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New study findings highlight a potential strategy for preventing or slowing disease progression for type 1 diabetes (T1D) by focusing on a specific inflammation-related protein known to play a key role in its development. Researchers at the Indiana University School of Medicine suggest the findings could influence the repurposing of an existing FDA-approved psoriasis drug as a novel treatment for T1D, potentially leading to new clinical trials.1,2
Image credit: Sherry Young | stock.adobe.com
Polymorphisms in tyrosine protein kinase 2 (TYK2), a member of the Janus kinase family, relate to a reduced risk of several autoimmune diseases, such as T1D, ulcerative colitis, and rheumatoid arthritis.2 Researchers used 3 in vitro human model systems and 2 in vivo preclinical mouse models to assess whether the pharmacological inhibition of TYK2 facilitates crosstalk between the immune system and β cells in T1D.1
The results demonstrated that applying a molecular method to block inflammation signaling through the TYK2 protein reduced harmful inflammation in the pancreas, according to the researchers.1,2
Further results demonstrated that the treatment also affected the location within the cell of key ISG messenger RNAs, notably increasing cytoplasmic CD274 mRNA, suggesting that inflammation reduction might influence mRNA localization. Additionally, PD-L1 protein levels in islets were initially lower in treated mice but became similar to control mice later in the study in both models.1,2—Kennedy Ferruggia, Assistant Editor
Given the 2025 expansion of the MTM program, researchers from the University of Minnesota College of Pharmacy set out to examine the impact of comprehensive medication reviews (CMRs), a critical medication therapy management (MTM) service, on medication quality measures. Their findings, published in the Journal of the American Geriatrics Society, indicate patients with T2D who received a CMR have improved oral antidiabetic drug (OAD) adherence and statin utilization compared with nonrecipients.1,2
The study results indicated statistically significant improvements of 2% and 1.4% in the proportion of OAD-adherent and statin users, respectively, in CMR recipients compared with nonrecipients. Even when the researchers increased the threshold of OAD adherence from 80% proportion of days covered to 90%, participants still experienced a significant improvement of 1.1%. In contrast, the 2 groups had similar emergency department/hospitalization rates and frequencies.2
The researchers suggest that the modest impact of CMR on OAD adherence could be due to appropriate pharmacist recommendations that may lower adherence rates. They also explain that the lack of impact of CMR on hospitalizations may be due to improvement of clinical outcomes, such as glycemic control. Outcomes like that would require more than 1 year to produce significant results.2
These results add to the growing body of evidence supporting the engagement of pharmacists to manage patients’ chronic health conditions. As key figures in patients’ medication management, pharmacists can help improve adherence during CMR encounters through personalized guidance and tailored counseling and support.—Huiqiao (Melinda) Fan, BSc
New findings from the University of Nevada, Las Vegas (UNLV) suggest that high blood sugar levels associated with type 2 diabetes rewire the brain, weakening key functions and mimicking symptoms of early Alzheimer disease.1
According to researchers at Harvard University, long-term diabetes has significant impacts on neurons in the brain. High blood glucose can affect functional connectivity, which links brain regions that share functional properties, and brain matter. This can cause the brain to atrophy and can lead to small vessel disease, which restricts blood flow and causes cognitive difficulties. In severe cases, this can lead to the development of vascular dementia.2
Now, according to their study findings, the UNLV researchers say it appears that diabetes weakens the function of the anterior cingulate cortex (ACC), which suppresses reward perception and memory signals. This induces mild cognitive impairment, like that observed during the early stages of Alzheimer disease.1
Hyperglycemic insulin levels seemed to impair the ACC’s information-processing ability surrounding rewards. This weakened reward signal was attributed to a dampened input into the ACC from the hippocampus, which is also crucial for Alzheimer disease and is involved in spatial and autobiographical memory.1
These findings could be significant given the global prevalence of diabetes, and particularly type 2 diabetes, which is associated with obesity and can lead to chronic damage to the nerves, blood vessels, and surrounding tissues and organs. The researchers also suggest that the hippocampus-to-ACC projection could be worth exploring as a treatment target for mood disorders, which the ACC is already known to affect.3—Aislinn Antrim, Managing Editor
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