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Article ; Online: Cdk5: a multifaceted kinase in neurodegenerative diseases.

Cheung, Zelda H / Ip, Nancy Y

2012 Volume 22, Issue 3, Page(s) 169–175

Abstract: Since the identification of cyclin-dependent kinase-5 (Cdk5) as a tau kinase and member of the Cdk family almost 20 years ago, deregulation of Cdk5 activity has been linked to an array of neurodegenerative diseases. As knowledge on the etiopathological ... ...

Abstract	Since the identification of cyclin-dependent kinase-5 (Cdk5) as a tau kinase and member of the Cdk family almost 20 years ago, deregulation of Cdk5 activity has been linked to an array of neurodegenerative diseases. As knowledge on the etiopathological mechanisms of these diseases evolved through the years, Cdk5 has also been implicated in additional cellular events that are affected under these pathological conditions. From the role of Cdk5 in the regulation of synaptic functions to its involvement in autophagy deregulation, significant insights have been obtained regarding the role of Cdk5 as a key regulator of neurodegeneration. Here, we summarize recent findings on the involvement of Cdk5 in the pathophysiological mechanisms underlying various neurodegenerative diseases.
MeSH term(s)	Animals ; Autophagy ; Cell Survival ; Cyclin-Dependent Kinase 5/metabolism ; Humans ; Neurodegenerative Diseases/enzymology ; Neurodegenerative Diseases/pathology ; Neurodegenerative Diseases/physiopathology ; Signal Transduction
Chemical Substances	Cyclin-Dependent Kinase 5 (EC 2.7.11.1)
Language	English
Publishing date	2012-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	30122-x
ISSN	1879-3088 ; 0962-8924
ISSN (online)	1879-3088
ISSN	0962-8924
DOI	10.1016/j.tcb.2011.11.003
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Article ; Online: Autophagy deregulation in neurodegenerative diseases - recent advances and future perspectives.

Cheung, Zelda H / Ip, Nancy Y

Journal of neurochemistry

2011 Volume 118, Issue 3, Page(s) 317–325

Abstract: Autophagy is an evolutionarily conserved homeostatic process for the turnover of cellular contents, organelles and misfolded proteins through the lysosomal machinery. Recently, the involvement of autophagy in the pathophysiology of neurodegenerative ... ...

Abstract	Autophagy is an evolutionarily conserved homeostatic process for the turnover of cellular contents, organelles and misfolded proteins through the lysosomal machinery. Recently, the involvement of autophagy in the pathophysiology of neurodegenerative diseases has attracted considerable interest because autophagy deregulation has been linked to some of these neurodegenerative disorders. This interest is further heightened by the demonstration that various autophagic pathways, including macroautophagy and chaperone-mediated autophagy, are implicated in the turnover of proteins that are prone to aggregation in cellular or animal disease models. These observations have stimulated new awareness in the pivotal role of the autophagic pathways in neurodegenerative disease pathophysiology, and have sparked extensive research aimed at deciphering the mechanisms by which autophagy is altered in these disorders. Here, we summarize the latest advances in our understanding of the role of autophagy deregulation in Parkinson's, Alzheimer's and Huntington's disease.
MeSH term(s)	Alzheimer Disease/pathology ; Animals ; Autophagy/physiology ; Humans ; Huntington Disease/pathology ; Neurodegenerative Diseases/pathology ; Parkinson Disease/pathology ; Signal Transduction/physiology
Language	English
Publishing date	2011-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/j.1471-4159.2011.07314.x
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Article ; Online: From understanding synaptic plasticity to the development of cognitive enhancers.

Cheung, Zelda H / Ip, Nancy Y

The international journal of neuropsychopharmacology

2011 Volume 14, Issue 9, Page(s) 1247–1256

Abstract: Accumulating evidence reveals that synaptic dysfunction precedes neuronal loss in neurodegenerative diseases such as Alzheimer's disease. Intriguingly, synaptic abnormality is also implicated in a myriad of psychiatric disorders including depression. In ... ...

