PTEN: A molecular target for neurodegenerative disorders

2012 ◽  
Vol 3 (2) ◽  
Author(s):  
Azza Ismail ◽  
Ke Ning ◽  
Abdulmonem Al-Hayani ◽  
Basil Sharrack ◽  
Mimoun Azzouz
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurodegenerative Disorders ◽  
Neuronal Development ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
Suppressor Activity ◽  
Tumour Suppressor Activity ◽  
The Central Nervous System

AbstractPTEN (phosphatase and tensin homologue deleted in chromosome 10) was first identified as a candidate tumour suppressor gene located on chromosome 10q23. It is considered as one of the most frequently mutated genes in human malignancies. Emerging evidence shows that the biological function of PTEN extends beyond its tumour suppressor activity. In the central nervous system PTEN is a crucial regulator of neuronal development, neuronal survival, axonal regeneration and synaptic plasticity. Furthermore, PTEN has been linked to the pathogenesis of neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis. Recently increased attention has been focused on PTEN as a potential target for the treatment of brain injury and neurodegeneration. In this review we discuss the essential functions of PTEN in the central nervous system and its involvement in neurodegeneration.

scholarly journals RBM5/LUCA-15 — Tumour Suppression by Control of Apoptosis and the Cell Cycle?

2002 ◽  
Vol 2 ◽  
pp. 1885-1890 ◽  
Author(s):  
Mirna Mourtada-Maarabouni ◽  
Gwyn T. Williams
Keyword(s):  
Gene Locus ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
Suppressor Activity ◽  
Tumour Suppression ◽  
Major Significance ◽  
Tumour Suppressor Activity ◽  
Alternatively Spliced ◽  
Candidate Tumour Suppressor

The candidate tumour suppressor gene, LUCA-15, maps to the lung cancer tumour suppressor locus 3p21.3. The LUCA-15 gene locus encodes at least four alternatively spliced transcripts, which have been shown to function as regulators of apoptosis, a fact that may have a major significance in tumour regulation. This review highlights evidence that implicates the LUCA-15 locus in the control of apoptosis and cell proliferation, and reports observations that significantly strengthen the case for tumour suppressor activity by this gene.

scholarly journals Mutations in the von Hippel-Lindau Tumour Suppressor Gene in Central Nervous System Hemangioblastomas

2004 ◽  
Vol 2 (2) ◽  
pp. 93 ◽  
Author(s):  
Cezary Cybulski ◽  
Joanna Matyjasik ◽  
Marianna Soroka ◽  
Janusz Szymaś ◽  
Bohdan Górski ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
Von Hippel Lindau

scholarly journals The Antiapoptotic RBM5/LUCA-15/H37 Gene and Its Role in Apoptosis and Human Cancer: Research Update

2006 ◽  
Vol 6 ◽  
pp. 1705-1712 ◽  
Author(s):  
Mirna M Maarabouni ◽  
Gwyn T Williams
Keyword(s):  
Gene Locus ◽  
Human Cancer ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
Suppressor Activity ◽  
Major Significance ◽  
Tumour Suppressor Activity ◽  
Alternatively Spliced ◽  
Candidate Tumour Suppressor

The candidate tumour-suppressor gene, LUCA-15/RBM5/H37, maps to the lung cancer tumour-suppressor locus 3p21.3. The LUCA-15 gene locus encodes at least four alternatively spliced transcripts that have been shown to function as regulators of apoptosis, a fact which may have major significance in tumour regulation. This review highlights recent evidence that further implicates the LUCA-15 locus in the control of apoptosis and cell proliferation, and focuses on the observations that confirm the tumour-suppressor activity of this gene.

