Journal of neuropathology and experimental neurology
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J. Neuropathol. Exp. Neurol. · Dec 2003
Biography Historical ArticleAANP award for meritorious service presented to Bernardino Ghetti, MD.
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J. Neuropathol. Exp. Neurol. · Aug 2003
ReviewFrom cell death to neuronal regeneration: building a new brain after traumatic brain injury.
During the past decade, there has been accumulating evidence of the involvement of passive and active cell death mechanisms in both the clinical setting and in experimental models of traumatic brain injury (TBI). Traditionally, research for a treatment of TBI consists of strategies to prevent cell death using acute pharmacological therapy. However, to date, encouraging experimental work has not been translated into successful clinical trials. ⋯ Recent experimental studies have identified a variety of candidate cell lines for transplantation into the injured CNS. Additionally, the characterization of the neurogenic potential of specific regions of the adult mammalian brain and the elucidation of the molecular controls underlying regeneration may allow for the development of neuronal replacement therapies that do not require transplantation of exogenous cells. These novel strategies may represent a new opportunity of great interest for delayed intervention in patients with TBI.
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Many of us who conduct research based on disorders that uniquely affect the human nervous system are involved directly or indirectly with brain banks. Brain banking is by its very nature a multi-disciplinary endeavor that requires close collaboration with our colleagues in clinical departments and also with the families and patients who are donors of brain tissue. These brain tissues will ultimately be used for many types of basic science investigations. ⋯ This paper represents a broad overview of brain banking and the issues that are common to all brain banks. Legal and ethical concerns regarding confidentiality of donor records and donor recruitment procedures, as well as safety precautions for technical staff, tissue banking methods and disbursement will be discussed. Finally, issues surrounding financial support for brain banks will be considered.
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J. Neuropathol. Exp. Neurol. · Jul 2003
Comparative StudyProinsulin C-peptide replacement in type 1 diabetic BB/Wor-rats prevents deficits in nerve fiber regeneration.
We recently reported that early gene responses and expression of cytoskeletal proteins are perturbed in regenerating nerve in type 1 insulinopenic diabetes but not in type 2 hyperinsulinemic diabetes. We hypothesized that these differences were due to impaired insulin action in the former type of diabetes. To test this hypothesis, type 1 diabetic BB/Wor-rats were replaced with proinsulin C-peptide, which enhances insulin signaling without lowering blood glucose. ⋯ These effects translated into normalization of axonal radial growth and significantly improved axonal elongation of regenerating fibers in C-peptide-replaced BB/Wor-rats. The findings in C-peptide replaced type 1 diabetic rats were similar to those previously reported in hyperinsulinemic and iso-hyperglycemic type 2 BB/Z-rats. We conclude that impaired insulin action may be more important than hyperglycemia in suppressing nerve fiber regeneration in type 1 diabetic neuropathy.
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J. Neuropathol. Exp. Neurol. · May 2003
Nitrosative and oxidative injury to premyelinating oligodendrocytes in periventricular leukomalacia.
Periventricular leukomalacia (PVL), the major substrate of cerebral palsy in survivors of prematurity, is defined as focal periventricular necrosis and diffuse gliosis in immature cerebral white matter. We propose that nitrosative and/or oxidative stress to premyelinating oligodendrocytes complicating cerebral ischemia in the sick premature infant is a key mechanism of injury interfering with maturation of these cells to myelin-producing oligodendrocytes and subsequent myelination. ⋯ These data establish that PVL is primarily a white matter disease that involves injury to premyelinating oligodendrocytes, potentially through activation of microglia and release of reactive oxygen and nitrogen species. Agents that prevent nitrosative and oxidative stress may play a key role in ameliorating PVL in premature infants in the intensive care nursery.