HOME > 상세정보

상세정보

Mitochondrial mechanisms of degeneration and repair in Parkinson's disease [electronic resource]

Mitochondrial mechanisms of degeneration and repair in Parkinson's disease [electronic resource]

자료유형
E-Book(소장)
개인저자
Buhlman, Lori M.
서명 / 저자사항
Mitochondrial mechanisms of degeneration and repair in Parkinson's disease [electronic resource] / Lori M. Buhlman, editor.
발행사항
Cham :   Springer International Publishing :   Imprint: Springer,   c2016.  
형태사항
1 online resource (xii, 275 p.) : ill. (some col.).
ISBN
9783319421391
요약
This volume brings together various theories of how aberrations in mitochondrial function and morphology contribute to neurodegeneration in idiopathic and familial forms of Parkinson’s disease. Moreover, it comprehensively reviews the current search for therapies, and proposes how molecules are involved in specific functions as attractive therapeutic targets. It is expected to facilitate critical thought and discussion about the fundamental aspects of neurodegeneration in Parkinson’s disease and foster the development of therapeutic strategies among researchers and graduate students. Theories of idiopathic Parkinson’s etiology support roles for chronic inflammation and exposure to heavy metals or pesticides. Interestingly, as this project proposes, a case can be made that abnormalities in mitochondrial morphology and function are at the core of each of these theories. In fact, the most common approach to the generation of animal and cell-culture models of idiopathic Parkinson’s disease involves exposure to mitochondrial toxins. Even more compelling is the fact that most familial patients harbor genetic mutations that cause disruptions in normal mitochondrial morphology and function. While there remains to be no effective treatment for Parkinson’s disease, efforts to postpone, prevent and “cure” onset mitochondrial aberrations and neurodegeneration associated with Parkinson’s disease in various models are encouraging. While only about ten percent of Parkinson’s patients inherit disease-causing mutations, discovering common mechanisms by which familial forms of Parkinson’s disease manifest will likely shed light on the pathophysiology of the more common idiopathic form and provide insight to the general process of neurodegeneration, thus revealing therapeutic targets that will become more and more accessible as technology improves.
일반주기
Title from e-Book title page.  
내용주기
Mitochondrial ROS and Apoptosis -- Dopamine Metabolism and Reactive Oxygen Species Production -- The Consequences of Damaged Mitochondrial DNA -- The role of chronic inflammation in the etiology of Parkinson’s disease -- Ion-Catalyzed Reactive Oxygen Species in Sporadic Models of Parkinson's Disease -- Toxin Mediated Complex I Inhibition and Parkinson’s Disease -- Parkinson Disease-Associated Mutations Affect Mitochondrial Function -- PARKIN/PINK1 Pathway for the Selective Isolation and Degradation of Impaired Mitochondria -- Mitochondrial Therapeutic approaches in Parkinson's Disease -- Altering Mitochondrial Fusion and Fission Protein Levels Rescues Parkin and PINK1 Loss-of-Function Phenotypes -- Early Nicotine Exposure is Protective in Familial and Idiopathic Models of Parkinson’s Disease -- Transcription Modulation of Mitochondrial Function and Related Pathways as a Therapeutic Opportunity in Parkinson’s Disease -- Delivery of Biologically Active Molecules to Mitochondria.
서지주기
Includes bibliographical references and index.
이용가능한 다른형태자료
Issued also as a book.  
일반주제명
Parkinson's disease --Molecular aspects.
바로가기
URL
000 00000nam u2200205 a 4500
001 000046029942
005 20200604112848
006 m d
007 cr
008 200601s2016 sz a ob 001 0 eng d
020 ▼a 9783319421391
040 ▼a 211009 ▼c 211009 ▼d 211009
050 4 ▼a QP356.3
082 0 4 ▼a 616.833 ▼2 23
084 ▼a 616.833 ▼2 DDCK
