1
40
2
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Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1517/13543776.2014.931375" target="_blank" rel="noreferrer noopener">http://doi.org/10.1517/13543776.2014.931375</a>
Pages
947–951
Issue
8
Volume
24
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Parkinson's disease biomarker: a patent evaluation of WO2013153386.
Publisher
An entity responsible for making the resource available
Expert opinion on therapeutic patents
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-08
Subject
The topic of the resource
Humans; Disease Progression; Biomarkers/metabolism; Phosphorylation; Mitochondria/pathology; mitophagy; autophagy; clinical testing; Dopaminergic Neurons/pathology; mitochondrial membrane potential; Parkinson Disease/*diagnosis/physiopathology; Patents as Topic; Protein Kinases/*metabolism; Ubiquitin-Protein Ligases/*metabolism
Creator
An entity primarily responsible for making the resource
Geldenhuys Werner J; Abdelmagid Samir M; Gallegos Patrick J; Safadi Fayez F
Description
An account of the resource
INTRODUCTION: Parkinson's disease (PD) is a neurodegenerative movement disorder resultant from the loss of dopaminergic neurons in the brain. There is an urgent need for effective biomarkers that can be used in the early diagnosis of PD. Mitochondrial dysfunction plays a significant role in PD pathology, which has led to the evaluation of mitophagy markers, PTEN-induced putative kinase 1 (PINK1), and PARKIN as possible biomarkers for the early diagnosis of PD. AREAS COVERED: The current patent describes the use of phosphorylation of PINK1 and PARKIN as a diagnostic measure. Specifically, Ser65 on PARKIN, which is phosphorylated by PINK1, and the autophosphorylation of PINK1 at Thr257 are described. EXPERT OPINION: This patent describes a much needed methodology that can easily be adapted in the clinical setting by which a biological sample, such as serum or cerebrospinal fluid, is collected and analyzed for the phosphorylation markers. Here, the phosphorylation activity seen in PINK1 and PARKIN can differentiate between age-matched controls and PD patients. This patent presents a novel diagnostic measure in early PD, as well as determines which medications would have a beneficial effect on a patient's disease progression.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1517/13543776.2014.931375" target="_blank" rel="noreferrer noopener">10.1517/13543776.2014.931375</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2014
Abdelmagid Samir M
Autophagy
Biomarkers/metabolism
clinical testing
Department of Anatomy & Neurobiology
Department of Pharmaceutical Sciences
Department of Pharmacy Practice
Disease Progression
Dopaminergic Neurons/pathology
Expert opinion on therapeutic patents
Gallegos Patrick J
Geldenhuys Werner J
Humans
Mitochondria/pathology
mitochondrial membrane potential
mitophagy
NEOMED College of Medicine
NEOMED College of Pharmacy
Parkinson Disease/*diagnosis/physiopathology
Patents as Topic
Phosphorylation
Protein Kinases/*metabolism
Safadi Fayez F
Ubiquitin-Protein Ligases/*metabolism
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/cne.24012" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/cne.24012</a>
Pages
3503–3517
Issue
17
Volume
524
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Persistence of intact retinal ganglion cell terminals after axonal transport loss in the DBA/2J mouse model of glaucoma.
Publisher
An entity responsible for making the resource available
The Journal of comparative neurology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-12
Subject
The topic of the resource
*Axonal Transport/physiology; *bouton; *mitochondria; *neurodegeneration; *retinal; *RRID:IMSRJAX:000671; *RRID:IMSRJAX:007048; *RRID:SCR002716; *RRID:SCR002865; *superior colliculus; *synapse; Animal; Animals; Disease Models; Electron; Glaucoma/metabolism/*pathology; Imaging; Inbred DBA; Mice; Microscopy; Mitochondria/pathology; Neuroanatomical Tract-Tracing Techniques; Regression Analysis; Retinal Ganglion Cells/metabolism/*pathology; Scanning; Superior Colliculi/metabolism/*pathology; Synapses/metabolism/*pathology; Three-Dimensional; Visual Pathways/metabolism/pathology
Creator
An entity primarily responsible for making the resource
Smith Matthew A; Xia Christina Z; Dengler-Crish Christine M; Fening Kelly M; Inman Denise M; Schofield Brett R; Crish Samuel D
Description
An account of the resource
Axonal transport defects are an early pathology occurring within the retinofugal projection of the DBA/2J mouse model of glaucoma. Retinal ganglion cell (RGC) axons and terminals are detectable after transport is affected, yet little is known about the condition of these structures. We examined the ultrastructure of the glaucomatous superior colliculus (SC) with three-dimensional serial block-face scanning electron microscopy to determine the distribution and morphology of retinal terminals in aged mice exhibiting varying levels of axonal transport integrity. After initial axonal transport failure, retinal terminal densities did not vary compared with either transport-intact or control tissue. Although retinal terminals lacked overt signs of neurodegeneration, transport-intact areas of glaucomatous SC exhibited larger retinal terminals and associated mitochondria. This likely indicates increased oxidative capacity and may be a compensatory response to the stressors that this projection is experiencing. Areas devoid of transported tracer label showed reduced mitochondrial volumes as well as decreased active zone number and surface area, suggesting that oxidative capacity and synapse strength are reduced as disease progresses but before degeneration of the synapse. Mitochondrial volume was a strong predictor of bouton size independent of pathology. These findings indicate that RGC axons retain connectivity after losing function early in the disease process, creating an important therapeutic opportunity for protection or restoration of vision in glaucoma. J. Comp. Neurol. 524:3503-3517, 2016. (c) 2016 Wiley Periodicals, Inc.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/cne.24012" target="_blank" rel="noreferrer noopener">10.1002/cne.24012</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Axonal Transport/physiology
*bouton
*Mitochondria
*neurodegeneration
*retinal
*RRID:IMSRJAX:000671
*RRID:IMSRJAX:007048
*RRID:SCR002716
*RRID:SCR002865
*superior colliculus
*synapse
2016
Animal
Animals
Crish Samuel D
Dengler-Crish Christine M
Department of Anatomy & Neurobiology
Department of Pharmaceutical Sciences
Disease Models
Electron
Fening Kelly M
Glaucoma/metabolism/*pathology
Imaging
Inbred DBA
Inman Denise M
Mice
Microscopy
Mitochondria/pathology
NEOMED College of Medicine
NEOMED College of Pharmacy
Neuroanatomical Tract-Tracing Techniques
Regression Analysis
Retinal Ganglion Cells/metabolism/*pathology
Scanning
Schofield Brett R
Smith Matthew A
Superior Colliculi/metabolism/*pathology
Synapses/metabolism/*pathology
The Journal of comparative neurology
Three-Dimensional
Visual Pathways/metabolism/pathology
Xia Christina Z