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Article: Intestine-derived α-synuclein initiates and aggravates pathogenesis of Parkinson's disease in Drosophila.

Liu, Wei / Lim, Kah-Leong / Tan, Eng-King

2022 Volume 11, Issue 1, Page(s) 44

Abstract: Background: Aberrant aggregation of α-synuclein (α-syn) is a key pathological feature of Parkinson's disease (PD), but the precise role of intestinal α-syn in the progression of PD is unclear. In a number of genetic Drosophila models of PD, α-syn was ... ...

Abstract	Background: Aberrant aggregation of α-synuclein (α-syn) is a key pathological feature of Parkinson's disease (PD), but the precise role of intestinal α-syn in the progression of PD is unclear. In a number of genetic Drosophila models of PD, α-syn was frequently ectopically expressed in the neural system to investigate the pathobiology. Method: We investigated the potential role of intestinal α-syn in PD pathogenesis using a Drosophila model. Human α-syn was overexpressed in Drosophila guts, and life span, survival, immunofluorescence and climbing were evaluated. Immunofluorescence, Western blotting and reactive oxygen species (ROS) staining were performed to assess the effects of intestinal α-syn on intestinal dysplasia. High-throughput RNA and 16S rRNA gene sequencing, quantitative RT-PCR, immunofluorescence, and ROS staining were performed to determine the underlying molecular mechanism. Results: We found that the intestinal α-syn alone recapitulated many phenotypic and pathological features of PD, including impaired life span, loss of dopaminergic neurons, and progressive motor defects. The intestine-derived α-syn disrupted intestinal homeostasis and accelerated the onset of intestinal ageing. Moreover, intestinal expression of α-syn induced dysbiosis, while microbiome depletion was efficient to restore intestinal homeostasis and ameliorate the progression of PD. Intestinal α-syn triggered ROS, and eventually led to the activation of the dual oxidase (DUOX)-ROS-Jun N-terminal Kinase (JNK) pathway. In addition, α-syn from both the gut and the brain synergized to accelerate the progression of PD. Conclusions: The intestinal expression of α-syn recapitulates many phenotypic and pathologic features of PD, and induces dysbiosis that aggravates the pathology through the DUOX-ROS-JNK pathway in Drosophila. Our findings provide new insights into the role of intestinal α-syn in PD pathophysiology.
MeSH term(s)	Animals ; Drosophila/genetics ; Drosophila/metabolism ; Dual Oxidases ; Dysbiosis/complications ; Dysbiosis/genetics ; Humans ; Intestines/pathology ; JNK Mitogen-Activated Protein Kinases ; Parkinson Disease/metabolism ; RNA, Ribosomal, 16S ; Reactive Oxygen Species ; alpha-Synuclein/genetics ; alpha-Synuclein/metabolism
Chemical Substances	RNA, Ribosomal, 16S ; Reactive Oxygen Species ; alpha-Synuclein ; Dual Oxidases (EC 1.11.1.-) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2022-10-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2653701-1
ISSN	2047-9158
ISSN	2047-9158
DOI	10.1186/s40035-022-00318-w
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Article ; Online: The Mood Stabilizer Lithium Slows Down Synaptic Vesicle Cycling at Glutamatergic Synapses.

Tang, Willcyn / Cory, Bradley / Lim, Kah-Leong / Fivaz, Marc

Neuromolecular medicine

2022 Volume 25, Issue 1, Page(s) 125–135

Abstract: Lithium is a mood stabilizer broadly used to prevent and treat symptoms of mania and depression in people with bipolar disorder (BD). Little is known, however, about its mode of action. Here, we analyzed the impact of lithium on synaptic vesicle (SV) ... ...

