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Article ; Online: Synaptic Paths to Neurodegeneration: The Emerging Role of TDP-43 and FUS in Synaptic Functions.

Ling, Shuo-Chien

2018 Volume 2018, Page(s) 8413496

Abstract: TAR DNA-binding protein-43 KDa (TDP-43) and fused in sarcoma (FUS) as the defining pathological hallmarks for amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), coupled with ALS-FTD-causing mutations in both genes, indicate that their ...

Abstract	TAR DNA-binding protein-43 KDa (TDP-43) and fused in sarcoma (FUS) as the defining pathological hallmarks for amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), coupled with ALS-FTD-causing mutations in both genes, indicate that their dysfunctions damage the motor system and cognition. On the molecular level, TDP-43 and FUS participate in the biogenesis and metabolism of coding and noncoding RNAs as well as in the transport and translation of mRNAs as part of cytoplasmic mRNA-ribonucleoprotein (mRNP) granules. Intriguingly, many of the RNA targets of TDP-43 and FUS are involved in synaptic transmission and plasticity, indicating that synaptic dysfunction could be an early event contributing to motor and cognitive deficits in ALS and FTD. Furthermore, the ability of the low-complexity prion-like domains of TDP-43 and FUS to form liquid droplets suggests a potential mechanism for mRNP assembly and conversion. This review will discuss the role of TDP-43 and FUS in RNA metabolism, with an emphasis on the involvement of this process in synaptic function and neuroprotection. This will be followed by a discussion of the potential phase separation mechanism for forming RNP granules and pathological inclusions.
MeSH term(s)	DNA-Binding Proteins/metabolism ; Humans ; Nerve Degeneration/metabolism ; Neurodegenerative Diseases/metabolism ; RNA-Binding Protein FUS/metabolism ; Synapses/metabolism
Chemical Substances	DNA-Binding Proteins ; RNA-Binding Protein FUS ; TARDBP protein, human
Language	English
Publishing date	2018-04-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1454938-4
ISSN	1687-5443 ; 2090-5904 ; 0792-8483
ISSN (online)	1687-5443
ISSN	2090-5904 ; 0792-8483
DOI	10.1155/2018/8413496
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Article ; Online: Central nervous system cholesterol metabolism in health and disease.

Ho, Wan Y / Hartmann, Hannelore / Ling, Shuo-Chien

IUBMB life

2022 Volume 74, Issue 8, Page(s) 826–841

Abstract: Cholesterol is a ubiquitous and essential component of cellular membranes, as it regulates membrane structure and fluidity. Furthermore, cholesterol serves as a precursor for steroid hormones, oxysterol, and bile acids, that are essential for maintaining ...

Abstract	Cholesterol is a ubiquitous and essential component of cellular membranes, as it regulates membrane structure and fluidity. Furthermore, cholesterol serves as a precursor for steroid hormones, oxysterol, and bile acids, that are essential for maintaining many of the body's metabolic processes. The biosynthesis and excretion of cholesterol is tightly regulated in order to maintain homeostasis. Although virtually all cells have the capacity to make cholesterol, the liver and brain are the two main organs producing cholesterol in mammals. Once produced, cholesterol is transported in the form of lipoprotein particles to other cell types and tissues. Upon formation of the blood-brain barrier (BBB) during embryonic development, lipoproteins cannot move between the central nervous system (CNS) and the rest of the body. As such, cholesterol biosynthesis and metabolism in the CNS operate autonomously without input from the circulation system in normal physiological conditions. Nevertheless, similar regulatory mechanisms for maintaining cholesterol homeostasis are utilized in both the CNS and peripheral systems. Here, we discuss the functions and metabolism of cholesterol in the CNS. We further focus on how different CNS cell types contribute to cholesterol metabolism, and how ApoE, the major CNS apolipoprotein, is involved in normal and pathophysiological functions. Understanding these basic mechanisms will aid our ability to elucidate how CNS cholesterol dysmetabolism contributes to neurogenerative diseases.
MeSH term(s)	Animals ; Biological Transport ; Brain ; Central Nervous System/metabolism ; Cholesterol/metabolism ; Lipid Metabolism ; Mammals/metabolism
Chemical Substances	Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2022-07-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1492141-8
ISSN	1521-6551 ; 1521-6543
ISSN (online)	1521-6551
ISSN	1521-6543
DOI	10.1002/iub.2662
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Article ; Online: Elevated FUS levels by overriding its autoregulation produce gain-of-toxicity properties that disrupt protein and RNA homeostasis.

