Chronological Molecular Changes in Neuronal Communication in Androgen-Deficient Rats

Fainanta, Taratorn; Jaroenporn, Sukanya; Wititsuwankul, Patteera; Malaivijitnond, Suchinda

doi:10.1007/s12031-019-01335-7

Cited by 10 publications

(10 citation statements)

References 71 publications

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“…[34][35][36][37][38] In addition to studies on the association of cognitive function and testosterone suppression in patients with PC receiving ADT, evidence suggests that age-related reduction in testosterone also is associated with cognitive decline. In preclinical studies, androgen deficiency has been linked to the induction of early onset neurodegeneration, 41 with oxidative stress being a well-documented contributing factor to brain aging and neurodegeneration. 42 In vitro studies have shown that testosterone has a protective effect on cerebellar granular cells, making them less vulnerable to oxidative stress-induced cell death.…”

Section: Systematic Reviews and Meta-analysesmentioning

confidence: 99%

Risk of Cognitive Effects in Comorbid Patients With Prostate Cancer Treated With Androgen Receptor Inhibitors

Morgans

Renzulli

Olivier

et al. 2021

Clinical Genitourinary Cancer

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Prostate cancer (PC) is pr imar ily a disease of older men. As the risk of neurocognitive decline increases as people age, cognitive dysfunction is a potential complication in men with PC, imposing detrimental effects on functional independence and quality of life. Importantly, risk of cognitive decline may increase with exposure to androgen deprivation therapy and other hormonal therapies. Particular consideration should be given to patients with castrationresistant PC (CRPC), many of whom require continuous, long-term androgen deprivation therapy combined with a second-generation androgen receptor inhibitor. Non-comparative evidence from interventional trials of androgen receptor inhibitors in men with non-metastatic CRPC suggests differential effects on cognitive function and central nervous system-related adverse events within this dr ug class. Dr ug-dr ug interactions with concomitant medications for chronic, non-malignant comorbidities differ among ARIs and thus may contribute further to cognitive impairment. Hence, establishing baseline cognitive function is a prerequisite to identifying subsequent clinical decline associated with androgen receptor-targeted therapies. Although brief, sensitive screening tools for cancer-related cognitive dysfunction are lacking, mental status can be ascertained from the initial medical history and neurocognitive examination, progressing to more in-depth evaluation when impairment is suspected. On-treatment neurocognitive monitoring should be integrated into regular clinical follow-up to preserve cognitive function and quality of life throughout disease management. This review summarizes the multiple factors that may contribute to cognitive decline in men with CRPC, awareness of which will assist clinicians to optimize individual treatment. Practical, clinic-based strategies for managing the risks for and symptoms of cognitive dysfunction are also discussed.

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Section: Systematic Reviews and Meta-analysesmentioning

confidence: 99%

Risk of Cognitive Effects in Comorbid Patients With Prostate Cancer Treated With Androgen Receptor Inhibitors

Morgans

Renzulli

Olivier

et al. 2021

Clinical Genitourinary Cancer

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“…For all of the rats assigned to either the place or response task, testosterone was observed to significantly alter concentrations of BDNF in the hippocampus and striatum in a dosedependent manner. A number of studies have shown that castration decreases total BDNF levels in the hippocampus of adult male rats (Ebrahimzadeh et al, 2015;Fainanta et al, 2019;Shin et al, 2016). This effect may, however, vary among the sub-regions of the hippocampus -an effect that our assay was too crude to detect.…”

Section: Changes In Bdnf Concentrationsmentioning

confidence: 88%

Dose-dependent effects of testosterone on spatial learning strategies and brain-derived neurotrophic factor in male rats

Zhang

Ramdev

Tuta

et al. 2020

Psychoneuroendocrinology

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“…Male rats have higher levels of BDNF within the dentate gyrus than do females [179], suggesting that BDNF levels may be regulated by sex hormones. In support of this, castration decreased BDNF levels in the hippocampus of male rats [99,168,180], and testosterone implants increased hippocampal BDNF in a transgenic male mouse model of Alzheimer's disease (SAMP8) [181]. Surprisingly, neither DHT nor testosterone influenced BDNF levels within the hippocampi of aged male rats [153,154].…”

Section: Possible Molecular Pathways Within the Hippocampusmentioning

confidence: 89%

“…The implications of these wide-ranging changes have not been well characterized, but it is noteworthy that NMDA receptors and GABA receptors were up-regulated in the hippocampus by castration [167], possibly compensating for reduced connectivity. Using a more focused approach, another study assessed changes in mRNA expression for specific genes involved in synaptic plasticity within the hippocampus of males rats within 9 days of castration [168]. Castration caused a decrease in transcripts for brain-derived neurotrophic factor (BDNF) and synaptophysin, while increasing expression of transcripts for acetylcholine receptors (α7-nicotinic and M 1 muscarinic) and an NMDA receptor subunit (GluN1).…”

Section: Possible Molecular Pathways Within the Hippocampusmentioning

confidence: 99%

“…Castration caused a decrease in transcripts for brain-derived neurotrophic factor (BDNF) and synaptophysin, while increasing expression of transcripts for acetylcholine receptors (α7-nicotinic and M 1 muscarinic) and an NMDA receptor subunit (GluN1). The authors suggest that the upregulation of receptors may have been a compensatory response to reduced synaptic signaling caused by down-regulation of synaptophysin and BDNF [168].…”

Section: Possible Molecular Pathways Within the Hippocampusmentioning

confidence: 99%

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Testosterone and Adult Neurogenesis

Spritzer

Roy

2020

Biomolecules

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It is now well established that neurogenesis occurs throughout adulthood in select brain regions, but the functional significance of adult neurogenesis remains unclear. There is considerable evidence that steroid hormones modulate various stages of adult neurogenesis, and this review provides a focused summary of the effects of testosterone on adult neurogenesis. Initial evidence came from field studies with birds and wild rodent populations. Subsequent experiments with laboratory rodents have tested the effects of testosterone and its steroid metabolites upon adult neurogenesis, as well as the functional consequences of induced changes in neurogenesis. These experiments have provided clear evidence that testosterone increases adult neurogenesis within the dentate gyrus region of the hippocampus through an androgen-dependent pathway. Most evidence indicates that androgens selectively enhance the survival of newly generated neurons, while having little effect on cell proliferation. Whether this is a result of androgens acting directly on receptors of new neurons remains unclear, and indirect routes involving brain-derived neurotrophic factor (BDNF) and glucocorticoids may be involved. In vitro experiments suggest that testosterone has broad-ranging neuroprotective effects, which will be briefly reviewed. A better understanding of the effects of testosterone upon adult neurogenesis could shed light on neurological diseases that show sex differences.

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Chronological Molecular Changes in Neuronal Communication in Androgen-Deficient Rats

Cited by 10 publications

References 71 publications

Risk of Cognitive Effects in Comorbid Patients With Prostate Cancer Treated With Androgen Receptor Inhibitors

Risk of Cognitive Effects in Comorbid Patients With Prostate Cancer Treated With Androgen Receptor Inhibitors

Dose-dependent effects of testosterone on spatial learning strategies and brain-derived neurotrophic factor in male rats

Testosterone and Adult Neurogenesis

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