Role of WWOX/WOX1 in Alzheimer's disease pathology and in cell death signaling

Chih Chung Teng, Ya Ting Yang, Yu Chi Chen, Yu-Min Kuo, Chun-I Sze

Research output: Contribution to journalReview article

7 Citations (Scopus)

Abstract

Alzheimer's disease (AD) is the most common form of dementia with a progressive course. AD pathology is a manifestation of the underlying severity and neuroanatomic involvement of specific vulnerable brain regions and circuits that are responsible for neuronal dysfunction and death. The etiology of AD is largely unknown. It has been hypothesized that multiple factors, including genetic components, oxidative stress, intracellular or extracellular accumulation of amyloid, dysfunction of cystoskeletal and synapse components, neuronal loss by apoptosis, neuronal excitotoxicity, inflammation, mitochondria dysfunction, etc., may play important roles in the onset of the disease. WWOX/WOX1 is a candidate tumor suppressor. Human WWOX gene, encoding the WW domain-containing oxidoreductase (designated WWOX, FOR, or WOX1) protein, has been mapped to a fragile site on the chromosome ch16q23.3-24.1. Functionally, the WW domain is not only a tumor suppressor, but also a participant in molecular interactions, signaling, and apoptosis in many diseases. In this article, we review the potential mechanism by which WWOX/WOX1 may participate in the pathogenesis of AD with a focus on cell death signaling pathways in neurons.

Original languageEnglish
Pages (from-to)1951-1965
Number of pages15
JournalFrontiers in Bioscience - Elite
Volume4 E
Issue number5
Publication statusPublished - 2012 Jan 1

Fingerprint

Pathology
Cell death
Alzheimer Disease
Cell Death
Chromosome Fragile Sites
Apoptosis
Tumors
Amyloid
Synapses
Dementia
Neoplasms
Mitochondria
Oxidoreductases
Oxidative Stress
Gene encoding
Oxidative stress
Molecular interactions
Chromosomes
Inflammation
Neurons

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)

Cite this

Teng, Chih Chung ; Yang, Ya Ting ; Chen, Yu Chi ; Kuo, Yu-Min ; Sze, Chun-I. / Role of WWOX/WOX1 in Alzheimer's disease pathology and in cell death signaling. In: Frontiers in Bioscience - Elite. 2012 ; Vol. 4 E, No. 5. pp. 1951-1965.
@article{0fbfd62aae7a48b09575580abf8f5d5a,
title = "Role of WWOX/WOX1 in Alzheimer's disease pathology and in cell death signaling",
abstract = "Alzheimer's disease (AD) is the most common form of dementia with a progressive course. AD pathology is a manifestation of the underlying severity and neuroanatomic involvement of specific vulnerable brain regions and circuits that are responsible for neuronal dysfunction and death. The etiology of AD is largely unknown. It has been hypothesized that multiple factors, including genetic components, oxidative stress, intracellular or extracellular accumulation of amyloid, dysfunction of cystoskeletal and synapse components, neuronal loss by apoptosis, neuronal excitotoxicity, inflammation, mitochondria dysfunction, etc., may play important roles in the onset of the disease. WWOX/WOX1 is a candidate tumor suppressor. Human WWOX gene, encoding the WW domain-containing oxidoreductase (designated WWOX, FOR, or WOX1) protein, has been mapped to a fragile site on the chromosome ch16q23.3-24.1. Functionally, the WW domain is not only a tumor suppressor, but also a participant in molecular interactions, signaling, and apoptosis in many diseases. In this article, we review the potential mechanism by which WWOX/WOX1 may participate in the pathogenesis of AD with a focus on cell death signaling pathways in neurons.",
author = "Teng, {Chih Chung} and Yang, {Ya Ting} and Chen, {Yu Chi} and Yu-Min Kuo and Chun-I Sze",
year = "2012",
month = "1",
day = "1",
language = "English",
volume = "4 E",
pages = "1951--1965",
journal = "Frontiers in Bioscience - Elite",
issn = "1945-0494",
publisher = "Frontiers in Bioscience",
number = "5",

}

Role of WWOX/WOX1 in Alzheimer's disease pathology and in cell death signaling. / Teng, Chih Chung; Yang, Ya Ting; Chen, Yu Chi; Kuo, Yu-Min; Sze, Chun-I.

In: Frontiers in Bioscience - Elite, Vol. 4 E, No. 5, 01.01.2012, p. 1951-1965.

Research output: Contribution to journalReview article

TY - JOUR

T1 - Role of WWOX/WOX1 in Alzheimer's disease pathology and in cell death signaling

AU - Teng, Chih Chung

AU - Yang, Ya Ting

AU - Chen, Yu Chi

AU - Kuo, Yu-Min

AU - Sze, Chun-I

PY - 2012/1/1

Y1 - 2012/1/1

N2 - Alzheimer's disease (AD) is the most common form of dementia with a progressive course. AD pathology is a manifestation of the underlying severity and neuroanatomic involvement of specific vulnerable brain regions and circuits that are responsible for neuronal dysfunction and death. The etiology of AD is largely unknown. It has been hypothesized that multiple factors, including genetic components, oxidative stress, intracellular or extracellular accumulation of amyloid, dysfunction of cystoskeletal and synapse components, neuronal loss by apoptosis, neuronal excitotoxicity, inflammation, mitochondria dysfunction, etc., may play important roles in the onset of the disease. WWOX/WOX1 is a candidate tumor suppressor. Human WWOX gene, encoding the WW domain-containing oxidoreductase (designated WWOX, FOR, or WOX1) protein, has been mapped to a fragile site on the chromosome ch16q23.3-24.1. Functionally, the WW domain is not only a tumor suppressor, but also a participant in molecular interactions, signaling, and apoptosis in many diseases. In this article, we review the potential mechanism by which WWOX/WOX1 may participate in the pathogenesis of AD with a focus on cell death signaling pathways in neurons.

AB - Alzheimer's disease (AD) is the most common form of dementia with a progressive course. AD pathology is a manifestation of the underlying severity and neuroanatomic involvement of specific vulnerable brain regions and circuits that are responsible for neuronal dysfunction and death. The etiology of AD is largely unknown. It has been hypothesized that multiple factors, including genetic components, oxidative stress, intracellular or extracellular accumulation of amyloid, dysfunction of cystoskeletal and synapse components, neuronal loss by apoptosis, neuronal excitotoxicity, inflammation, mitochondria dysfunction, etc., may play important roles in the onset of the disease. WWOX/WOX1 is a candidate tumor suppressor. Human WWOX gene, encoding the WW domain-containing oxidoreductase (designated WWOX, FOR, or WOX1) protein, has been mapped to a fragile site on the chromosome ch16q23.3-24.1. Functionally, the WW domain is not only a tumor suppressor, but also a participant in molecular interactions, signaling, and apoptosis in many diseases. In this article, we review the potential mechanism by which WWOX/WOX1 may participate in the pathogenesis of AD with a focus on cell death signaling pathways in neurons.

UR - http://www.scopus.com/inward/record.url?scp=84860868174&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84860868174&partnerID=8YFLogxK

M3 - Review article

C2 - 22202011

AN - SCOPUS:84860868174

VL - 4 E

SP - 1951

EP - 1965

JO - Frontiers in Bioscience - Elite

JF - Frontiers in Bioscience - Elite

SN - 1945-0494

IS - 5

ER -