Ho, Wan Yun / Ling, Shuo-Chien

Autophagy

2019 Volume 15, Issue 9, Page(s) 1665–1667

Abstract: Coding or non-coding mutations in FUS (fused in sarcoma) cause amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). In addition to familial ALS, abnormal aggregates of FUS are present in a portion of FTD and other neurodegenerative ... ...

Abstract	Coding or non-coding mutations in FUS (fused in sarcoma) cause amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). In addition to familial ALS, abnormal aggregates of FUS are present in a portion of FTD and other neurodegenerative diseases independent of their mutations. Broad expression within the central nervous system of either wild-type or two ALS-linked human FUS mutants produces progressive motor phenotypes accompanied by characteristic ALS-like pathology. FUS levels are autoregulated to maintain an optimal steady-state level. Increasing FUS expression by saturating its autoregulatory mechanism results in rapidly progressive neurological phenotypes and dose-dependent lethality. Genome-wide expression analysis reveals genetic mis-regulations distinct from those via FUS reduction. Among these are increased expression of lysosomal proteins, suggestive of disruption in protein homeostasis as a potential gain-of-toxicity mechanism. Indeed, increased expression of wild-type FUS or ALS-linked mutant forms of FUS inhibit macroautophagy/autophagy. Collectively, our results demonstrate that: (1) mice expressing FUS develop progressive motor deficits, (2) increased FUS expression by overriding its autoregulatory mechanism accelerates neurodegeneration, providing a basis for FUS involvement without mutation, and (3) disruption in both protein homeostasis and RNA processing contribute to FUS-mediated toxicity.
MeSH term(s)	Amyotrophic Lateral Sclerosis ; Animals ; Autophagy ; Homeostasis ; Humans ; Mice ; Mutation ; RNA ; RNA-Binding Protein FUS/genetics
Chemical Substances	FUS protein, human ; RNA-Binding Protein FUS ; RNA (63231-63-0)
Language	English
Publishing date	2019-06-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2019.1633162
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Article: Deciphering lipid dysregulation in ALS: from mechanisms to translational medicine.

Agrawal, Ira / Lim, Yong Shan / Ng, Shi-Yan / Ling, Shuo-Chien

Translational neurodegeneration

2022 Volume 11, Issue 1, Page(s) 48

Abstract: Lipids, defined by low solubility in water and high solubility in nonpolar solvents, can be classified into fatty acids, glycerolipids, glycerophospholipids, sphingolipids, and sterols. Lipids not only regulate integrity and fluidity of biological ... ...

Abstract	Lipids, defined by low solubility in water and high solubility in nonpolar solvents, can be classified into fatty acids, glycerolipids, glycerophospholipids, sphingolipids, and sterols. Lipids not only regulate integrity and fluidity of biological membranes, but also serve as energy storage and bioactive molecules for signaling. Causal mutations in SPTLC1 (serine palmitoyltransferase long chain subunit 1) gene within the lipogenic pathway have been identified in amyotrophic lateral sclerosis (ALS), a paralytic and fatal motor neuron disease. Furthermore, lipid dysmetabolism within the central nervous system and circulation is associated with ALS. Here, we aim to delineate the diverse roles of different lipid classes and understand how lipid dysmetabolism may contribute to ALS pathogenesis. Among the different lipids, accumulation of ceramides, arachidonic acid, and lysophosphatidylcholine is commonly emerging as detrimental to motor neurons. We end with exploring the potential ALS therapeutics by reducing these toxic lipids.
MeSH term(s)	Humans ; Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/therapy ; Amyotrophic Lateral Sclerosis/metabolism ; Translational Science, Biomedical ; Motor Neurons/pathology ; Motor Neuron Disease/metabolism ; Ceramides/metabolism
Chemical Substances	Ceramides
Language	English
Publishing date	2022-11-07
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2653701-1
ISSN	2047-9158
ISSN	2047-9158
DOI	10.1186/s40035-022-00322-0
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Article ; Online: Cholesterol dyshomeostasis in amyotrophic lateral sclerosis: cause, consequence, or epiphenomenon?

Hartmann, Hannelore / He, Wanyun / Chang, Jer‐Cherng / Ling, Shuo‐Chien

The FEBS Journal. 2022 Dec., v. 289, no. 24 p.7688-7709

2022

Abstract: Amyotrophic lateral sclerosis (ALS), the most common adult‐onset motor neuron disease, is characterized by the selective degeneration of motor neurons leading to paralysis and eventual death. Multiple pathogenic mechanisms, including systemic ... ...

