Interleukin-1β: A common cause of alzheimer's disease and diabetes mellitus

Holden, R.J.; Mooney, Phyllis

doi:10.1016/0306-9877(95)90240-6

Cited by 15 publications

(5 citation statements)

References 86 publications

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“…IL-1b secreted by activated monocytes and other various cells is an important mediators regulating the host response to inflammation and immunity (Dinarello, 1984;Dinarello & Mier, 1987). In previous reports, IL-1b production by PBMCs was higher in obesity and IDDM (Plouffe et al, 1978;Ciampolillo et al, 1993;Holden & Mooney, 1995;Bunout et al, 1996), although only a few papers have reported that NIDDM shows high levels of IL-1b (Davaraj & Jialal, 2000). Our investigation demonstrated that this cytokine was produced at significantly high levels in obese NIDDM and obese-non NIDDM compared with non-obese NIDDM.…”

Section: Discussionmentioning

confidence: 98%

Effect of obesity and insulin on immunity in non-insulin-dependent diabetes mellitus

et al. 2002

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Objective: To understand the effect of obesity and insulin on immune functions in non-insulin-dependent diabetes mellitus (NIDDM). Subject: Fourteen obese NIDDM (body mass index (BMI) ¼ 30.6 AE 1.1), seven non-obese NIDDM (BMI ¼ 24.2 AE 0.5) and five obese non-NIDDM (BMI ¼ 28.3 AE 0.67). Interventions: We first examined the influence of insulin on the proliferation of several human cell lines. Second, we compared several immune functions between obese and non-obese NIDDM, and obese non-NIDDM patients using peripheral blood mononuclear cells. Result: Insulin decreased proliferation of T-cell lines but not that of other types of cell lines. Furthermore, obesity augmented the production of IL-1b which could have cytotoxity against islet b cells in NIDDM. Conclusion: Our data suggested that the pathophysiology of NIDDM could be affected by the change of immunity due to obesity, and the treatment of obesity in NIDDM may be important from an immunological aspect.

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Section: Discussionmentioning

confidence: 98%

Effect of obesity and insulin on immunity in non-insulin-dependent diabetes mellitus

et al. 2002

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“…In the early 1990's, there was a great dilemma regarding the direct or inverse relationship between DM and AD in which some supported its correlation by insulin abnormalities, glycation, and IL-1β (Gambassi & Bernabei, 1998;Holden & Mooney, 1995;Landi, Bernabei, & Gambassi, 1997;Smith, Sayre, & Perry, 1996). Hoyer's studies were the first to establish the links between diabetes and Alzheimer's.…”

Section: Studies Exploring Correlations Between Diabetes and Alzheimentioning

confidence: 99%

Cognitive dysfunction: A growing link between diabetes and Alzheimer's disease

Jash

Gondaliya

Kirave

et al. 2019

Drug Development Research

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Diabetes mellitus (DM) is a gradually rising metabolic disease which is currently affecting millions of people worldwide. Diabetes is associated with various complications like nephropathy, neuropathy, retinopathy, diabetic foot, cognitive impairment, and many more. Evidence suggests that cognitive dysfunction is a rising complication of diabetes which adversely affects the brain of patients suffering from diabetes. Age‐related memory impairment is a complication having its major effect on people suffering from diabetes and Alzheimer's. Patients suffering from diabetes are at two times higher risk of developing cognitive dysfunction as compared with normal individuals. Multiple factors which are involved in diabetes related complications are found to play a role in the development of neurodegeneration in Alzheimer's. The problem of insulin deficiency and insulin resistance is well reported in diabetes but there are many studies which suggest dysregulation of insulin levels as a reason behind the development of Alzheimer's. As the link between diabetes and Alzheimer disease (AD) is deepening, there is a need to understand the plausible tie‐ins between the two. Emerging role of major factors like insulin imbalance, advanced glycation end products and micro‐RNA's involved in diabetes and Alzheimer's have been discussed here. This review helps in understanding the plausible mechanism underlying the pathophysiology of amyloid beta (Aβ) plaque formation and tau hyperphosphorylation as well provides information about studies carried out in this area of research. The final thought is to enhance the scientific knowledge on this correlation and develop future therapeutics to treat the same.

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“…Administration of interleukin-1 beta impairs memory . In addition, Ah deposits seen in Alzheimer's disease share the same alpha-helix conformation as amylin deposits found in pancreatic beta-cells (Holden and Mooney, 1995), and diabetes doubles the risk of developing Alzheimer's disease. In addition, the hippocampus, an area important in learning and memory and affected in Alzheimer's disease, has a large number of insulin receptors (Holden and Mooney, 1995).…”

Section: Introductionmentioning

confidence: 98%

“…In addition, Ah deposits seen in Alzheimer's disease share the same alpha-helix conformation as amylin deposits found in pancreatic beta-cells (Holden and Mooney, 1995), and diabetes doubles the risk of developing Alzheimer's disease. In addition, the hippocampus, an area important in learning and memory and affected in Alzheimer's disease, has a large number of insulin receptors (Holden and Mooney, 1995). Administration of insulin improves memory in diabetic mice, in normal healthy young men, and in Alzheimer's patients without the apolipoprotein-E genotype (Craft et al, 2000;Flood et al, 1990;Kern et al, 2001).…”

Section: Introductionmentioning

confidence: 98%