090 ▼a 616.833
245 0 0 ▼a Mitochondrial mechanisms of degeneration and repair in Parkinson's disease ▼h [electronic resource] / ▼c Lori M. Buhlman, editor.
260 ▼a Cham : ▼b Springer International Publishing : ▼b Imprint: Springer, ▼c c2016.
300 ▼a 1 online resource (xii, 275 p.) : ▼b ill. (some col.).
500 ▼a Title from e-Book title page.
504 ▼a Includes bibliographical references and index.
505 0 ▼a Mitochondrial ROS and Apoptosis -- Dopamine Metabolism and Reactive Oxygen Species Production -- The Consequences of Damaged Mitochondrial DNA -- The role of chronic inflammation in the etiology of Parkinson’s disease -- Ion-Catalyzed Reactive Oxygen Species in Sporadic Models of Parkinson's Disease -- Toxin Mediated Complex I Inhibition and Parkinson’s Disease -- Parkinson Disease-Associated Mutations Affect Mitochondrial Function -- PARKIN/PINK1 Pathway for the Selective Isolation and Degradation of Impaired Mitochondria -- Mitochondrial Therapeutic approaches in Parkinson's Disease -- Altering Mitochondrial Fusion and Fission Protein Levels Rescues Parkin and PINK1 Loss-of-Function Phenotypes -- Early Nicotine Exposure is Protective in Familial and Idiopathic Models of Parkinson’s Disease -- Transcription Modulation of Mitochondrial Function and Related Pathways as a Therapeutic Opportunity in Parkinson’s Disease -- Delivery of Biologically Active Molecules to Mitochondria.
520 ▼a This volume brings together various theories of how aberrations in mitochondrial function and morphology contribute to neurodegeneration in idiopathic and familial forms of Parkinson’s disease. Moreover, it comprehensively reviews the current search for therapies, and proposes how molecules are involved in specific functions as attractive therapeutic targets. It is expected to facilitate critical thought and discussion about the fundamental aspects of neurodegeneration in Parkinson’s disease and foster the development of therapeutic strategies among researchers and graduate students. Theories of idiopathic Parkinson’s etiology support roles for chronic inflammation and exposure to heavy metals or pesticides. Interestingly, as this project proposes, a case can be made that abnormalities in mitochondrial morphology and function are at the core of each of these theories. In fact, the most common approach to the generation of animal and cell-culture models of idiopathic Parkinson’s disease involves exposure to mitochondrial toxins. Even more compelling is the fact that most familial patients harbor genetic mutations that cause disruptions in normal mitochondrial morphology and function. While there remains to be no effective treatment for Parkinson’s disease, efforts to postpone, prevent and “cure” onset mitochondrial aberrations and neurodegeneration associated with Parkinson’s disease in various models are encouraging. While only about ten percent of Parkinson’s patients inherit disease-causing mutations, discovering common mechanisms by which familial forms of Parkinson’s disease manifest will likely shed light on the pathophysiology of the more common idiopathic form and provide insight to the general process of neurodegeneration, thus revealing therapeutic targets that will become more and more accessible as technology improves.
530 ▼a Issued also as a book.
538 ▼a Mode of access: World Wide Web.
650 0 ▼a Parkinson's disease ▼x Molecular aspects.
700 1 ▼a Buhlman, Lori M.
856 4 0 ▼u https://oca.korea.ac.kr/link.n2s?url=http://dx.doi.org/10.1007/978-3-319-42139-1
945 ▼a KLPA
991 ▼a E-Book(소장)

소장정보

No. 소장처 청구기호 등록번호 도서상태 반납예정일 예약 서비스
No. 1 소장처 중앙도서관/e-Book 컬렉션/ 청구기호 CR 616.833 등록번호 E14022886 도서상태 대출불가(열람가능) 반납예정일 예약 서비스 M

관련분야 신착자료

김혜금 (2021)
방영주 (2021)
대한소화기내시경학회. 내시경대사비만연구회 (2021)
대한소화기내시경학회. 교육수련연구회 (2021)
연세대학교. 의과대학. 의학을 쉽게 푸는 모임 (2021)
서울대학교. 의과대학. 영상의학교실 (2021)