There is no definite cure for Alzheimer's disease (AD) due to its multifactorial origin. Drugs that inhibit acetylcholinesterase (AChE), such as rivastigmine, are promising symptomatic treatments for AD. Emerging evidence suggests that insulin therapy can hinder several aspects of AD pathology. Insulin has been shown to modify the activity of AChE, but it is still unknown how insulin and AChE interact. Combination therapy, which targets several features of the disease based on existing medications, can provide a worthy therapy option for AD management. However, to date, no studies have examined the potential interaction of insulin with AChE and/or rivastigmine in vitro. In the present study, we employed the Response Surface Methodology (RSM) as an in vitro assessment to investigate the effect of insulin on both AChE activity and rivastigmine inhibitory action using a common spectrophotometric assay for cholinesterase activity, Ellman's method. Our results showed that insulin, even at high concentrations, has an insignificant effect on both the activity of AChE and rivastigmine's inhibitory action. The variance of our data is near zero, which means that the dispersion is negligible. However, to improve our understanding of the possible interaction of insulin and rivastigmine, or its target AChE, more in silico modelling and in vivo studies are needed.
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http://dx.doi.org/10.3390/ph14111136 | DOI Listing |
J Neurogenet
March 2025
Department of Neurology, Faculty of Medicine, Universitas Udayana/Ngoerah Hospital, Bali, Indonesia.
Painful diabetic neuropathy (PDN) is a common complication in patients with type 2 diabetes mellitus (T2DM) with disruption of vitamin D (VD) activity as one of the risk factors. Active VD exerts its biological functions through the vitamin D receptor (VDR), which polymorphisms in the VDR gene can impair. This study aims to establish VDR FokI and ApaI polymorphisms as risk factors for PDN.
View Article and Find Full Text PDFEur J Pain
April 2025
Chair in Clinical Psychoneuroimmunology, University of Granada, Melilla, Spain.
Objective: To investigate the relationship between leptin levels, insulin resistance (measured by HOMA), and clinical outcomes related to pain, disability, and shoulder range of motion (ROM) in patients with frozen shoulder (FS).
Methods: This cross-sectional study included 34 patients diagnosed with FS. Leptin and HOMA levels were measured and analysed in relation to pain and disability scores, as assessed by the Shoulder Pain and Disability Index (SPADI), along with shoulder ROM (flexion, extension, abduction, adduction, and internal/external rotation).
Elife
March 2025
Ache Lab, Neurobiology and Genetics, Theodor-Boveri-Institute, Biocenter, Julius-Maximilians-University of Würzburg, Am Hubland, Würzburg, Germany.
Insulin plays a critical role in maintaining metabolic homeostasis. Since metabolic demands are highly dynamic, insulin release needs to be constantly adjusted. These adjustments are mediated by different pathways, most prominently the blood glucose level, but also by feedforward signals from motor circuits and different neuromodulatory systems.
View Article and Find Full Text PDFBMC Complement Med Ther
March 2025
Department of Cardiology and Diabetology, Paracelsus-Harz-Clinic, Quedlinburg, Germany.
Background: For Diabetic polyneuropathy, the most prevalent form of polyneuropathy, there is a lack of evidence-based treatment options. Current approaches include pain management, alpha-lipoic acid, and antidepressants. Physical interventions, such as electrical stimulation (four-chamber galvanic bath) have been suggested but have limited supporting evidence.
View Article and Find Full Text PDFMitochondrion
March 2025
Mitochondria and Metabolism Center, Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA 98109, USA. Electronic address:
Obesity is an independent risk factor for heart failure with preserved ejection fraction (HFpEF). Dynamin related protein 1 (Drp1) is a key regulator of mitochondrial morphology, bioenergetics and quality control. The role of endogenous Drp1 in obesity induced HFpEF remains largely unknown.
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