Abstract	Lithium is a mood stabilizer broadly used to prevent and treat symptoms of mania and depression in people with bipolar disorder (BD). Little is known, however, about its mode of action. Here, we analyzed the impact of lithium on synaptic vesicle (SV) cycling at presynaptic terminals releasing glutamate, a neurotransmitter previously implicated in BD and other neuropsychiatric conditions. We used the pHluorin-based synaptic tracer vGpH and a fully automated image processing pipeline to quantify the effect of lithium on both SV exocytosis and endocytosis in hippocampal neurons. We found that lithium selectively reduces SV exocytic rates during electrical stimulation, and markedly slows down SV recycling post-stimulation. Analysis of single-bouton responses revealed the existence of functionally distinct excitatory synapses with varying sensitivity to lithium-some terminals show responses similar to untreated cells, while others are markedly impaired in their ability to recycle SVs. While the cause of this heterogeneity is unclear, these data indicate that lithium interacts with the SV machinery and influences glutamate release in a large fraction of excitatory synapses. Together, our findings show that lithium down modulates SV cycling, an effect consistent with clinical reports indicating hyperactivation of glutamate neurotransmission in BD.
MeSH term(s)	Lithium Compounds/pharmacology ; Glutamic Acid/metabolism ; Synaptic Vesicles/drug effects ; Synaptic Vesicles/metabolism ; Synapses/drug effects ; Synapses/metabolism ; Synaptic Transmission/drug effects ; Action Potentials/drug effects ; Bipolar Disorder/metabolism ; Bipolar Disorder/pathology ; Presynaptic Terminals/drug effects ; Presynaptic Terminals/metabolism ; Hippocampus/pathology ; Exocytosis/drug effects ; Endocytosis/drug effects ; Animals ; Rats ; Cells, Cultured
Chemical Substances	Lithium Compounds ; Glutamic Acid (3KX376GY7L)
Language	English
Publishing date	2022-11-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2077809-0
ISSN	1559-1174 ; 1535-1084
ISSN (online)	1559-1174
ISSN	1535-1084
DOI	10.1007/s12017-022-08729-8
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Article ; Online: BACE2: A Promising Neuroprotective Candidate for Alzheimer's Disease.

Yeap, Yee Jie / Kandiah, Nagaendran / Nizetic, Dean / Lim, Kah-Leong

Journal of Alzheimer's disease : JAD

2022 Volume 94, Issue s1, Page(s) S159–S171

Abstract: Alzheimer's disease (AD) is the most common cause of dementia that affects millions of predominantly elderly individuals worldwide. Despite intensive research over several decades, controversies still surround the etiology of AD and the disease remains ... ...

Abstract	Alzheimer's disease (AD) is the most common cause of dementia that affects millions of predominantly elderly individuals worldwide. Despite intensive research over several decades, controversies still surround the etiology of AD and the disease remains incurable. Meanwhile, new molecular players of the central amyloid cascade hypothesis have emerged and among these is a protease known as β-site APP cleavage enzyme 2 (BACE2). Unlike BACE1, BACE2 cleaves the amyloid-β protein precursor within the Aβ domain that accordingly prevents the generation of Aβ42 peptides, the aggregation of which is commonly regarded as the toxic entity that drives neurodegeneration in AD. Given this non-amyloidogenic role of BACE2, it is attractive to position BACE2 as a therapeutic target for AD. Indeed, several groups including ours have demonstrated a neuroprotective role for BACE2 in AD. In this review, we discuss emerging evidence supporting the ability of BACE2 in mitigating AD-associated pathology in various experimental systems including human pluripotent stem cell-derived cerebral organoid disease models. Alongside this, we also provide an update on the identification of single nucleotide polymorphisms occurring in the BACE2 gene that are linked to increased risk and earlier disease onset in the general population. In particular, we highlight a recently identified point mutation on BACE2 that apparently leads to sporadic early-onset AD. We believe that a better understanding of the role of BACE2 in AD would provide new insights for the development of viable therapeutic strategies for individuals with dementia.
MeSH term(s)	Humans ; Aged ; Alzheimer Disease/pathology ; Amyloid Precursor Protein Secretases/metabolism ; Aspartic Acid Endopeptidases/genetics ; Aspartic Acid Endopeptidases/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/metabolism
Chemical Substances	Amyloid Precursor Protein Secretases (EC 3.4.-) ; Aspartic Acid Endopeptidases (EC 3.4.23.-) ; Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; BACE2 protein, human (EC 3.4.23.45)
Language	English
Publishing date	2022-11-30
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-220867
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Article ; Online: Seipin Deficiency Leads to Energy Dyshomeostasis via Inducing Hypothalamic Neuroinflammation and Aberrant Expression of Neuropeptides.

Cui, Wenli / Chen, Hong / Lei, Lingfeng / Wang, Wenru / Lim, Kah-Leong / Zhang, Chengwu / Lu, Li

Neuromolecular medicine

2024 Volume 26, Issue 1, Page(s) 18

Abstract: Seipin is a key regulator of lipid metabolism, the deficiency of which leads to severe lipodystrophy. Hypothalamus is the pivotal center of brain that modulates appetite and energy homeostasis, where Seipin is abundantly expressed. Whether and how Seipin ...

