Mechanism of Schwann cells in diabetic peripheral neuropathy: A review

Li, Jingjing; Guan, Ruiqian; Pan, Limin

doi:10.1097/md.0000000000032653

Cited by 18 publications

(9 citation statements)

References 30 publications

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“…Diabetes-induced alterations in Schwann cells are linked to neuronal damage, leading to diabetic peripheral neuropathy [ 91 , 92 ]. These alterations compromise the synthesis and release of neuronal support factors and result in the build-up of neurotoxic and pro-inflammatory factors, including tumor necrosis factor (TNF-α), interleukin (IL)-1α, IL-1β, monocyte chemoattractant protein-1 (MCP-1), and CXCL2, which in turn contribute to endothelial dysfunction, axonal degeneration, and neuronal damage [ 93 , 94 , 95 ].…”

Section: Myelinating Glia: Oligodendrocytes and Schwann Cellsmentioning

confidence: 99%

Effects of a Diabetic Microenvironment on Neurodegeneration: Special Focus on Neurological Cells

Chavda,

Yadav,

Patel

et al. 2024

Brain Sciences

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Diabetes is a chronic metabolic condition associated with high levels of blood glucose which leads to serious damage to the heart, kidney, eyes, and nerves. Elevated blood glucose levels damage brain function and cognitive abilities. They also lead to various neurological and neuropsychiatric disorders, including chronic neurodegeneration and cognitive decline. High neuronal glucose levels can cause drastic neuronal damage due to glucose neurotoxicity. Astrocytes, a type of glial cell, play a vital role in maintaining brain glucose levels through neuron–astrocyte coupling. Hyperglycemia leads to progressive decline in neuronal networks and cognitive impairment, contributing to neuronal dysfunction and fostering a neurodegenerative environment. In this review, we summarize the various connections, functions, and impairments of glial cells due to metabolic dysfunction in the diabetic brain. We also summarize the effects of hyperglycemia on various neuronal functions in the diabetic brain.

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Section: Myelinating Glia: Oligodendrocytes and Schwann Cellsmentioning

confidence: 99%

Effects of a Diabetic Microenvironment on Neurodegeneration: Special Focus on Neurological Cells

Chavda,

Yadav,

Patel

et al. 2024

Brain Sciences

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“…Several laboratories have reported that inhibition of PKCβ improves vascular and neural function in diabetic rodents ( 51 – 54 ). In addition, dysregulation of Schwann cells in part through altered PKC activity can contribute to DPN ( 50 , 55 – 58 ). In streptozotocin-induced diabetic rats’ activity of PKCα was decreased in neurons and Schwann cells that was corrected by treatment with methylcobalamin ( 59 ).…”

Section: Protein Kinase C Pathwaymentioning

confidence: 99%

Combination therapy is it in the future for successfully treating peripheral diabetic neuropathy?

Yorek

2024

Front. Endocrinol.

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In 2022, the Center for Disease Control and Prevention reported that 11.3% of the United States population, 37.3 million people, had diabetes and 38% of the population had prediabetes. A large American study conducted in 2021 and supported by many other studies, concluded that about 47% of diabetes patients have peripheral neuropathy and that diabetic neuropathy was present in 7.5% of patients at the time of diabetes diagnosis. In subjects deemed to be pre-diabetes and impaired glucose tolerance there was a wide range of prevalence estimates (interquartile range (IQR): 6%-34%), but most studies (72%) reported a prevalence of peripheral neuropathy ≥10%. There is no recognized treatment for diabetic peripheral neuropathy (DPN) other than good blood glucose control. Good glycemic control slows progression of DPN in patients with type 1 diabetes but for patients with type 2 diabetes it is less effective. With obesity and type 2 diabetes at epidemic levels the need of a treatment for DPN could not be more important. In this article I will first present background information on the “primary” mechanisms shown from pre-clinical studies to contribute to DPN and then discuss mono- and combination therapies that have demonstrated efficacy in animal studies and may have success when translated to human subjects. I like to compare the challenge of finding an effective treatment for DPN to the ongoing work being done to treat hypertension. Combination therapy is the recognized approach used to normalize blood pressure often requiring two, three or more drugs in addition to lifestyle modification to achieve the desired outcome. Hypertension, like DPN, is a progressive disease caused by multiple mechanisms. Therefore, it seems likely as well as logical that combination therapy combined with lifestyle adjustments will be required to successfully treat DPN.

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“…They secrete various neuroprotective factors that provide neural support against reactive oxygen species (ROS), and inflammation in pathological as well as physiologic states [13,14]. Both peripheral neurons (PN) and Schwann cells are sensitive to excessive ROS levels like those seen in T2D.…”

Section: Diabetic Peripheral Neuropathymentioning

confidence: 99%

Early Detection of Peripheral Neuropathy by Assessment of Sudomotor Function

Whaley,,

Danev,

Alexander

et al. 2024

Neuro Neurosci

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Chronic hyperglycemia in both type 1 and type 2 diabetes commonly lead to diabetic peripheral neuropathy (DPN) which commonly affects small nerve fibers, including autonomic sudomotor nerves, of the lower limbs. DPN results from nerve damage leading to gradual onset of foot pain, tingling, numbness, muscle weakness, extreme sensitivity to touch, and heat intolerance. Peripheral neuropathy is associated with increased all-cause mortality and morbidities such as foot ulcers, poor wound healing, local and systemic infection, limb amputation, and painful neuropathic symptoms. DPN is also typically diagnosed during later stages when disease progression has already led to irreversible nerve damage and associated severe symptoms. As such, early detection of peripheral neuropathy is important in implementing early interventions and can help preserve nerve function and prevent serious complications of DPN. Non-invasive methods of testing for early DPN rely on assessment of sudomotor nerve function. One method includes quantitative sudomotor axon reflex test (QSART) which measures postganglionic sympathetic function via iontophoresis which allows quantification of sweat production, and by extension, autonomic function. In general, QSART provides a non-invasive, reproducible, and precise evaluation of autonomic function in both controls and diabetics. It can be used to evaluate a large number of autonomic diseases, and the quantitative data it generates provides a measure of the extent and location of the peripheral neuropathy in each individual. Another assessment method includes the sympathetic skin response (SSR) test which measures the change in electrical potential of the skin which itself comes from activated eccrine sweat glands. The SSR test has a well-established protocol, and the results are easily-measured, and the results are quantifiable. It can be used reliably in the diagnosis of numerous autonomic disorders including DPN where a diminished or absent response correlate with sudomotor nerve damage. SudoCheck by VitalScan is an FDA-cleared, non-invasive autonomic sdomotor assessment tool that combines QSART, SSR, BIA, and EIS to provide rapid results with a specificity of 95% and a sensitivity of 80%. It was created to enable a precise evaluation of sweat gland function, and by extension, the presence and progression of diabetic peripheral neuropathy including early sub-clinical disease

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Mechanism of Schwann cells in diabetic peripheral neuropathy: A review

Cited by 18 publications

References 30 publications

Effects of a Diabetic Microenvironment on Neurodegeneration: Special Focus on Neurological Cells

Effects of a Diabetic Microenvironment on Neurodegeneration: Special Focus on Neurological Cells

Combination therapy is it in the future for successfully treating peripheral diabetic neuropathy?

Early Detection of Peripheral Neuropathy by Assessment of Sudomotor Function

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