Abstract	Accumulating evidence reveals that synaptic dysfunction precedes neuronal loss in neurodegenerative diseases such as Alzheimer's disease. Intriguingly, synaptic abnormality is also implicated in a myriad of psychiatric disorders including depression. In particular, alterations in spine density and morphology have been associated with aberrant synaptic activity in these diseased brains. Understanding the molecular mechanisms underlying the regulation of spine morphogenesis, synaptic function and plasticity under physiological and pathological conditions will therefore provide critical insights for the development of potential therapeutic agents against these diseases. Here we summarize existing knowledge on some of the molecular players in synaptic plasticity, and highlight how these findings from basic neuroscientific research aid in the identification of novel drug leads for the development of therapeutics.
MeSH term(s)	Animals ; Dementia/drug therapy ; Dementia/metabolism ; Dementia/physiopathology ; Dendritic Spines/drug effects ; Dendritic Spines/metabolism ; Humans ; Molecular Targeted Therapy ; Neuronal Plasticity/drug effects ; Neurons/drug effects ; Neurons/physiology ; Nootropic Agents/pharmacology ; Nootropic Agents/therapeutic use
Chemical Substances	Nootropic Agents
Language	English
Publishing date	2011-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1440129-0
ISSN	1469-5111 ; 1461-1457
ISSN (online)	1469-5111
ISSN	1461-1457
DOI	10.1017/S1461145710001537
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Article ; Online: The emerging role of autophagy in Parkinson's disease.

Cheung, Zelda H / Ip, Nancy Y

Molecular brain

2009 Volume 2, Page(s) 29

Abstract: Parkinson's disease (PD) is the most common neurodegenerative movement disorder that affects about 1% of the population worldwide. Despite significant advances in the identification of genetic mutations and signaling pathways that are associated with the ...

Abstract	Parkinson's disease (PD) is the most common neurodegenerative movement disorder that affects about 1% of the population worldwide. Despite significant advances in the identification of genetic mutations and signaling pathways that are associated with the disease, the precise mechanisms implicated in the pathophysiology of the disease are not well understood. More importantly, treatments that are effective in reversing the progression of the disease is essentially lacking. Further investigation into the pathogenic mechanisms of PD thus presents a pressing concern for neuroscientists. Recently, deregulation of the autophagic pathway is observed in the brains of PD patients and in models of PD. In this review we summarize current literature on the emerging involvement of autophagy in PD, and the implication for future development of treatment against the disorder.
MeSH term(s)	Animals ; Autophagy ; Cytoprotection ; Humans ; Parkinson Disease/pathology ; Signal Transduction
Language	English
Publishing date	2009-09-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2436057-0
ISSN	1756-6606 ; 1756-6606
ISSN (online)	1756-6606
ISSN	1756-6606
DOI	10.1186/1756-6606-2-29
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Endophilin B1: Guarding the gate to destruction.

Cheung, Zelda H / Ip, Nancy Y

Communicative & integrative biology

2009 Volume 2, Issue 2, Page(s) 130–132

Abstract: Endophilin B1 is a member of the endophilin family that is localized predominantly to intracellular membranes. Also known as Bax-interacting factor-1 (Bif-1), this protein has been observed to regulate the membrane dynamics of various intracellular ... ...

Abstract	Endophilin B1 is a member of the endophilin family that is localized predominantly to intracellular membranes. Also known as Bax-interacting factor-1 (Bif-1), this protein has been observed to regulate the membrane dynamics of various intracellular compartments, such as the control of mitochondrial morphology and autophagosome formation in fibroblast. Endophilin B1 is expressed in the brain, but its functions in neurons had remained unknown. Recently, we have observed a novel role of endophilin B1 in neurons where it controls the trafficking of TrkA, cognate receptor for the prototypic neurotrophin nerve growth factor (NGF). Knock-down of endophilin B1 expression induces precocious targeting of NGF/TrkA to late endosomes and lysosomes, thereby leading to reduced TrkA levels. This is accompanied by marked attenuation of NGF-induced gene transcription and neurite outgrowth. Our observations suggest that endophilin B1 regulates TrkA level and downstream functions by controlling the movement of TrkA to late endosomes/lysosomes, possibly acting at the level of early endosomes.
Language	English
Publishing date	2009-08-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	2451097-X
ISSN	1942-0889 ; 1942-0889
ISSN (online)	1942-0889
ISSN	1942-0889
DOI	10.4161/cib.7745
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Article: Cdk5: a multifaceted kinase in neurodegenerative diseases