Abstract	Seipin is a key regulator of lipid metabolism, the deficiency of which leads to severe lipodystrophy. Hypothalamus is the pivotal center of brain that modulates appetite and energy homeostasis, where Seipin is abundantly expressed. Whether and how Seipin deficiency leads to systemic metabolic disorders via hypothalamus-involved energy metabolism dysregulation remains to be elucidated. In the present study, we demonstrated that Seipin-deficiency induced hypothalamic inflammation, reduction of anorexigenic pro-opiomelanocortin (POMC), and elevation of orexigenic agonist-related peptide (AgRP). Importantly, administration of rosiglitazone, a thiazolidinedione antidiabetic agent, rescued POMC and AgRP expression, suppressed hypothalamic inflammation, and restored energy homeostasis in Seipin knockout mice. Our findings offer crucial insights into the mechanism of Seipin deficiency-associated energy imbalance and indicates that rosiglitazone could serve as potential intervening agent towards metabolic disorders linked to Seipin.
MeSH term(s)	Animals ; Mice ; Hypothalamus/metabolism ; Energy Metabolism/drug effects ; Pro-Opiomelanocortin/genetics ; Pro-Opiomelanocortin/biosynthesis ; Agouti-Related Protein/genetics ; Mice, Knockout ; Homeostasis ; GTP-Binding Protein gamma Subunits/genetics ; Rosiglitazone/pharmacology ; Male ; Neuroinflammatory Diseases/etiology ; Mice, Inbred C57BL ; Hypoglycemic Agents/pharmacology ; Hypoglycemic Agents/therapeutic use ; Neuropeptides/genetics ; Neuropeptides/deficiency ; Gene Expression Regulation/drug effects
Chemical Substances	Pro-Opiomelanocortin (66796-54-1) ; Agouti-Related Protein ; Bscl2 protein, mouse ; GTP-Binding Protein gamma Subunits ; Rosiglitazone (05V02F2KDG) ; Agrp protein, mouse ; Hypoglycemic Agents ; Neuropeptides
Language	English
Publishing date	2024-05-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2077809-0
ISSN	1559-1174 ; 1535-1084
ISSN (online)	1559-1174
ISSN	1535-1084
DOI	10.1007/s12017-024-08788-z
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Article ; Online: From 2D to 3D: Development of Monolayer Dopaminergic Neuronal and Midbrain Organoid Cultures for Parkinson's Disease Modeling and Regenerative Therapy.

Yeap, Yee Jie / Teddy, Tng J W / Lee, Mok Jung / Goh, Micaela / Lim, Kah Leong

International journal of molecular sciences

2023 Volume 24, Issue 3

Abstract: Parkinson's Disease (PD) is a prevalent neurodegenerative disorder that is characterized pathologically by the loss of A9-specific dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) of the midbrain. Despite intensive research, the ... ...

Abstract	Parkinson's Disease (PD) is a prevalent neurodegenerative disorder that is characterized pathologically by the loss of A9-specific dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) of the midbrain. Despite intensive research, the etiology of PD is currently unresolved, and the disease remains incurable. This, in part, is due to the lack of an experimental disease model that could faithfully recapitulate the features of human PD. However, the recent advent of induced pluripotent stem cell (iPSC) technology has allowed PD models to be created from patient-derived cells. Indeed, DA neurons from PD patients are now routinely established in many laboratories as monolayers as well as 3D organoid cultures that serve as useful toolboxes for understanding the mechanism underlying PD and also for drug discovery. At the same time, the iPSC technology also provides unprecedented opportunity for autologous cell-based therapy for the PD patient to be performed using the patient's own cells as starting materials. In this review, we provide an update on the molecular processes underpinning the development and differentiation of human pluripotent stem cells (PSCs) into midbrain DA neurons in both 2D and 3D cultures, as well as the latest advancements in using these cells for drug discovery and regenerative medicine. For the novice entering the field, the cornucopia of differentiation protocols reported for the generation of midbrain DA neurons may seem daunting. Here, we have distilled the essence of the different approaches and summarized the main factors driving DA neuronal differentiation, with the view to provide a useful guide to newcomers who are interested in developing iPSC-based models of PD.
MeSH term(s)	Humans ; Parkinson Disease/therapy ; Mesencephalon ; Dopaminergic Neurons ; Pluripotent Stem Cells ; Induced Pluripotent Stem Cells ; Organoids
Language	English
Publishing date	2023-01-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24032523
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Article ; Online: Visualization of accessible cholesterol using a GRAM domain-based biosensor.

