Hormonal Expression Associated with Alzheimer's Disease and Neurodegenerative Diseases

Verdile, Giuseppe; Barron, Anna M.; Martins, Ralph N.

doi:10.1002/9781119356752.ch12

Cited by 1 publication

(1 citation statement)

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“…The immunohistochemistry analysis shows that there is a co‐localization between ER and mitochondria in human brain tissues from both of the experimental groups (Marin, 2011). These results are congruent with the findings of the studies conducted on rodents (Verdile et al, 2019). The group that had been diagnosed with AD showed a lower expression of ERβ in both the total cell lysates and the mitochondrial fractions when compared to the control group within the same age range (Tang et al, 1996).…”

Section: The Role Of Erβ In the Pathogenesis Of Adsupporting

confidence: 93%

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: The Role Of Erβ In the Pathogenesis Of Adsupporting

confidence: 93%