effect [87–89]. The SERM tamoxifen, has been found to protect memory from Aβ-induced toxicity by acting as a ER agonist while enhancing spatial and contextual memory by reducing dopamine metabolism and increasing neurotransmitter acetylcholine [90]. …”

Section: 27hc Is Associated With Cognitive Impairmentmentioning

confidence: 99%

27-Hydroxycholesterol, an endogenous selective estrogen receptor modulator

Nelson

2017

Maturitas

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Estrogen receptors (ERs) mediate the actions of the steroidal estrogens, and are important for the regulation of several physiological and pathophysiological processes, including reproduction, bone physiology, cardiovascular physiology and breast cancer. The unique pharmacology of the ERs allows for certain ligands, such as tamoxifen, to elicit tissue- and context-specific responses, ligands now referred to as selective estrogen receptor modulators (SERMs). Recently, the cholesterol metabolite 27-hydroxychoelsterol (27HC) has been defined as an endogenous SERM, with activities in atherosclerosis, osteoporosis, breast and prostate cancers, and neural degenerative diseases. Since 27HC concentrations closely mirror those of cholesterol, it is possible that 27HC mediates many of the biological effects of cholesterol. This paper provides an overview of ER pharmacology and summarizes the work to date implicating 27HC in various diseases. Wherever possible, we highlight clinical data in support of a role for 27HC in the diseases discussed.

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Memory enhancement by Tamoxifen on amyloidosis mouse model

Cited by 32 publications

References 18 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

The Working Memory and Dorsolateral Prefrontal-Hippocampal Functional Connectivity Changes in Long-Term Survival Breast Cancer Patients Treated with Tamoxifen

27-Hydroxycholesterol, an endogenous selective estrogen receptor modulator

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