Koh, Dylan Hong Zheng / Naito, Tomoki / Na, Minyoung / Yeap, Yee Jie / Rozario, Pritisha / Zhong, Franklin L / Lim, Kah-Leong / Saheki, Yasunori

Nature communications

2023 Volume 14, Issue 1, Page(s) 6773

Abstract: Cholesterol is important for membrane integrity and cell signaling, and dysregulation of the distribution of cellular cholesterol is associated with numerous diseases, including neurodegenerative disorders. While regulated transport of a specific pool of ...

Abstract	Cholesterol is important for membrane integrity and cell signaling, and dysregulation of the distribution of cellular cholesterol is associated with numerous diseases, including neurodegenerative disorders. While regulated transport of a specific pool of cholesterol, known as "accessible cholesterol", contributes to the maintenance of cellular cholesterol distribution and homeostasis, tools to monitor accessible cholesterol in live cells remain limited. Here, we engineer a highly sensitive accessible cholesterol biosensor by taking advantage of the cholesterol-sensing element (the GRAM domain) of an evolutionarily conserved lipid transfer protein, GRAMD1b. Using this cholesterol biosensor, which we call GRAM-W, we successfully visualize in real time the distribution of accessible cholesterol in many different cell types, including human keratinocytes and iPSC-derived neurons, and show differential dependencies on cholesterol biosynthesis and uptake for maintaining levels of accessible cholesterol. Furthermore, we combine GRAM-W with a dimerization-dependent fluorescent protein (ddFP) and establish a strategy for the ultrasensitive detection of accessible plasma membrane cholesterol. These tools will allow us to obtain important insights into the molecular mechanisms by which the distribution of cellular cholesterol is regulated.
MeSH term(s)	Humans ; Cell Membrane/metabolism ; Cholesterol/metabolism ; Biological Transport ; Homeostasis ; Biosensing Techniques
Chemical Substances	Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2023-10-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-42498-7
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Article ; Online: Lysosomal acidification dysfunction in microglia: an emerging pathogenic mechanism of neuroinflammation and neurodegeneration.

Quick, Joseph D / Silva, Cristian / Wong, Jia Hui / Lim, Kah Leong / Reynolds, Richard / Barron, Anna M / Zeng, Jialiu / Lo, Chih Hung

Journal of neuroinflammation

2023 Volume 20, Issue 1, Page(s) 185

Abstract: Microglia are the resident innate immune cells in the brain with a major role in orchestrating immune responses. They also provide a frontline of host defense in the central nervous system (CNS) through their active phagocytic capability. Being a ... ...

Abstract	Microglia are the resident innate immune cells in the brain with a major role in orchestrating immune responses. They also provide a frontline of host defense in the central nervous system (CNS) through their active phagocytic capability. Being a professional phagocyte, microglia participate in phagocytic and autophagic clearance of cellular waste and debris as well as toxic protein aggregates, which relies on optimal lysosomal acidification and function. Defective microglial lysosomal acidification leads to impaired phagocytic and autophagic functions which result in the perpetuation of neuroinflammation and progression of neurodegeneration. Reacidification of impaired lysosomes in microglia has been shown to reverse neurodegenerative pathology in Alzheimer's disease. In this review, we summarize key factors and mechanisms contributing to lysosomal acidification impairment and the associated phagocytic and autophagic dysfunction in microglia, and how these defects contribute to neuroinflammation and neurodegeneration. We further discuss techniques to monitor lysosomal pH and therapeutic agents that can reacidify impaired lysosomes in microglia under disease conditions. Finally, we propose future directions to investigate the role of microglial lysosomal acidification in lysosome-mitochondria crosstalk and in neuron-glia interaction for more comprehensive understanding of its broader CNS physiological and pathological implications.
MeSH term(s)	Humans ; Microglia/metabolism ; Neuroinflammatory Diseases ; Alzheimer Disease/metabolism ; Lysosomes/metabolism ; Hydrogen-Ion Concentration
Language	English
Publishing date	2023-08-05
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-023-02866-y
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Article ; Online: Parkin-independent mitophagy-FKBP8 takes the stage.

