vincristine/atrophy

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Spatiotemporal localization of injury potentials in DRG neurons during vincristine-induced axonal degeneration.

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The distal to proximal degeneration of axons, or "dying back" is a common pattern of neuropathology in many diseases of the PNS and CNS. A long-standing debate has centered on whether this pattern of neurodegeneration is due to an insult to the cell body or to the axon itself, although it is likely

Retinal and optic nerve atrophy induced by intravitreous vincristine in the primate.

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Vincristine is known to be toxic to neural tissue, where it is thought to react with microtubules and impair axonal transport. Intravitreous vincristing-induced changes of the retina have been reported to be reversible after 10 micrograms. In the present study, the effects of 0.01 to 100 micrograms

[Study of the effects of isaxonine on retrograde axon degeneration induced by vincristine in man (author's transl)].

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Fifteen patients with Hodgkin's disease were examined before and after each administration of vincristine sulfate (2 intravenous injections of 1.4 mg/m2 of body surface, during the first week of each month for 3 months). Moreover, each patient received daily, according to a double blind protocol,

Topical application of colchicine, vinblastine and vincristine prevents strychnine-enhanced transsynaptic degeneration in the medullary dorsal horn following transection of the inferior alveolar nerve in adult rats.

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The effect of topical application of axonal transport blockers to the transected peripheral nerve was assessed by quantitating the strychnine-enhanced transsynaptic degeneration following transection of the inferior alveolar nerve in adult rats. Systemic administration of strychnine (1 mg/kg/day)

Optic atrophy induced by vincristine.

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Bilateral optic atrophy developed in a 15-year-old patient receiving concomitant neuraxis radiation therapy and weekly vincristine sulfate for medulloblastoma. Other neurologic manifestations that have been associated with vincristine therapy, including inappropriate secretion of antidiuretic

Pathogenesis of axonal degeneration: parallels between Wallerian degeneration and vincristine neuropathy.

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Peripheral neuropathies and Wallerian degeneration share a number of pathological features; the most prominent of which is axonal degeneration. We asked whether common pathophysiologic mechanisms are involved in these 2 disorders by directly comparing in vitro models of axonal degeneration after

CRMP4 mediates MAG-induced inhibition of axonal outgrowth and protection against Vincristine-induced axonal degeneration.

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Suppression of inhibition of axonal outgrowth and promotion of axonal protection from progressive axonal degeneration are both therapeutic strategies for the treatment of neuronal diseases characterized by axonal loss. Myelin-associated inhibitors (MAIs) have been shown to suppress axonal outgrowth,

Mitochondrial Dynamics Decrease Prior to Axon Degeneration Induced by Vincristine and are Partially Rescued by Overexpressed cytNmnat1.

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Axon degeneration is a prominent feature of various neurodegenerative diseases, such as Parkinson's and Alzheimer's, and is often characterized by aberrant mitochondrial dynamics. Mitochondrial fission, fusion, and motility have been shown to be particularly important in progressive

The gene for slow Wallerian degeneration (Wld(s)) is also protective against vincristine neuropathy.

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Neurological diseases are frequently associated with axonal degeneration, which leads to dysfunction though separation of neurons from their targets. The mechanisms of axonal degeneration are largely unknown and in many cases are independent of those occurring within cell bodies in neurodegenerative

Vincristine and bortezomib use distinct upstream mechanisms to activate a common SARM1-dependent axon degeneration program.

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Chemotherapy-induced peripheral neuropathy is one of the most prevalent dose-limiting toxicities of anticancer therapy. Development of effective therapies to prevent chemotherapy-induced neuropathies could be enabled by a mechanistic understanding of axonal breakdown following exposure to

Acute deterioration of Charcot-Marie-Tooth disease IA (CMT IA) following 2 mg of vincristine chemotherapy.

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BACKGROUND Severe up to life-threatening neuropathy has been observed in patients with hereditary neuropathies receiving vincristine. METHODS A 52-year-old female painter suffering from high-grade non-Hodgkin's lymphoma (stage IVB) was treated with a total of 4 mg of vincristine during two courses

Neurofibrillary degeneration induced by vincristine therapy.

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Spheromembranous degeneration of muscle induced by vincristine.

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Effects of colchicine, vinblastine and vincristine on degeneration transmitter release after sympathetic denervation studied in the conscious rat.

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Self-hypnosis misinterpreted as CNS deterioration in an adolescent with leukemia and vincristine toxicity.

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