Cheung, Zelda H / Ip, Nancy Y

Trends in cell biology. 2012 Mar., v. 22, no. 3

2012

Abstract	Since the identification of cyclin-dependent kinase-5 (Cdk5) as a tau kinase and member of the Cdk family almost 20 years ago, deregulation of Cdk5 activity has been linked to an array of neurodegenerative diseases. As knowledge on the etiopathological mechanisms of these diseases evolved through the years, Cdk5 has also been implicated in additional cellular events that are affected under these pathological conditions. From the role of Cdk5 in the regulation of synaptic functions to its involvement in autophagy deregulation, significant insights have been obtained regarding the role of Cdk5 as a key regulator of neurodegeneration. Here, we summarize recent findings on the involvement of Cdk5 in the pathophysiological mechanisms underlying various neurodegenerative diseases.
Keywords	autophagy ; neurodegenerative diseases ; tau-protein kinase
Language	English
Dates of publication	2012-03
Size	p. 169-175.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	30122-x
ISSN	1879-3088 ; 0962-8924
ISSN (online)	1879-3088
ISSN	0962-8924
DOI	10.1016/j.tcb.2011.11.003
Database	NAL-Catalogue (AGRICOLA)

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Article: Molecular machinery of macroautophagy and its deregulation in diseases.

Wong, Alan S L / Cheung, Zelda H / Ip, Nancy Y

Biochimica et biophysica acta

2011 Volume 1812, Issue 11, Page(s) 1490–1497

Abstract: Macroautophagy maintains cellular homeostasis through targeting cytoplasmic contents and organelles into autophagosomes for degradation. This process begins with the assembly of protein complexes on isolation membrane to initiate the formation of ... ...

Abstract	Macroautophagy maintains cellular homeostasis through targeting cytoplasmic contents and organelles into autophagosomes for degradation. This process begins with the assembly of protein complexes on isolation membrane to initiate the formation of autophagosome, followed by its nucleation, elongation and maturation. Fusion of autophagosomes with lysosomes then leads to degradation of the cargo. In the past decade, significant advances have been made on the identification of molecular players that are implicated in various stages of macroautophagy. Post-translational modifications of macroautophagy regulators have also been demonstrated to be critical for the selective targeting of cytoplasmic contents into autophagosomes. In addition, recent demonstration of distinct macroautophagy regulators has led to the identification of different subtypes of macroautophagy. Since deregulation of macroautophagy is implicated in diseases including neurodegenerative disorders, cancers and inflammatory disorders, understanding the molecular machinery of macroautophagy is crucial for elucidating the mechanisms by which macroautophagy is deregulated in these diseases, thereby revealing new potential therapeutic targets and strategies. Here we summarize current knowledge on the regulation of mammalian macroautophagy machineries and their disease-associated deregulation.
MeSH term(s)	Animals ; Autophagy ; Humans ; Inflammation/physiopathology ; Neoplasms/physiopathology ; Neurodegenerative Diseases/physiopathology
Language	English
Publishing date	2011-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2011.07.005
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Article ; Online: The roles of cyclin-dependent kinase 5 in dendrite and synapse development.

Cheung, Zelda H / Ip, Nancy Y

Biotechnology journal

2007 Volume 2, Issue 8, Page(s) 949–957

Abstract: Since the isolation of cyclin-dependent kinase 5 (Cdk5), this proline-directed serine/threonine kinase has been demonstrated as an important regulator of neuronal migration, neuronal survival and synaptic functions. Recently, a number of players ... ...

