Diabetes Mellitus-Related Dysfunction of the Motor System

Muramatsu, Ken

doi:10.3390/ijms21207485

Cited by 42 publications

(33 citation statements)

References 219 publications

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“…As such, much of the diabetic body of literature focuses on sensory neuropathy as this is the primary clinical concern, but the contributive impact of AGEs in diabetic neuropathogenesis needs further study. It has been posited that motor neurons are partially protected by the central nervous system blood–brain barrier from the glycolytic attack that sensory nerve cell bodies experience in the diabetic state [ 140 , 141 ]. Additionally, other compensatory mechanisms likely exist for motor nerves (e.g., single motor unit action potential enlargement) that sensory nerves lack [ 142 ].…”

Section: Peripheral Nerve Involvement In Aging and Atrophymentioning

confidence: 99%

Advanced Glycation End-Products in Skeletal Muscle Aging

et al. 2021

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Advanced age causes skeletal muscle to undergo deleterious changes including muscle atrophy, fast-to-slow muscle fiber transition, and an increase in collagenous material that culminates in the age-dependent muscle wasting disease known as sarcopenia. Advanced glycation end-products (AGEs) non-enzymatically accumulate on the muscular collagens in old age via the Maillard reaction, potentiating the accumulation of intramuscular collagen and stiffening the microenvironment through collagen cross-linking. This review contextualizes known aspects of skeletal muscle extracellular matrix (ECM) aging, especially the role of collagens and AGE cross-linking, and underpins the motor nerve’s role in this aging process. Specific directions for future research are also discussed, with the understudied role of AGEs in skeletal muscle aging highlighted. Despite more than a half century of research, the role that intramuscular collagen aggregation and cross-linking plays in sarcopenia is well accepted yet not well integrated with current knowledge of AGE’s effects on muscle physiology. Furthermore, the possible impact that motor nerve aging has on intramuscular cross-linking and muscular AGE levels is posited.

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Section: Peripheral Nerve Involvement In Aging and Atrophymentioning

confidence: 99%

Advanced Glycation End-Products in Skeletal Muscle Aging

et al. 2021

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“…T1DM causes insulin deficiency with effects on the expression of neurotrophic factors, neurotransmission, loss of functional integrity, and defects in brain connectivity. T2DM causes cognitive decline and dementia due to decreased insulin sensitivity [111][112].…”

Section: Cyclo-oxygenase Pathwaymentioning

confidence: 99%

“…Imaging shows a decreased volume of the hippocampus and electrophysiological studies reveal a reduction in long-term potentiation. This causes a decline in learning, memory, and affective expression [112,114].…”

Section: Cyclo-oxygenase Pathwaymentioning

confidence: 99%

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A Comprehensive Review of Neuronal Changes in Diabetics

Luna¹,

Manjunatha²,

Bollu³

et al. 2021

Cureus

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“…These motor dysfunctions were previously believed to be caused by a combination of sensory neuropathy and muscle wasting [ 5 ]. However, recent studies have revealed that motor system dysfunction, including the cerebral cortex and spinal cord, can also cause motor dysfunction in these patients [ 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

Functional and Structural Changes in the Corticospinal Tract of Streptozotocin-Induced Diabetic Rats

Muramatsu

Shimo²,

Tamaki³

et al. 2021

IJMS

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This study aimed to reveal functional and morphological changes in the corticospinal tract, a pathway shown to be susceptible to diabetes. Type 1 diabetes was induced in 13-week-old male Wistar rats administered streptozotocin. Twenty-three weeks after streptozotocin injection, diabetic animals and age-matched control animals were used to demonstrate the conduction velocity of the corticospinal tract. Other animals were used for morphometric analyses of the base of the dorsal funiculus of the corticospinal tract in the spinal cord using both optical and electron microscopy. The conduction velocity of the corticospinal tract decreased in the lumbar spinal cord in the diabetic animal, although it did not decrease in the cervical spinal cord. Furthermore, atrophy of the fibers of the base of the dorsal funiculus was observed along their entire length, with an increase in the g-ratio in the lumbar spinal cord in the diabetic animal. This study indicates that the corticospinal tract fibers projecting to the lumbar spinal cord experience a decrease in conduction velocity at the lumbar spinal cord of these axons in diabetic animals, likely caused by a combination of axonal atrophy and an increased g-ratio due to thinning of the myelin sheath.

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Diabetes Mellitus-Related Dysfunction of the Motor System

Cited by 42 publications

References 219 publications

Advanced Glycation End-Products in Skeletal Muscle Aging

Advanced Glycation End-Products in Skeletal Muscle Aging

A Comprehensive Review of Neuronal Changes in Diabetics

Functional and Structural Changes in the Corticospinal Tract of Streptozotocin-Induced Diabetic Rats

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