Lim, Grace Gy / Lim, Kah-Leong

EMBO reports

2017 Volume 18, Issue 6, Page(s) 864–865

Abstract: Although the Parkin/PINK1 pathway has received considerable attention in recent years as a key regulator of mitophagy in mammals, it is important to recognize that multiple mitophagy receptors like BNIP3, NIX, and FUNDC1 exist that can promote the ... ...

Abstract	Although the Parkin/PINK1 pathway has received considerable attention in recent years as a key regulator of mitophagy in mammals, it is important to recognize that multiple mitophagy receptors like BNIP3, NIX, and FUNDC1 exist that can promote the selective clearance of mitochondria in the absence of Parkin. In this issue, Bhujabal
MeSH term(s)	Animals ; Apoptosis ; Mitochondria ; Mitophagy ; Ubiquitin-Protein Ligases
Chemical Substances	Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2017-05-17
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	2020896-0
ISSN	1469-3178 ; 1469-221X
ISSN (online)	1469-3178
ISSN	1469-221X
DOI	10.15252/embr.201744313
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Zs.A 5433: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Vitamin B12 Ameliorates the Pathological Phenotypes of Multiple Parkinson’s Disease Models by Alleviating Oxidative Stress

Wu, Yue / Zhao, Zhongting / Yang, Naidi / Xin, Chenqi / Li, Zheng / Xu, Jiajia / Ma, Bo / Lim, Kah-Leong / Li, Lin / Wu, Qiong / Yu, Changmin / Zhang, Chengwu

Antioxidants. 2023 Jan. 09, v. 12, no. 1

2023

Abstract: Parkinson’s disease (PD) is the second most common neurodegenerative disease characterized by progressive loss of dopaminergic neurons in the substantia nigra of the midbrain. The etiology of PD has yet to be elucidated, and the disease remains incurable. ...

Abstract	Parkinson’s disease (PD) is the second most common neurodegenerative disease characterized by progressive loss of dopaminergic neurons in the substantia nigra of the midbrain. The etiology of PD has yet to be elucidated, and the disease remains incurable. Increasing evidence suggests that oxidative stress is the key causative factor of PD. Due to their capacity to alleviate oxidative stress, antioxidants hold great potential for the treatment of PD. Vitamins are essential organic substances for maintaining the life of organisms. Vitamin deficiency is implicated in the pathogenesis of various diseases, such as PD. In the present study, we investigated whether administration of vitamin B12 (VB12) could ameliorate PD phenotypes in vitro and in vivo. Our results showed that VB12 significantly reduced the generation of reactive oxygen species (ROS) in the rotenone-induced SH-SY5Y cellular PD model. In a Parkin gene knockout C. elegans PD model, VB12 mitigated motor dysfunction. Moreover, in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse PD model, VB12 also displayed protective effects, including the rescue of mitochondrial function, dopaminergic neuron loss, and movement disorder. In summary, our results suggest that vitamin supplementation may be a novel method for the intervention of PD, which is safer and more feasible than chemical drug treatment.
Keywords	brain ; drug therapy ; etiology ; gene targeting ; mice ; mitochondria ; models ; neurodegenerative diseases ; neurons ; oxidative stress ; pathogenesis ; reactive oxygen species ; vitamin B12 ; vitamin deficiencies ; vitamin supplements
Language	English
Dates of publication	2023-0109
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article ; Online
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox12010153
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Complete Genome Sequence of Serratia marcescens FY, Isolated from Drosophila melanogaster.

Liu, Wei / Kang, Ruxue / Lim, Kah Leong / Tan, Eng King

Microbiology resource announcements

2020 Volume 9, Issue 45

Abstract: In nature, the fruit fly frequently encounters various pathogens that cause a decrease in host fitness. Here, we present the genome sequence ... ...

Abstract	In nature, the fruit fly frequently encounters various pathogens that cause a decrease in host fitness. Here, we present the genome sequence of
Language	English
Publishing date	2020-11-05
Publishing country	United States
Document type	Journal Article
ISSN	2576-098X
ISSN (online)	2576-098X
DOI	10.1128/MRA.00755-20
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