We are analyzing https://link.springer.com/article/10.1007/s00702-010-0498-0.

Title:
Traumatic brain injury and recovery mechanisms: peptide modulation of periventricular neurogenic regions by the choroid plexus–CSF nexus | Journal of Neural Transmission
Description:
In traumatic brain injury (TBI), severe disruptions occur in the choroid plexus (CP)–cerebrospinal fluid (CSF) nexus that destabilize the nearby hippocampal and subventricular neurogenic regions. Following invasive and non-invasive injuries to cortex, several adverse sequelae harm the brain interior: (i) structural damage to CP epithelium that opens the blood–CSF barrier (BCSFB) to protein, (ii) altered CSF dynamics and intracranial pressure (ICP), (iii) augmentation of leukocyte traffic across CP into the CSF–brain, (iv) reduction in CSF sink action and clearance of debris from ventricles, and (v) less efficient provision of micronutritional and hormonal support for the CNS. However, gradual post-TBI restitution of the injured CP epithelium and ependyma, and CSF homeostatic mechanisms, help to restore subventricular/subgranular neurogenesis and the cognitive abilities diminished by CNS damage. Recovery from TBI is faciltated by upregulated choroidal/ependymal growth factors and neurotrophins, and their secretion into ventricular CSF. There, by an endocrine-like mechanism, CSF bulk flow convects the neuropeptides to target cells in injured cortex for aiding repair processes; and to neurogenic niches for enhancing conversion of stem cells to new neurons. In the recovery from TBI and associated ischemia, the modulating neuropeptides include FGF2, EGF, VEGF, NGF, IGF, GDNF, BDNF, and PACAP. Homeostatic correction of TBI-induced neuropathology can be accelerated or amplified by exogenously boosting the CSF concentration of these growth factors and neurotrophins. Such intraventricular supplementation via the CSF route promotes neural restoration through enhanced neurogenesis, angiogenesis, and neuroprotective effects. CSF translational research presents opportunities that involve CP and ependymal manipulations to expedite recovery from TBI.
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Keywords {🔍}

csf, brain, google, scholar, tbi, pubmed, injury, johanson, cells, cas, fluid, choroid, growth, bcsfb, factor, plexus, epithelium, epithelial, neurogenesis, peptide, fig, recovery, traumatic, sharma, cns, cerebrospinal, flow, system, barrier, ventricles, factors, ischemia, trauma, rat, neurogenic, transporters, rats, res, neural, cell, membrane, formation, damage, injured, effects, cerebral, icp, bbb, lateral, response,

Topics {✒️}

leukocyte traffic dentate gyrus–hippocampus restore subventricular/subgranular neurogenesis dentate gyrus involves leukocyte permeation subventricular zone blood-brain barrier permeability organic anion-transporting polypeptide blood–cerebrospinal fluid barrier blood-cerebrospinal fluid barrier cp–csf–ependyma/svz distributional nexus brain fluid/pressure imbalance vegfr-2/flk-1 kinase receptor na–k-atpase inhibitors cogent research/therapeutic challenge quasi-lymphatic excretory system establishing brain homeostasis organic anion-transporting polypeptides article download pdf mild hypoxic/ischemic damage local autocrine/paracrine processes decreases interleukin-1beta level choroid plexus-csf route post-traumatic cerebral ischemia blood-cerebrospinal fluid barriers ventriculo-subarachnoid spaces acts sudden/intense lateral movement modulates beta-amyloid neurotrophin-promoted neurogenesis enhance reaching large-cavity csf intracranial pressure regulation single-cell epithelial layer choroid plexus-csf system adenovirus-mediated gene transfer fgf-2-induced hydrocephalus choroid plexus–csf nexus inter-epithelial paracellular pathway bilirubin-induced neurological diseases subventricular neurogenic regions injury 1–3 day post-contusion csf-borne substances diffuse csf-borne peptides confers small water-soluble molecules high-pressure hydrocephalus restore cognition post-tbi enhanced vascular permeability gradual post-tbi restitution reveal cp–csf mechanisms cp-attached kolmer cells blood–brain barrier

Questions {❓}

A related question: Is there an increased number of CP dark cells in TBI?
Deserving elucidation is whether injury signals (cytokines?
Remarkably in the TFI experiments, the choroid epithelial cells were largely recovered (or replaced?
Why not also include CP epithelium as a potential target for facilitating the recovery from TBI-generated damage, or at least preventing a greater degree of injury?

