An updated meta-analysis of cohort studies: Diabetes and risk of Alzheimer's disease

Zhang, Jieyu; Chen, Chunxiang; Hua, Shuizhen; Liao, Hairong; Wang, Mei‐Xiang; Xiong, Yan; Cao, Fei

doi:10.1016/j.diabres.2016.10.024

Cited by 280 publications

(239 citation statements)

References 32 publications

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“…There is an abundance of evidence that T2D increases the risk of AD and may be in the causative pathway. In a recent meta-analysis of longitudinal population-based studies, the relative risk for the development of AD among people with diabetes was 1.53, consistent with results from a previous meta-analysis of longitudinal epidemiological studies (33,51). Data suggest that AD risk may be increased based on the degree of hyperglycaemia and not simply on the presence or absence of T2D.…”

Section: Evidence Of Hyperglycaemia and Type 2 Diabetes As A Risk Facsupporting

confidence: 81%

Obesity as a risk factor for Alzheimer's disease: weighing the evidence

et al. 2017

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Alzheimer's disease (AD) is the sixth leading cause of death in the USA today; therefore, it is imperative that public health initiatives and clinical strategies are developed to prevent and effectively treat AD. Despite the enormous impact that AD has on individuals, families, society, and the health care system, there are no biomarkers to clearly identify those at risk for AD, public health prevention strategies in place, or treatments to address the underlying pathology or stop the progression of AD. There is ample scientific as well as empirical evidence that obesity and its metabolic and vascular comorbidities are related to AD and likely in the causative pathway. Obesity prevention and treatment could prove to be an efficacious and safe approach to preventing AD, a serious and daunting epidemic disease. In this review, we present the current pathophysiological and clinical evidence linking obesity and obesity-related comorbidities (eg, insulin resistance, hyperglycaemia, and type 2 diabetes) with AD. Additionally, we discuss which population to target and when to consider treatment for AD. Finally, we summarize the current evidence regarding the efficacy of anti-obesity and anti-diabetic pharmacotherapeutic agents for the treatment of AD.

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Section: Evidence Of Hyperglycaemia and Type 2 Diabetes As A Risk Facsupporting

confidence: 81%

Obesity as a risk factor for Alzheimer's disease: weighing the evidence

et al. 2017

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“…3B and 3C) showed that the diabetic pathophysiological factors could upregulate ROCK1 and 14-3-3σ which are associated with neurodegeneration [32, 33]. Thus it would be interesting to investigate whether ROCK1 or 14-3-3σ is a link between type 2 diabetes and Alzheimer's disease which shows an increased risk in type 2 diabetes [34]. …”

Section: Discussionmentioning

confidence: 99%

Type 2 Diabetes Promotes Cell Centrosome Amplification via AKT-ROS-Dependent Signalling of ROCK1 and 14-3-3σ

Wang¹,

Lü²,

Wang³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Type 2 diabetes is associated with oxidative stress and DNA damage which can cause centrosome amplification. Thus, the study investigated centrosome amplification in type 2 diabetes and the underlying mechanisms. Methods: Centrosome numbers in human peripheral blood mononuclear blood cells (PBMC) from healthy subjects and patients with type 2 diabetes were compared to access the association between type 2 diabetes and centrosome amplification. Colon cancer cells were used to investigate the molecular mechanisms underlying the centrosome amplification triggered by high glucose, insulin and palmitic acid. Western blot analysis was used to quantify the level of protein and protein phosphorylation. Immunofluorescent staining was performed to detect centrosomes. ROS was quantified using flow cytometry technique. Transcriptpmic profiling was performed using Illumina HiSeq^TM500 platform. Results: We found that centrosome amplification was increased PBMC from the type 2 diabetic patients, which correlated with the levels of fasting blood glucose and HbA1c. High glucose, insulin and palmitic acid, alone or in combinations, induced ROS production and centrosome amplification. Together, they increased AKT activation as well as the expression, binding and centrosome translation of ROCK1 and 14-3-3σ. Results from further analyses showed that AKT-ROS-dependent upregulations of expression, binding and centrosome translocation of ROCK1 and 14-3-3σ was the molecular pathway underlying the centrosome amplification in vitro triggered by high glucose, insulin and palmitic acid. Moreover, the key in vitro molecular signalling events activated by high glucose, insulin and palmitic acid were verified in PBMC from the patients with type 2 diabetes. Conclusion: Our results show that type 2 diabetes promotes cell centrosome amplification, and suggest that the diabetic pathophysiological factors-activated AKT-ROS-dependent signalling of ROCK1 and 14-3-3σ is the underlying molecular mechanism.

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“…A recent study reviewed cohort studies and pooled results to examine the relationship between diabetes and AD. They found that diabetes was associated with a higher risk of AD; however, this association was observed in both Western and Eastern populations-Eastern populations having higher risk [66]. This study did not examine other ethnic differences.…”

Section: Comorbiditiesmentioning

confidence: 75%