Nonenzymatic incorporation of glucose and galactose into brain cytoskeletal proteins in vitro

Brown, M. R. W.; Keith, Tim J.; Knull, Harvey R.

doi:10.1016/0197-0186(92)90144-g

Cited by 10 publications

(2 citation statements)

References 36 publications

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“…They hypothesized that this pattern may be a result of reduced accumulation of cytoskeletal elements distally because of impaired transport [164]. Additional cytoskeletal protein defectsinclude direct actin and neurofilament glycation in the setting of hyperglycemia in vitro [34], andin vivo [69, 191](as reviewed in [163]), as well as reduced expression of heavy and light neurofilament, and α -tubulin in the DRGs of type I diabetic animals [172]. It should be noted, however, that while actin glycationdoes not interfere with its ability to polymerize [191], glycosylated tubulin has a reduced polymerization ability [274].…”

Section: Mechanisms Of Peripheral Neuropathymentioning

confidence: 99%

Mechanisms of distal axonal degeneration in peripheral neuropathies

Cashman

Höke²

2015

Neuroscience Letters

168

181

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Peripheral neuropathy is a common complication of a variety of diseases and treatments, including diabetes, cancer chemotherapy, and infectious causes (HIV, hepatitis C, and Campylobacter jejuni). Despite the fundamental difference between these insults, peripheral neuropathy develops as a combination of just six primary mechanisms: altered metabolism, covalent modification, altered organelle function and reactive oxygen species formation, altered intracellular and inflammatory signaling, slowed axonal transport, and altered ion channel dynamics and expression. All of these pathways converge to lead to axon dysfunction and symptoms of neuropathy. The detailed mechanisms of axon degeneration itself have begun to be elucidated with studies of animal models with altered degeneration kinetics, including the slowed Wallerian degeneration (Wlds) and Sarmknockout animal models. These studies have shown axonal degeneration to occur througha programmed pathway of injury signaling and cytoskeletal degradation. Insights into the common disease insults that converge on the axonal degeneration pathway promise to facilitate the development of therapeutics that may be effective against other mechanisms of neurodegeneration.

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Section: Mechanisms Of Peripheral Neuropathymentioning

confidence: 99%

Mechanisms of distal axonal degeneration in peripheral neuropathies

Cashman

Höke²

2015

Neuroscience Letters

168

181

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“…In fact, axonal transport abnormalities have been implicated in diabetic peripheral neuropathy for nearly 30 years ( Medori et al, 1985 ). DM may cause alterations in cytoskeletal components, such as actin, neurofilaments, and tubulin, which are essential for normal intracellular (axonal) transport, either by direct glycation under hyperglycemic conditions or due to impaired gene expression ( Cullum et al, 1991 ; Brown et al, 1992 ; Mohiuddin and Tomlinson, 1997 ). For example, tubulin glycation in DM impairs polymerization and alters microtubule dynamics, which are crucial for the transport of intracellular macromolecules and organelles ( Williams et al, 1982 ).…”

Section: The Challenges Axon Faces During Agingmentioning

confidence: 99%

Alzheimer’s disease: an axonal injury disease?

Dan,

Zhang

2023

Front. Aging Neurosci.

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Alzheimer’s disease (AD) is the primary cause of dementia and is anticipated to impose a substantial economic burden in the future. Over a significant period, the widely accepted amyloid cascade hypothesis has guided research efforts, and the recent FDA approval of an anti- amyloid-beta (Aβ) protofibrils antibody, believed to decelerate AD progression, has further solidified its significance. However, the excessive emphasis placed on the amyloid cascade hypothesis has overshadowed the physiological nature of Aβ and tau proteins within axons. Axons, specialized neuronal structures, sustain damage during the early stages of AD, exerting a pivotal influence on disease progression. In this review, we present a comprehensive summary of the relationship between axonal damage and AD pathology, amalgamating the physiological roles of Aβ and tau proteins, along with the impact of AD risk genes such as APOE and TREM2. Furthermore, we underscore the exceptional significance of axonal damage in the context of AD.

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Immunological detection of glycated proteins in normal and streptozotocin-induced diabetic rats using anti hexitol-lysine IgG

Myint

Hoshi

Ookawara

et al. 1995

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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A polyclonal antibody specific for the Amadori compound, a product of an early stage of the Maillard reaction, was raised in rabbits by immunization with hexitol-lysine (1-glucitol-lysine or 1-mannitol-lysine) coupled with various carrier proteins. The affinity purified antibody has a high titre and preferentially recognizes the glucose adduct, in the presence of sodium borohydride, as judged on enzyme-linked immunosorbent assay as well as immunoblot analysis. The glycated proteins (Amadori products) in various tissues of normal and streptozotocin-induced diabetic rats were examined by immunoblot analysis. In diabetic conditions, kidney, liver, lens, brain and lung proteins are more susceptible to glycation than other tissue proteins. Heart, spleen, adrenal gland and muscle proteins exhibit similar extents of glycation in both normal and diabetic conditions. This is the first demonstration of a specific antibody against the Amadori compound being raised with a synthetic compound, and of the tissue distribution of glycated proteins in normal and diabetic conditions. The antibody was very useful for in vitro and in vivo experiments on the Maillard reaction.

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Nonenzymatic incorporation of glucose and galactose into brain cytoskeletal proteins in vitro

Cited by 10 publications

References 36 publications

Mechanisms of distal axonal degeneration in peripheral neuropathies

Mechanisms of distal axonal degeneration in peripheral neuropathies

Alzheimer’s disease: an axonal injury disease?

Immunological detection of glycated proteins in normal and streptozotocin-induced diabetic rats using anti hexitol-lysine IgG

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