Abstract	Amyotrophic lateral sclerosis (ALS), the most common adult‐onset motor neuron disease, is characterized by the selective degeneration of motor neurons leading to paralysis and eventual death. Multiple pathogenic mechanisms, including systemic dysmetabolism, have been proposed to contribute to ALS. Among them, dyslipidemia, i.e., abnormal level of cholesterol and other lipids in the circulation and central nervous system (CNS), has been reported in ALS patients, but without a consensus. Cholesterol is a constituent of cellular membranes and a precursor of steroid hormones, oxysterols, and bile acids. Consequently, optimal cholesterol levels are essential for health. Due to the blood–brain barrier (BBB), cholesterol cannot move between the CNS and the rest of the body. As such, cholesterol metabolism in the CNS is proposed to operate autonomously. Despite its importance, it remains elusive how cholesterol dyshomeostasis may contribute to ALS. In this review, we aim to describe the current state of cholesterol metabolism research in ALS, identify unresolved issues, and provide potential directions.
Keywords	amyotrophic lateral sclerosis ; bile ; blood-brain barrier ; central nervous system ; cholesterol metabolism ; death ; hyperlipidemia ; motor neurons ; oxysterols ; paralysis
Language	English
Dates of publication	2022-12
Size	p. 7688-7709.
Publishing place	John Wiley & Sons, Ltd
Document type	Article ; Online
Note	REVIEW
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.16175
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Cholesterol dyshomeostasis in amyotrophic lateral sclerosis: cause, consequence, or epiphenomenon?

Hartmann, Hannelore / Ho, Wan Yun / Chang, Jer-Cherng / Ling, Shuo-Chien

The FEBS journal

2021

Abstract: Amyotrophic lateral sclerosis (ALS), the most common adult-onset motor neuron disease, is characterized by the selective degeneration of motor neurons leading to paralysis and eventual death. Multiple pathogenic mechanisms, including systemic ... ...

Abstract	Amyotrophic lateral sclerosis (ALS), the most common adult-onset motor neuron disease, is characterized by the selective degeneration of motor neurons leading to paralysis and eventual death. Multiple pathogenic mechanisms, including systemic dysmetabolism, have been proposed to contribute to ALS. Among them, dyslipidemia, i.e., abnormal level of cholesterol and other lipids in the circulation and central nervous system (CNS), has been reported in ALS patients, but without a consensus. Cholesterol is a constituent of cellular membranes and a precursor of steroid hormones, oxysterols, and bile acids. Consequently, optimal cholesterol levels are essential for health. Due to the blood-brain barrier (BBB), cholesterol cannot move between the CNS and the rest of the body. As such, cholesterol metabolism in the CNS is proposed to operate autonomously. Despite its importance, it remains elusive how cholesterol dyshomeostasis may contribute to ALS. In this review, we aim to describe the current state of cholesterol metabolism research in ALS, identify unresolved issues, and provide potential directions.
Language	English
Publishing date	2021-09-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.16175
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Article ; Online: Deregulated expression of a longevity gene, Klotho, in the C9orf72 deletion mice with impaired synaptic plasticity and adult hippocampal neurogenesis.

Ho, Wan Yun / Navakkode, Sheeja / Liu, Fujia / Soong, Tuck Wah / Ling, Shuo-Chien

Acta neuropathologica communications

2020 Volume 8, Issue 1, Page(s) 155

Abstract: Hexanucleotide repeat expansion of C9ORF72 is the most common genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia. Synergies between loss of C9ORF72 functions and gain of toxicities from the repeat expansions contribute to C9ORF72- ... ...

