Akt activation ameliorates deficits in hippocampal-dependent memory and activity-dependent synaptic protein synthesis in an Alzheimer’s disease mouse model

Kommaddi, Reddy Peera; Gowaikar, Ruturaj; P A, Haseena; Diwakar, Latha; Singh, Kunal; Mondal, Amrita

doi:10.1016/j.jbc.2023.105619

Cited by 3 publications

(1 citation statement)

References 104 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, it was observed that estrogens augmented the uptake of accumulated Aβ by microglia in the human cortex (Testo et al, 2024;Yamada et al, 2024). 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).…”

Section: Modulation Of Estrogen Signallingmentioning

confidence: 99%

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

Rishabh,

Rohilla,

Bansal

et al. 2024

Eur J of Neuroscience

View full text Add to dashboard Cite

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.

show abstract

Section: Modulation Of Estrogen Signallingmentioning

confidence: 99%

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

Rishabh,

Rohilla,

Bansal

et al. 2024

Eur J of Neuroscience

View full text Add to dashboard Cite

show abstract

Nanocurcumin prevents memory impairment, hippocampal apoptosis, Akt and CaMKII-α signaling disruption in the central STZ model of Alzheimer’s disease in rat

Moosavi,

soukhaklari,

Bagheri-Mohammadi

et al. 2024

Behavioural Brain Research

View full text Add to dashboard Cite

Resistance Exercise Training as a New Trend in Alzheimer’s Disease Research: From Molecular Mechanisms to Prevention

Sepúlveda-Lara,

Sepúlveda,

Marzuca-Nassr

2024

IJMS

View full text Add to dashboard Cite

Alzheimer’s disease is a pathology characterized by the progressive loss of neuronal connections, which leads to gray matter atrophy in the brain. Alzheimer’s disease is the most prevalent type of dementia and has been classified into two types, early onset, which has been associated with genetic factors, and late onset, which has been associated with environmental factors. One of the greatest challenges regarding Alzheimer’s disease is the high economic cost involved, which is why the number of studies aimed at prevention and treatment have increased. One possible approach is the use of resistance exercise training, given that it has been shown to have neuroprotective effects associated with Alzheimer’s disease, such as increasing cortical and hippocampal volume, improving neuroplasticity, and promoting cognitive function throughout the life cycle. However, how resistance exercise training specifically prevents or ameliorates Alzheimer’s disease has not been fully characterized. Therefore, the aim of this review was to identify the molecular basis by which resistance exercise training could prevent or treat Alzheimer’s disease.

show abstract

Akt activation ameliorates deficits in hippocampal-dependent memory and activity-dependent synaptic protein synthesis in an Alzheimer’s disease mouse model

Cited by 3 publications

References 104 publications

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

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

Nanocurcumin prevents memory impairment, hippocampal apoptosis, Akt and CaMKII-α signaling disruption in the central STZ model of Alzheimer’s disease in rat

Resistance Exercise Training as a New Trend in Alzheimer’s Disease Research: From Molecular Mechanisms to Prevention

Contact Info

Product

Resources

About