Given sparse relevant data, the aim of this study was to determine whether Helicobacter pylori infection, including cytotoxin-associated gene-A (CagA) producing strains, is associated with dementia in type 2 diabetes (T2DM).

Longitudinal data from 1115 participants in the community-based Fremantle Diabetes Study Phase I (mean age 64.0 years, 48.0 % males; 38.0 % H. pylori seronegative, 24.3 % H. pylori seropositive/CagA seronegative, and 37.7 % H. pylori/CagA seropositive at baseline) were analyzed.

During up to 19 years of follow-up, 50.3 % and 83.5 % of participants without and with incident dementia, respectively, died. In Cox proportional hazards models, H. pylori/CagA seropositivity (hazard ratio (95 % CI) 1.68 (1.15, 2.46), P = 0.008), but not H. pylori seropositivity/CagA seronegativity (P = 0.541) was an independent predictor of incident dementia, but neither H. pylori seropositivity/CagA seronegativity nor H. pylori/CagA seropositivity were significant predictors in competing risks models (P ≥ 0.280).

Although CagA seropositivity in T2DM may have a contributory etiologic role in the risk of dementia, this may be through its association with reduced cardiovascular/all-cause mortality.

Diabetes raises the risk of dementia, mortality, and cognitive decline in the elderly, potentially because of hereditary variables such as APOE. In this study, we aim to evaluate Diabetes mellitus and the risk of incident dementia in APOE ɛ4 carriers.

We thoroughly searched PubMed (Medline), Scopus, and Google Scholar databases for related articles up to September 2023. The titles, abstracts, and full texts of articles were reviewed; data were extracted and analyzed.

This meta-analysis included nine cohorts and seven cross-sectional articles with a total of 42,390 population. The study found that APOE ɛ4 carriers with type 2 diabetes (T2D) had a 48% higher risk of developing dementia compared to non-diabetic carriers (Hazard Ratio;1.48, 95%CI1.36-1.60). The frequency of dementia was 3 in 10 people (frequency: 0.3; 95%CI (0.15-0.48). No significant heterogeneity was observed. Egger's test, which we performed, revealed no indication of publication bias among the included articles (p = 0.2).

Overall, diabetes increases the risk of dementia, but further large-scale studies are still required to support the results of current research.

Type 2 diabetes can cause a variety of complications, significantly affecting people's health. Given their ability to suppress carbohydrate digestion, alpha-glucosidase inhibitors are effective treatments for diabetes. However, the current approved glucosidase inhibitors' side effects of abdominal discomfort limit their use. We used the compound Pg3R from the natural fruit berry as a reference, screening against a large database of 22 million compounds to identify potential health-friendly alpha-glucosidase inhibitors. Ligand-based screening enables us to identify 3968 ligands that exhibit structural similarity compared to the natural compound. These lead hits were used for LeDock, and their binding free energies were evaluated by MM/GBSA. Among the top-scoring candidates, ZINC263584304 exhibited the strongest binding affinity to alpha-glucosidase, with a "low-fat" structural characteristic. Its recognition mechanism was further investigated by microsecond MD simulations and free energy landscapes, exhibiting novel conformational changes during the binding process. Our study provided a novel alpha-glucosidase inhibitor with the potential to treat type 2 diabetes.

Our study aimed to identify the common themes, knowledge gaps and to evaluate the quality of data linkage research on diabetes in Australia.

This systematic review was developed in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (the PRISMA Statement). Six biomedical databases and the Australian Population Health Research Network (PHRN) website were searched. A narrative synthesis was conducted to comprehensively identify the common themes and knowledge gaps. The guidelines for studies involving data linkage were used to appraise methodological quality of included studies.

After screening and hand-searching, 118 studies were included in the final analysis. Data linkage publications confirmed negative health outcomes in people with diabetes, reported risk factors for diabetes and its complications, and found an inverse association between primary care use and hospitalization. Linked data were used to validate data sources and diabetes instruments. There were limited publications investigating healthcare expenditure and adverse drug reactions (ADRs) in people with diabetes. Regarding methodological assessment, important information about the linkage performed was under-reported in included studies.

In the future, more up to date data linkage research addressing costs of diabetes and its complications in a contemporary Australian setting, as well as research assessing ADRs of recently approved antidiabetic medications, are required.