Abstract	Since the isolation of cyclin-dependent kinase 5 (Cdk5), this proline-directed serine/threonine kinase has been demonstrated as an important regulator of neuronal migration, neuronal survival and synaptic functions. Recently, a number of players implicated in dendrite and synapse development have been identified as Cdk5 substrates. Neurite extension, synapse and spine maturation are all modulated by a myriad of extracellular guidance cues or trophic factors. Cdk5 was recently demonstrated to regulate signaling downstream of some of these extracellular factors, in addition to modulating Rho GTPase activity, which regulates cytoskeletal dynamics. In this communication, we summarize our existing knowledge on the pathways and mechanisms through which Cdk5 affects dendrite, synapse and spine development.
MeSH term(s)	Animals ; Brain/enzymology ; Cell Enlargement ; Cyclin-Dependent Kinase 5/metabolism ; Dendrites/physiology ; Humans ; Nerve Tissue Proteins/metabolism ; Phosphorylation ; Synapses/physiology
Chemical Substances	Nerve Tissue Proteins ; Cyclin-Dependent Kinase 5 (EC 2.7.11.1) ; CDK5 protein, human (EC 2.7.11.22)
Language	English
Publishing date	2007-08
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2221885-3
ISSN	1860-7314 ; 1860-6768
ISSN (online)	1860-7314
ISSN	1860-6768
DOI	10.1002/biot.200700056
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Article: Beta-catenin in reverse action.

Fu, Amy K Y / Cheung, Zelda H / Ip, Nancy Y

Nature neuroscience

2008 Volume 11, Issue 3, Page(s) 244–246

MeSH term(s)	Animals ; Cell Communication/physiology ; Cell Differentiation/physiology ; Humans ; Mice ; Mice, Knockout ; Motor Neurons/metabolism ; Muscle, Skeletal/embryology ; Muscle, Skeletal/innervation ; Neuromuscular Junction/embryology ; Presynaptic Terminals/metabolism ; Presynaptic Terminals/ultrastructure ; Receptor Aggregation/physiology ; Receptors, Cholinergic/metabolism ; Signal Transduction/physiology ; Wnt Proteins/genetics ; Wnt Proteins/metabolism ; beta Catenin/metabolism
Chemical Substances	Receptors, Cholinergic ; Wnt Proteins ; beta Catenin
Language	English
Publishing date	2008-03
Publishing country	United States
Document type	Comment ; News
ZDB-ID	1420596-8
ISSN	1546-1726 ; 1097-6256
ISSN (online)	1546-1726
ISSN	1097-6256
DOI	10.1038/nn0308-244
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Article ; Online: The emerging role of autophagy in Parkinson's disease

Cheung Zelda H / Ip Nancy Y

Molecular Brain, Vol 2, Iss 1, p

2009 Volume 29

Abstract: Abstract Parkinson's disease (PD) is the most common neurodegenerative movement disorder that affects about 1% of the population worldwide. Despite significant advances in the identification of genetic mutations and signaling pathways that are associated ...

Abstract	Abstract Parkinson's disease (PD) is the most common neurodegenerative movement disorder that affects about 1% of the population worldwide. Despite significant advances in the identification of genetic mutations and signaling pathways that are associated with the disease, the precise mechanisms implicated in the pathophysiology of the disease are not well understood. More importantly, treatments that are effective in reversing the progression of the disease is essentially lacking. Further investigation into the pathogenic mechanisms of PD thus presents a pressing concern for neuroscientists. Recently, deregulation of the autophagic pathway is observed in the brains of PD patients and in models of PD. In this review we summarize current literature on the emerging involvement of autophagy in PD, and the implication for future development of treatment against the disorder.
Keywords	Neurology. Diseases of the nervous system ; RC346-429 ; Neurosciences. Biological psychiatry. Neuropsychiatry ; RC321-571 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Neurology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	610
Language	English
Publishing date	2009-09-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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