The lower regeneration potential reported for C57BL/6J mice strain after peripheral nerve lesion may result from alterations in crucial events during Wallerian degeneration. We analysed neurofilament and myelin breakdown, macrophage recruitment, NADPH-diaphorase reaction and inducible nitric oxide synthase (iNOS) expression in transected sciatic nerves of C57BL/6J and A/J mice. The neurofilament volume density was lower in C57BL/6J strain mice at 1 and 3 days after lesion, and later equalled the density observed in A/J. C57BL/6J mice presented a high number of cells containing myelin debris, 3 and 5 days after the lesion. In both strains iNOS immunoreactivity was intense in macrophages and less evident in Schwann cells. However, a delay in macrophage recruitment and a lower percentage of iNOS-expressing macrophages on the third day were observed in C57BL/6J mice. NADPH-diaphorase reaction disclosed a similar pattern for both strains until the seventh day. However, at 5 days, cells with slender processes involving ellipsoid segments showed a well-defined cytoplasmic labelling in C57BL/6J whereas in A/J most of these cells exhibited a more granular and disperse labelling. We propose that these differences between A/J and C57BL/6J strains during Wallerian degeneration may be implicated in the lower regeneration potential observed in the latter.
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http://dx.doi.org/10.1046/j.1469-7580.2003.00248.x | DOI Listing |
Cell Death Dis
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In vitro Toxicology and Biomedicine, Dept. inaugurated by the Doerenkamp-Zbinden foundation, University of Konstanz, 78457, Konstanz, Germany.
Neurite degeneration (ND) precedes cell death in many neurodegenerative diseases. However, it remains unclear how this compartmentalized cell death process is orchestrated in the central nervous system (CNS). The establishment of a CNS axotomy model (using modified 3D LUHMES cultures) allowed us to study metabolic control of ND in human midbrain-derived neurons without the use of toxicants or other direct disturbance of cellular metabolism.
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Department of Clinical Neuroscience, Division of Eye and Vision, St. Erik Eye Hospital, Karolinska Institutet, Stockholm, Sweden.
Heliyon
January 2025
Department of Neurology, Xinhua Hospital Affiliated with Dalian University, Dalian, Liaoning Province, China.
Wallerian degeneration (WD) was first discovered by Augustus Waller in 1850 in a transection of the glossopharyngeal and hypoglossal nerves in frogs. Initial studies suggested that the formation mechanism of WD is related to the nutrition of neuronal cell bodies to axons. However, with the wide application of transgenic mice in experiments, the latest studies have found that the mechanism of WD is related to axonal degeneration, myelin clearance and extracellular matrix.
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Department of Radiology, Jawaharlal Nehru Medical College, Datta Meghe Institute of Higher Education & Research, Sawangi, Meghe, Wardha, India.
Dyke-Davidoff-Masson syndrome (DDMS) is a rare neurological disorder characterized by cerebral hemiatrophy, leading to seizures, hemiparesis, and cognitive deficits. We report the case of a 20-year-old female with a history of chronic seizure disorder and left-sided hemiparesis. The patient experienced her first seizure at 6 months of age, followed by recurrent generalized tonic seizures throughout childhood.
View Article and Find Full Text PDFbioRxiv
January 2025
Department of Biology, University of Iowa, Iowa City, IA 52242 USA.
Neurotrophic factors are critical for establishing functional connectivity in the nervous system and sustaining neuronal survival through adulthood. As the first neurotrophic factor purified, nerve growth factor (NGF) is extensively studied for its prolific role in axon outgrowth, pruning, and survival. Applying NGF to diseased neuronal tissue is an exciting therapeutic option and understanding how NGF regulates local axon susceptibility to pathological degeneration is critical for exploiting its full potential.
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