Epidemiologic studies have documented an association between diabetes and increased risk of cognitive decline in the elderly. Based on animal model studies, several mechanisms have been proposed to explain such an association, including central insulin signaling, neurodegeneration, brain amyloidosis, and neuroinflammation. Nevertheless, the exact mechanisms in humans remain poorly defined. It is reasonable, however, that many pathways may be involved in these patients leading to cognitive impairment. A major aim of clinicians is identifying early onset of neurologic signs and symptoms in elderly diabetics to improve quality of life of those with cognitive impairment and reduce costs associated with long-term complications. Several biomarkers have been proposed to identify diabetics at higher risk of developing dementia and diagnose early stage dementia. Although biomarkers of brain amyloidosis, neurodegeneration and synaptic plasticity are commonly used to diagnose dementia, especially Alzheimer disease, their role in diabetes remains unclear. The aim of this review is to explore the molecular mechanisms linking diabetes with cognitive decline and present the most important findings on the clinical use of biomarkers for diagnosing and predicting early cognitive decline in diabetics.

Cognitive dysfunction is increasingly recognized as an important comorbidity of type 2 diabetes (T2D). We aimed to establish if the risk of accelerated cognitive decline (ACD) is higher in females with T2D than males.

3163 participants (38% female) with T2D from the cognition substudy of CAROLINA® (NCT01243424) were included (mean age 64.4 ± 9.2 years; T2D duration 7.6 ± 6.1 years). The cognitive outcome was occurrence of ACD at end of follow-up, defined as a regression based index score ≤16th percentile on either the Mini-Mental State Examination (MMSE) or a composite measure of attention and executive functioning (Trail Making and Verbal Fluency Test). Potential confounders, were taken into account at an individual patient level. Logistic regression analysis was used to investigate ACD risk by sex. We assessed potential mediators for sex differences in ACD using Causal Mediation Analysis (CMA). After a median follow-up duration of 6.1 ± 0.7 years, 361 (30.0%) females compared to 494 (25.2%) males exhibited ACD (OR 1.27 [95%CI 1.08-1.49], p = .003). Depressive symptoms, which were more common in females (24.3% vs 12.5%), mediated between sex and ACD (mediation effect 20.3%, p = 0.03). There were no other significant mediators.

Females with T2D had a higher risk of ACD compared to males. This was partly explained by depressive symptoms. After evaluation of vascular and diabetes-related risk factors, complications and treatment, a major share of the higher risk of ACD in females remained unexplained. Our results highlight the need for further research on causes of sex-specific ACD in T2D.

Physical inactivity is a risk factor for type 2 diabetes (T2D) and dementia. However, it is unknown if physical activity (PA) intensity is associated with brain health in people with T2D. Therefore, this study aimed to determine 1) associations between PA intensity and step count with both cognition and brain structure and 2) if apolipoprotein E-ε4 (APOE-ε4) or insulin-therapy modifies any associations.

Participants were people with T2D (n=220; aged 55-86 years). An accelerometer worn over the left hip was used to obtain step count and moderate-to-vigorous PA (MVPA) averaged over 7 days. Cognition in 7 domains was obtained using a battery of neuropsychological tests. Brain structure was measured by Magnetic Resonance Imaging (MRI). Linear regression models were used to examine associations between step count, MVPA and each cognitive and MRI measure. APOE-ε4 x PA and insulin-therapy x PA product terms were added to the models to examine effect modification.

The mean age of participants was 67.9 (SD 6.3). Higher step count was associated with greater hippocampal volume (β=0.028 95%CI 0.005, 0.051). Insulin-therapy modified the association between MVPA and attention-processing speed, such that associations were significant in people receiving insulin-therapy (P for interaction=0.019). There were no other significant associations.

Higher step count and greater time spent in MVPA may be associated with better hippocampal volume and attention-processing speed respectively in people with T2D. People with greater diabetes severity (receiving insulin-therapy) may get more cognitive benefit from MVPA.

There is evidence that diabetes-related complications are declining but most data sources have limitations.

To characterize temporal changes in incidence rates (IRs) of chronic complications and mortality in well-characterized, community-based Australians.

Longitudinal observational study.

Urban population.

