Impact of micronutrients and nutraceuticals on cognitive function and performance in Alzheimer's disease

Guarnieri, Lorenza; Bosco, Francesca; Leo, Antonio; Citraro, Rita; Palma, Ernesto; De Sarro, Giovambattista; Mollace, Vincenzo

doi:10.1016/j.arr.2024.102210

Cited by 8 publications

(1 citation statement)

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“…The potential of estrogens to reduce plaque load in animal models has been observed through their actions (Kommaddi et al, 2024). The findings suggest that estradiol has the potential to reduce Aβ levels in HEK293 cells, enhance soluble APP in ZR-75-1 human carcinoma cells and promote APP trafficking in the trans-Golgi network in vesicles, leading to a decrease in Aβ synthesis (Guarnieri et al, 2024). The characteristics exhibited by estrogen are in line with its capacity to reduce the production of neuronal Aβ (Mitra et al, 2023).…”

Section: Modulation Of Estrogen Signallingmentioning

confidence: 86%

Estrogen signalling and Alzheimer's disease: Decoding molecular mechanisms for therapeutic breakthrough

Rishabh,

Rohilla,

Bansal

et al. 2024

Eur J of Neuroscience

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In females, Alzheimer's disease (AD) incidences increases as compared to males due to estrogen deficiency after menopause. Estrogen therapy is the mainstay therapy for menopause and associated complications. Estrogen, a hormone with multifaceted physiological functions, has been implicated in AD pathophysiology. Estrogen plays a crucial role in amyloid precursor protein (APP) processing and overall neuronal health by regulating various factors such as brain‐derived neurotrophic factor (BDNF), intracellular calcium signalling, death domain‐associated protein (Daxx) translocation, glutamatergic excitotoxicity, Voltage‐Dependent Anion Channel, Insulin‐Like Growth Factor 1 Receptor, estrogen‐metabolising enzymes and apolipoprotein E (ApoE) protein polymorphisms. All these factors impact the physiology of postmenopausal women. Estrogen replacement therapies play an important treatment strategy to prevent AD after menopause. However, use of these therapies may lead to increased risks of breast cancer, venous thromboembolism and cardiovascular disease. Various therapeutic approaches have been used to mitigate the effects of estrogen on AD. These include hormone replacement therapy, Selective Estrogen Receptor Modulators (SERMs), Estrogen Receptor Beta (ERβ)‐Selective Agonists, Transdermal Estrogen Delivery, Localised Estrogen Delivery, Combination Therapies, Estrogen Metabolism Modulation and Alternative Estrogenic Compounds like genistein from soy, a notable phytoestrogen from plant sources. However, mechanism via which these approaches modulate AD in postmenopausal women has not been explained earlier thoroughly. Present review will enlighten all the molecular mechanisms of estrogen and estrogen replacement therapies in AD. Along‐with this, the association between estrogen, estrogen‐metabolising enzymes and ApoE protein polymorphisms will also be discussed in postmenopausal AD.

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Section: Modulation Of Estrogen Signallingmentioning

confidence: 86%