Subscribe: pubmed: 0002-9440
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pubmed: 0002-9440



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Function and Dysfunction of Adult Hippocampal Neurogenesis in Regeneration and Disease.
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Function and Dysfunction of Adult Hippocampal Neurogenesis in Regeneration and Disease.

Am J Pathol. 2017 Oct 10;:

Authors: Peng L, Bonaguidi MA

Abstract
The hippocampus is the only known brain region where physiological neurogenesis continues into adulthood across mammalian species and in humans. However, disease and injury can change the level of adult hippocampal neurogenesis, which plays an important role in regulating cognitive and emotional abilities. Alterations in hippocampal neurogenesis can mediate treatment of mental illness or affect the brain's capacity for repair and regeneration. In the present review, we evaluate how adult neurogenesis contributes to the repair and regeneration of hippocampal circuitry in the face of diseases and injuries. We also discuss possible future directions for harnessing adult neurogenesis for therapeutic use.

PMID: 29030053 [PubMed - as supplied by publisher]




Primary Cilia in Brain Development and Diseases.
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Primary Cilia in Brain Development and Diseases.

Am J Pathol. 2017 Oct 10;:

Authors: Youn YH, Han YG

Abstract
The primary cilium, a sensory appendage that is present in most mammalian cells, plays critical roles in signaling pathways and cell cycle progression. Mutations that affect the structure or function of primary cilia result in ciliopathies, a group of developmental and degenerative diseases that affect almost all organs and tissues. Our understanding of the constituents, development, and function of primary cilia has advanced considerably in recent years, revealing pathogenic mechanisms that potentially underlie ciliopathies. In the brain, the primary cilia are crucial for early patterning, neurogenesis, neuronal maturation and survival, and tumorigenesis, mostly through regulating cell cycle progression, Hedgehog signaling, and WNT signaling. We review these advances in our knowledge of primary cilia, focusing on brain development, and discuss the mechanisms that may underlie brain abnormalities in ciliopathies.

PMID: 29030052 [PubMed - as supplied by publisher]




Determinants of axon growth, plasticity, and regeneration in the context of spinal cord injury.
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Determinants of axon growth, plasticity, and regeneration in the context of spinal cord injury.

Am J Pathol. 2017 Oct 10;:

Authors: Filous AR, Schwab JM

Abstract
The mechanisms that underlie recovery after injury of the central nervous system have rarely been definitively established. Axon re-growth remains the major prerequisite for plasticity, regeneration, circuit formation, and eventually functional recovery. The attributed functional relevance of axon regrowth however will depend on a number of subsequent conditional neurobiological modifications, including myelination and synapse formation but also pruning of aberrant connectivity. Despite the ability to revamp axon outgrowth by altering an increasing number of extracellular and intracellular targets, disentangling which axons are responsible for the recovery of function from those that are functionally silent, or even contributing to aberrant functions, remains a crucial link between enhancing axonal growth profiles to functional improvement. Anatomical hallmarks of regeneration are not static and are largely activity dependent. Here we survey mechanisms leading to the formation of dystrophic growth cone at the injured axonal tip, the subsequent axonal dieback, and the molecular determinants of axon growth, plasticity, and regeneration in the context of spinal cord injury.

PMID: 29030051 [PubMed - as supplied by publisher]




Neural Regeneration a Century after Ramón y Cajal's Decree.
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Neural Regeneration a Century after Ramón y Cajal's Decree.

Am J Pathol. 2017 Oct 10;:

Authors: Otero JJ

Abstract
This Guest Editorial introduces this month’s special Neural Regeneration Theme Issue, a series of reviews intended to highlight the advances in modern neuroscience as well as to depict the chasms in our understanding of the brain.

PMID: 29030050 [PubMed - as supplied by publisher]




Inhibition of Mammalian Target of Rapamycin Signaling with Rapamycin Prevents Trauma-Induced Heterotopic Ossification.
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Inhibition of Mammalian Target of Rapamycin Signaling with Rapamycin Prevents Trauma-Induced Heterotopic Ossification.

Am J Pathol. 2017 Oct 05;:

Authors: Qureshi AT, Dey D, Sanders EM, Seavey JG, Tomasino AM, Moss K, Wheatley B, Cholok D, Loder S, Li J, Levi B, Davis TA

Abstract
A pressing clinical need exists for 63% to 65% of combat-wounded service members and 11% to 20% of civilians who develop heterotopic ossification (HO) after blast-related extremity injury and traumatic injuries, respectively. The mammalian target of rapamycin pathway is a central cellular sensor of injury. We evaluated the prophylactic effects of rapamycin, a selective inhibitor of mammalian target of rapamycin signaling, on HO formation in a rat model of blast-related, polytraumatic extremity injury. Rapamycin was administered intraperitoneally daily for 14 days at 0.5 mg/kg or 2.5 mg/kg. Ectopic bone formation was monitored by micro-computed tomography and confirmed by histologic examination. Connective tissue progenitor cells, platelet-derived growth factor receptor-α-positive cells, and α-smooth muscle actin-positive blood vessels were assayed at postoperative day 7 by colony formation and immunofluorescence. Early gene expression changes were determined by low-density microarray. There was significant attenuation of 1) total new bone and soft tissue ectopic bone with 0.5 mg/kg (38.5% and 14.7%) and 2.5 mg/kg rapamycin (90.3% and 82.9%), respectively, 2) connective tissue progenitor cells, 3) platelet-derived growth factor receptor-α-positive cells, 4) α-smooth muscle actin-positive blood vessels, and 5) of key extracellular matrix remodeling (CD44, Col1a1, integrins), osteogenesis (Sp7, Runx2, Bmp2), inflammation (Cxcl5, 10, IL6, Ccl2), and angiogenesis (Angpt2) genes. No wound healing complications were noted. Our data demonstrate the efficacy of rapamycin in inhibiting blast trauma-induced HO by a multipronged mechanism.

PMID: 29029772 [PubMed - as supplied by publisher]