Participants with type 2 diabetes from the Fremantle Diabetes Study phases I (FDS1; n = 1291 recruited 1993-1996) and II (FDS2; n = 1509 recruited 2008-2011) age-, sex,- and ZIP code-matched 1:4 to people without diabetes.

First hospitalizations for/with myocardial infarction (MI), stroke, heart failure (HF), lower extremity amputation, and cardiovascular disease (CVD) and all-cause mortality. Five-year IRs, IR ratios for those with versus without diabetes in FDS1 and FDS2, and IR differences (IRDs), were calculated.

The 13,995 participants had a mean age of 64.8 years and 50.4% were males. There were lower IR ratios for MI, stroke, HF, and CVD death in FDS2 versus FDS1. IRDs for people with versus without type 2 diabetes had reduced by >50% between phases for MI, stroke, HF, lower extremity amputation, and CVD death, with no change in IRD for all-cause mortality. Within the pooled type 2 diabetes cohort, FDS2 versus FDS1 participation was an independent inverse predictor of stroke, HF, CVD death, and all-cause mortality after adjustment in Cox proportional hazards models.

Cardiovascular outcomes in Australians have improved since the 1990s, especially in type 2 diabetes. The difference in all-cause mortality between those with and without type 2 diabetes has persisted despite longer survival.

Diabetes can take a tremendous toll on physical and psychological health. Given the growing evidence of the benefits of humor, this study examined the association between diabetes and humor. The sample consisted of 249 participants: 72.3% with type 1 diabetes, 70.3% female, 89.5% Caucasian, and 70.9% college educated. Participants completed the Humor Styles Questionnaire (HSQ) and were compared with HSQ norms. On the affiliative humor scale, the diabetes group did not differ from the norm (P >0.05), nor did those with type 1 diabetes (P >0.05). Scores of those with type 2 diabetes were lower than the norm (P <0.05). On the self-enhancing humor scale, the diabetes group did not differ from the norm (P >0.05), nor did the subgroups with type 1 diabetes (P >0.05) or type 2 diabetes (P >0.05). The diabetes group was lower than the norm on aggressive humor (P <0.01), as were the subgroups with type 1 diabetes (P <0.01) and type 2 diabetes (P <0.05). The diabetes group was higher than the norm on self-defeating humor (P <0.01), as were the subgroups with type 1 diabetes (P <0.01) and type 2 diabetes (P <0.01). Results suggest that people with either type of diabetes are more inclined toward self-enhancing humor, are less inclined toward aggressive humor, and score higher on self-defeating humor, and those with type 1 diabetes are also inclined toward affiliative humor. Results are discussed relative to the sample being comprised of individuals with good glycemic control (mean A1C 7.06 ± 1.39%). This study offers a preliminary comparison of humor among people with diabetes versus those in a healthy norm group without diabetes.

The clinical profile differs between old and young patients with type 2 diabetes mellitus (T2DM). We explored, based on a large real-world database, patient and disease characteristics and actual treatment patterns by age.

The analysis was based on the DIVE and DPV registries of patients with T2DM. Patients were analyzed by age groups 50-59 (middle-young), 60-69 (young-old), 70-79 (middle-old), 80-89 (old), and 90 years or more (oldest-old).

A total of 396,719 patients were analyzed, of which 17.7% were 50-59 years, 27.7% 60-69 years, 34.3% 70-79 years, 18.3% 80-89 years and 2.0% at least 90 years. We found that (a) T2DM in old and oldest-old patients was characterized much less by the presence of metabolic risk factors such as hypertension, obesity, dyslipidemia and smoking than in younger patients; (b) the HbA1c was much lower in oldest-old than in middle-young patients (7.2 ± 1.6% versus 8.0 ± 2.2%; p < 0.001), but it was associated with higher proportions of patients with severe hypoglycemia (7.0 versus 1.6%; p < 0.001); (c) this was potentially associated with the higher and increasing rates of insulin use in older patients (from 17.6% to 37.6%, p < 0.001) and the particular comorbidity profile of these patients, for example, chronic kidney disease (CKD); (d) patients with late diabetes onset had lower HbA1c values, lower bodyweight and less cardiovascular risk factors; (e) patients with a longer diabetes duration had a considerable increase in macrovascular and even more microvascular complications.

In very old patients there is a need for frequent careful routine assessment and a tailored pharmacotherapy in which patient safety is much more important than blood-glucose-lowering efficacy.