Alzheimer's disease (AD), the leading cause of dementia, involves microglial activation, pro-inflammatory cytokine release, and impaired insulin signaling via insulin receptor substrate 1 (IRS-1) inhibition. Brain insulin resistance (BIR) is a key factor in AD progression, disrupting synaptic plasticity and neuronal function. Additionally, glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) signaling, which regulate insulin pathways, are compromised in AD. GLP-1/GIP receptor activation or their analogs, such as tirzepatide, show potential in mitigating AD neuropathology. However, the precise neuroprotective mechanisms of tirzepatide remain unclear. This mini-review explores tirzepatide's potential therapeutic effects in AD, focusing on its role in restoring insulin signaling, reducing neuroinflammation, and improving cognitive function. Understanding these mechanisms could offer new insights into AD treatment strategies.

Tirzepatide (TRZ) is a dual agonist of glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) receptors that were recently approved for the treatment of type 2 diabetes (T2D) and obesity. Of note is that T2D and obesity, by inducing peripheral low-grade inflammation and oxidative stress, provoke the development of central neuroinflammation and oxidative stress. Together, T2D and obesity are regarded as potential risk factors implicated in the development and progression of Alzheimer’s disease (AD), which is the most common neurodegenerative disease and represents the most typical cause of dementia. Hence, targeting low-grade inflammation and oxidative stress in T2D and obesity by TRZ may reduce AD neuropathology. In addition, TRZ can inhibit the production of amyloid beta (Aβ) and associated neuroinflammation, oxidative stress, and neuronal apoptosis. However, the underlying neuroprotective mechanism of TRZ against AD is not entirely explained. Consequently, this mini-review aims to discuss the possible molecular mechanism of TRZ in AD.

This study aimed to determine the estimated proportion of contraindications among women taking combined oral contraceptives (COCs) and to assess the risk factors associated with their contraindications. This study was cross-sectional. Reproductive-aged women (18–49 years) on any COCs between 2018 and 2020 were recruited from one obstetrics–gynaecology clinic in a university-affiliated hospital and were included. Contraindications were defined using the World Health Organization (WHO) Medical Eligibility Criteria (MEC) for Contraceptive Use. Data were collected from electronic medical records for all included women, as well as a standardised, pretested, structured survey for one-third of the women. In this cross-sectional study, 380 women using COCs were included. Their mean age was 31.645 ± 7.366 years. Among them, 131 (34.5%) participated via a survey and electronic records, while the other 249 (65.5%) participated via electronic records only. The majority of the participants had a Bachelor’s degree (59.0%) and were married (62.1%). The overall estimated proportion of patients with at least one contraindication to COCs according to category 3 (relative contraindications) or 4 (absolute contraindications) was 31.3% (95% CI 26.63–35.99). The most common contraindications observed were controlled hypertension, category 3 (12.1%); major surgery with prolonged immobilisation, category 4 (4.7%); migraine with aura at any age, category 4 (4.2%); breastfeeding from six weeks to less than six months postpartum, category 3 (4.0%); and diabetes mellitus with complications, category 4 (3.2%). Significant factors associated with contraindications to COCs were married women (OR 2.19, 95% CI 1.38–3.46), those aged 35 years or more (OR 2.33, 95% CI 1.49–3.66), and those with one or more live births (OR 2.19, 95% CI 1.38–3.46). Ensuring proper assessment prior to prescribing and considering alternatives suitable for long-term use among women taking an oral contraceptive regularly is recommended.

Background: Medication safety incidents commonly occur in mental health hospitals. There is a need to improve the understanding of the circumstances that are thought to have played a part in the origin of these incidents to design safer systems to improve patient safety. Aim: This study aimed to undertake a mixed-methods analysis of medication safety incidents reported to the National Reporting and Learning System in England and Wales in 2010 to 2017. Method: Quantitative analyses of anonymized medication safety incidents occurring in mental health hospitals that were reported to the National Reporting and Learning System during an 8-year period were undertaken to characterize their type, severity, and the medication(s) involved. Second, a content analysis of the free-text reports associated with all incidents of at least moderate harm severity was undertaken to identify the underlying contributory factors. Results: Overall, 94,134 medication incident reports were examined, of which 10.4% (n = 9811) were reported to have resulted in harm. The 3 most frequent types of reported medication incidents involved omission of medication (17,302; 18.3%), wrong frequency (11,882; 12.6%), and wrong/unclear dose of medication (10,272; 10.9%). Medicines from the central nervous system (42,609; 71.0%), cardiovascular (4537; 7.6%), and endocrine (3669; 6.1%) medication classes were the most frequently involved with incidents. Failure to follow protocols (n = 93), lack of continuity of care (n = 92), patient behaviors (n = 62), and lack of stock (n = 51) were frequently reported as contributory factors. Conclusions: Medication incidents pose an enduring threat to patient safety in mental health hospitals. This study has identified important targets that can guide the tailored development of remedial interventions.

Metformin is an anti-diabetic drug used in the management of type 2 diabetes (T2D). Metformin has different pleiotropic effects, such as anti-inflammatory, antioxidant, antithrombotic, and vasculoprotective. Metformin has neuroprotective effects against neurodegenerative diseases and ischemic stroke. Conversely, metformin may exacerbate the pathogenesis of ischemic stroke. This controversial point may be related to the impact of metformin on the different signaling pathways, such as AMP-activated protein kinase (AMPK) and growth differentiation factor 15 (GDF-15). Many studies have reported the effect of metformin on ischemic stroke, with AMPK signaling only. However, little has been explored about the impact of metformin on the GDF-15 signaling in ischemic stroke. Accordingly, this review aims to discuss the role of metformin in the neuropathology of ischemic stroke regarding the AMPK and GDF-15 signaling pathways.