Schema {🗺️}

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         headline:Traumatic brain injury and recovery mechanisms: peptide modulation of periventricular neurogenic regions by the choroid plexus–CSF nexus
         description:In traumatic brain injury (TBI), severe disruptions occur in the choroid plexus (CP)–cerebrospinal fluid (CSF) nexus that destabilize the nearby hippocampal and subventricular neurogenic regions. Following invasive and non-invasive injuries to cortex, several adverse sequelae harm the brain interior: (i) structural damage to CP epithelium that opens the blood–CSF barrier (BCSFB) to protein, (ii) altered CSF dynamics and intracranial pressure (ICP), (iii) augmentation of leukocyte traffic across CP into the CSF–brain, (iv) reduction in CSF sink action and clearance of debris from ventricles, and (v) less efficient provision of micronutritional and hormonal support for the CNS. However, gradual post-TBI restitution of the injured CP epithelium and ependyma, and CSF homeostatic mechanisms, help to restore subventricular/subgranular neurogenesis and the cognitive abilities diminished by CNS damage. Recovery from TBI is faciltated by upregulated choroidal/ependymal growth factors and neurotrophins, and their secretion into ventricular CSF. There, by an endocrine-like mechanism, CSF bulk flow convects the neuropeptides to target cells in injured cortex for aiding repair processes; and to neurogenic niches for enhancing conversion of stem cells to new neurons. In the recovery from TBI and associated ischemia, the modulating neuropeptides include FGF2, EGF, VEGF, NGF, IGF, GDNF, BDNF, and PACAP. Homeostatic correction of TBI-induced neuropathology can be accelerated or amplified by exogenously boosting the CSF concentration of these growth factors and neurotrophins. Such intraventricular supplementation via the CSF route promotes neural restoration through enhanced neurogenesis, angiogenesis, and neuroprotective effects. CSF translational research presents opportunities that involve CP and ependymal manipulations to expedite recovery from TBI.
         datePublished:2010-10-10T00:00:00Z
         dateModified:2010-10-10T00:00:00Z
         pageStart:115
         pageEnd:133
         license:https://creativecommons.org/licenses/by-nc/2.0
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         keywords:
            CSF homeostasis
            Subventricular zone
            Blood–CSF barrier permeability
            Periventricular lesions
            Hydrocephalus
            Leukocyte traffic
            Neurogenesis
            Intracranial pressure
            Ischemia
            Traumatic brain injury models
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            Hippocampus
            Cerebrospinal formation and drainage
            CSF dynamics
            Neuropeptides
            Neurology
            Psychiatry
            Neurosciences
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ScholarlyArticle:
      headline:Traumatic brain injury and recovery mechanisms: peptide modulation of periventricular neurogenic regions by the choroid plexus–CSF nexus
      description:In traumatic brain injury (TBI), severe disruptions occur in the choroid plexus (CP)–cerebrospinal fluid (CSF) nexus that destabilize the nearby hippocampal and subventricular neurogenic regions. Following invasive and non-invasive injuries to cortex, several adverse sequelae harm the brain interior: (i) structural damage to CP epithelium that opens the blood–CSF barrier (BCSFB) to protein, (ii) altered CSF dynamics and intracranial pressure (ICP), (iii) augmentation of leukocyte traffic across CP into the CSF–brain, (iv) reduction in CSF sink action and clearance of debris from ventricles, and (v) less efficient provision of micronutritional and hormonal support for the CNS. However, gradual post-TBI restitution of the injured CP epithelium and ependyma, and CSF homeostatic mechanisms, help to restore subventricular/subgranular neurogenesis and the cognitive abilities diminished by CNS damage. Recovery from TBI is faciltated by upregulated choroidal/ependymal growth factors and neurotrophins, and their secretion into ventricular CSF. There, by an endocrine-like mechanism, CSF bulk flow convects the neuropeptides to target cells in injured cortex for aiding repair processes; and to neurogenic niches for enhancing conversion of stem cells to new neurons. In the recovery from TBI and associated ischemia, the modulating neuropeptides include FGF2, EGF, VEGF, NGF, IGF, GDNF, BDNF, and PACAP. Homeostatic correction of TBI-induced neuropathology can be accelerated or amplified by exogenously boosting the CSF concentration of these growth factors and neurotrophins. Such intraventricular supplementation via the CSF route promotes neural restoration through enhanced neurogenesis, angiogenesis, and neuroprotective effects. CSF translational research presents opportunities that involve CP and ependymal manipulations to expedite recovery from TBI.
      datePublished:2010-10-10T00:00:00Z
      dateModified:2010-10-10T00:00:00Z
      pageStart:115
      pageEnd:133
      license:https://creativecommons.org/licenses/by-nc/2.0
      sameAs:https://doi.org/10.1007/s00702-010-0498-0
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         CSF homeostasis
         Subventricular zone
         Blood–CSF barrier permeability
         Periventricular lesions
         Hydrocephalus
         Leukocyte traffic
         Neurogenesis
         Intracranial pressure
         Ischemia
         Traumatic brain injury models
         Dentate gyrus
         Hippocampus
         Cerebrospinal formation and drainage
         CSF dynamics
         Neuropeptides
         Neurology
         Psychiatry
         Neurosciences
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                     type:PostalAddress
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            affiliation:
                  name:University Hospital, Uppsala University
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                     name:Laboratory of Cerebrovascular Research, Institute of Surgical Sciences, Department of Anaesthesiology and Intensive Care, University Hospital, Uppsala University, Uppsala, Sweden
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         type:PostalAddress
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         name:Department of Pathology, Warren Alpert Medical School at Brown University, Providence, USA
         type:PostalAddress
      name:UCSD School of Medicine
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         type:PostalAddress
      name:University Hospital, Uppsala University
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               type:PostalAddress
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      name:Andrew Baird
      affiliation:
            name:UCSD School of Medicine
            address:
               name:Department of Surgery, UCSD School of Medicine, San Diego, USA
               type:PostalAddress
            type:Organization
      name:Hari Sharma
      affiliation:
            name:University Hospital, Uppsala University
            address:
               name:Laboratory of Cerebrovascular Research, Institute of Surgical Sciences, Department of Anaesthesiology and Intensive Care, University Hospital, Uppsala University, Uppsala, Sweden
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Neurosurgery, Warren Alpert Medical School at Brown University, Providence, USA
      name:Department of Neurosurgery, Brown Medical School, Providence, USA
      name:Department of Pathology, Warren Alpert Medical School at Brown University, Providence, USA
      name:Department of Surgery, UCSD School of Medicine, San Diego, USA
      name:Laboratory of Cerebrovascular Research, Institute of Surgical Sciences, Department of Anaesthesiology and Intensive Care, University Hospital, Uppsala University, Uppsala, Sweden

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