vitamin d

Is there a Place for Klotho in Alzheimer’s disease?

Published on: 29th February, 2024

Alzheimer’s disease, a major healthcare concern, lacks an effective pharmacological therapy to change its irreversible progression. In this work, we present Klotho, a protein associated with aging that is involved in the regulation of numerous physiological processes and is a serious candidate to be a pharmacological target to act on. Klotho’s mRNA has been found in neurons of a variety of brain regions (cortex, hippocampus). The best studied and prominent function of Klotho is as the co-receptor of fibroblast growth factor 23 (FGF23), through which Klotho controls renal phosphate excretion and vitamin D metabolism. Reduced serum levels of Klotho in mice have been associated with a shorter life expectancy and with numerous pathological conditions such as renal disease, vascular calcification, neurodegeneration, and others. Moreover, overexpression of Klotho leads to opposite effects resulting in increased survival rates. In this review we address different signaling pathways in which Klotho is involved in one way or another, focusing on those pathways that could serve as pharmacological targets to modify the evolution of Alzheimer’s disease. We describe how Klotho inhibits signaling cascades involved in cellular senescence, fibrosis, inflammation, and apoptosis all of which are mediated by tumor growth factor β (TGF- β), nuclear factor kappa K (NF- κ B), insulin-like growth factor 1 (IGF-1) or Wnt. We also highlight how Klotho is able to activate anti-inflammatory and antioxidant signaling pathways.  Although there are no drugs that act specifically on Klotho, compounds currently on the market such as hormone-based drugs, pravastatin, losartan, fosinopril, and rapamycin have been shown to increase the expression of this protein and are also discussed.
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A Prospective Observational Study on Neurotoxicity of Chemotherapy - A Critical Analysis

Published on: 2nd April, 2024

Background: Cancer treatment frequently depends on the intricate and potent effects that are acknowledged for their potential to save lives. Chemotherapy can have adverse effects on both the central and peripheral nervous systems, posing significant challenges.Objective: •    To assess the causative agent, development, and timing of occurrence.•    To improve management of neurological complications.•    To discriminate the iatrogenic effects of cancer therapy and neurological progression.Method: A prospective observational study was conducted in a hospital setting, focusing on the neurotoxic effects of chemotherapy in cancer patients over a span of six months. The research involved participants from both the oncology in-patient and daycare departments. After obtaining informed consent, individuals in the study population were interviewed to gather information about any neurological symptoms they encountered following their chemotherapy sessions.Results and discussion: Within our study population, a predominant 67% comprised female patients, while male patients constituted 33%. Of the total participants, 66% reported experiencing neurological symptoms. Among these symptoms, the majority of patients encountered sensations such as tingling, numbness, and a burning sensation. Other reported symptoms included headaches, distal weakness, myalgia, seizures, and ataxia.Conclusion: In this current study, 66% of the study population encountered neurological side effects. Generally, the presence of comorbidities, vitamin deficiencies, and advanced age can significantly contribute to the development of peripheral neuropathy. Depending on the severity of neuropathy, recommendations for interventions include the prescription of vitamin supplements, calcium supplements, duloxetine, and pregabalin.
Cite this ArticleCrossMarkPublonsHarvard Library HOLLISGrowKudosResearchGateBase SearchOAI PMHAcademic MicrosoftScilitSemantic ScholarUniversite de ParisUW LibrariesSJSU King LibrarySJSU King LibraryNUS LibraryMcGillDET KGL BIBLiOTEKJCU DiscoveryUniversidad De LimaWorldCatVU on WorldCat
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