Autophagosomes and multivesicular bodies in neuronal development and degeneration

2012 ◽  
Vol 3 (4) ◽  
Author(s):  
Andrea Diana
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurodegenerative Disorders ◽  
Neuronal Development ◽  
Developmental Stages ◽  
Intersection Point ◽  
Multivesicular Bodies ◽  
Growing Body ◽  
The Central Nervous System ◽  
The Relationship

AbstractA growing body of research deals with the relationship between the endosomal and autophagic/lysosomal pathways during developmental stages of the central nervous system. This includes their possible influence regarding the onset and progression of specific neurodegenerative disorders. In this review we focus our attention on major alterations affecting two organelles: autophagosomes and multivesicular bodies, both of which are located at the intersection point of their respective pathways.

scholarly journals Targeting innate immunity for neurodegenerative disorders of the central nervous system

2016 ◽  
Vol 138 (5) ◽  
pp. 653-693 ◽  
Author(s):  
Katrin I. Andreasson ◽  
Adam D. Bachstetter ◽  
Marco Colonna ◽  
Florent Ginhoux ◽  
Clive Holmes ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Innate Immunity ◽  
Nervous System ◽  
Neurodegenerative Disorders ◽  
The Central Nervous System

The Neuroimmune Interface in Prion Diseases

Physiology ◽  
2000 ◽  
Vol 15 (5) ◽  
pp. 250-255
Author(s):  
Michael A. Klein ◽  
Adriano Aguzzi
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Immune System ◽  
Prion Disease ◽  
Neurodegenerative Disorders ◽  
Prion Diseases ◽  
The Central Nervous System

Prion diseases are fatal neurodegenerative disorders of animals and humans. Here we address the role of the immune system in the spread of prions from peripheral sites to the central nervous system and its potential relevance to iatrogenic prion disease.

scholarly journals Niacin in the Central Nervous System: An Update of Biological Aspects and Clinical Applications

2019 ◽  
Vol 20 (4) ◽  
pp. 974 ◽  
Author(s):  
Valeria Gasperi ◽  
Matteo Sibilano ◽  
Isabella Savini ◽  
Maria Catani
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Nicotinamide Adenine Dinucleotide ◽  
Cell Cycle Progression ◽  
Neuronal Development ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Nicotinamide Adenine ◽  
Vitamin B3 ◽  
Traumatic Injuries ◽  
The Central Nervous System

Niacin (also known as “vitamin B3” or “vitamin PP”) includes two vitamers (nicotinic acid and nicotinamide) giving rise to the coenzymatic forms nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). The two coenzymes are required for oxidative reactions crucial for energy production, but they are also substrates for enzymes involved in non-redox signaling pathways, thus regulating biological functions, including gene expression, cell cycle progression, DNA repair and cell death. In the central nervous system, vitamin B3 has long been recognized as a key mediator of neuronal development and survival. Here, we will overview available literature data on the neuroprotective role of niacin and its derivatives, especially focusing especially on its involvement in neurodegenerative diseases (Alzheimer’s, Parkinson’s, and Huntington’s diseases), as well as in other neuropathological conditions (ischemic and traumatic injuries, headache and psychiatric disorders).

scholarly journals Death of developing neurons: New insights and implications for connectivity

2013 ◽  
Vol 203 (3) ◽  
pp. 385-393 ◽  
Author(s):  
Martijn P.J. Dekkers ◽  
Vassiliki Nikoletopoulou ◽  
Yves-Alain Barde
Keyword(s):  
Central Nervous System ◽  
Cell Death ◽  
Nervous System ◽  
Growth Factors ◽  
Axonal Degeneration ◽  
Neuronal Development ◽  
Critical Role ◽  
Synaptic Function ◽  
The Central Nervous System ◽  
Developing Neurons

The concept that target tissues determine the survival of neurons has inspired much of the thinking on neuronal development in vertebrates, not least because it is supported by decades of research on nerve growth factor (NGF) in the peripheral nervous system (PNS). Recent discoveries now help to understand why only some developing neurons selectively depend on NGF. They also indicate that the survival of most neurons in the central nervous system (CNS) is not simply regulated by single growth factors like in the PNS. Additionally, components of the cell death machinery have begun to be recognized as regulators of selective axonal degeneration and synaptic function, thus playing a critical role in wiring up the nervous system.

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