Abstract	Hexanucleotide repeat expansion of C9ORF72 is the most common genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia. Synergies between loss of C9ORF72 functions and gain of toxicities from the repeat expansions contribute to C9ORF72-mediated pathogenesis. However, how loss of C9orf72 impacts neuronal and synaptic functions remains undetermined. Here, we showed that long-term potentiation at the dentate granule cells and long-term depression at the Schaffer collateral/commissural synapses at the area CA1 were reduced in the hippocampus of C9orf72 knockout mice. Using unbiased transcriptomic analysis, we identified that Klotho, a longevity gene, was selectively dysregulated in an age-dependent manner. Specifically, Klotho protein expression in the hippocampus of C9orf72 knockout mice was incorrectly enriched in the dendritic regions of CA1 with concomitant reduction in granule cell layer of dentate gyrus at 3-month of age followed by an accelerating decline during aging. Furthermore, adult hippocampal neurogenesis was reduced in C9orf72 knockout mice. Taken together, our data suggest that C9ORF72 is required for synaptic plasticity and adult neurogenesis in the hippocampus and Klotho deregulations may be part of C9ORF72-mediated toxicity.
MeSH term(s)	Animals ; C9orf72 Protein/deficiency ; Glucuronidase/metabolism ; Hippocampus/metabolism ; Hippocampus/pathology ; Mice ; Mice, Knockout ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Neurogenesis/physiology ; Neuronal Plasticity/physiology ; Transcriptome
Chemical Substances	C9orf72 Protein ; C9orf72 protein, mouse ; Glucuronidase (EC 3.2.1.31) ; klotho protein (EC 3.2.1.31)
Keywords	covid19
Language	English
Publishing date	2020-09-04
Publishing country	England
Document type	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-020-01030-4
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Article ; Online: The vulnerability of motor and frontal cortex-dependent behaviors in mice expressing ALS-linked mutation in TDP-43.

Wong, Peiyan / Ho, Wan Yun / Yen, Yi-Chun / Sanford, Emma / Ling, Shuo-Chien

Neurobiology of aging

2020 Volume 92, Page(s) 43–60

Abstract: TDP-43 aggregates are the defining pathological hallmark for amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Strikingly, these TDP-43 proteinopathies are also found in other neurodegenerative diseases, including Alzheimer's disease ...

Abstract	TDP-43 aggregates are the defining pathological hallmark for amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Strikingly, these TDP-43 proteinopathies are also found in other neurodegenerative diseases, including Alzheimer's disease and are prevalent in the brains of old-aged humans. Furthermore, disease-causal mutations in TDP-43 have been identified for ALS and FTD. Collectively, the evidence indicates that TDP-43 dysfunctions lead to motor and cognitive deficits. To determine whether the mouse line expressing an ALS-linked mutation in TDP-43 (Q331K) can be used to study ALS-FTD spectrum disorders, we performed a systematic and longitudinal behavioral assessment that covered motor and cognitive functions. Deficits in motor and cognitive abilities were observed as early as 3 months of age and persisted through to 12 months of age. Within the cognitive modalities, the hippocampus-mediated spatial learning and memory, and contextual fear conditioning, were normal; whereas the frontal cortex-mediated working memory and cognitive flexibility were impaired. Biochemically, the human TDP-43 transgene downregulates endogenous mouse TDP-43 mRNA and protein, resulting in human TDP-43 protein that is comparable with the physiological level in cerebral cortex and hippocampus. Furthermore, Q331K TDP-43 is largely retained at the nucleus without apparent aggregates. Taken together, our data suggest that motor and frontal cortex may be more vulnerable to disease-linked mutation in TDP-43 and, this mouse model may be used to assess ALS-FTD-related spectrum diseases and the molecular underpinnings associated with the phenotypes.
MeSH term(s)	Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/physiopathology ; Animals ; Cognition ; DNA-Binding Proteins/genetics ; Disease Models, Animal ; Female ; Frontal Lobe/physiopathology ; Male ; Mice, Inbred C57BL ; Mice, Transgenic ; Motor Activity ; Motor Cortex/physiopathology ; Mutation
Chemical Substances	DNA-Binding Proteins ; TARDBP protein, human
Language	English
Publishing date	2020-04-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604505-4
ISSN	1558-1497 ; 0197-4580
ISSN (online)	1558-1497
ISSN	0197-4580
DOI	10.1016/j.neurobiolaging.2020.03.019
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Zs.A 1685: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: A degradative to secretory autophagy switch mediates mitochondria clearance in the absence of the mATG8-conjugation machinery.

Tan, Hayden Weng Siong / Lu, Guang / Dong, Han / Cho, Yik-Lam / Natalia, Auginia / Wang, Liming / Chan, Charlene / Kappei, Dennis / Taneja, Reshma / Ling, Shuo-Chien / Shao, Huilin / Tsai, Shih-Yin / Ding, Wen-Xing / Shen, Han-Ming

Nature communications

2022 Volume 13, Issue 1, Page(s) 3720

Abstract: PINK1-Parkin mediated mitophagy, a selective form of autophagy, represents one of the most important mechanisms in mitochondrial quality control (MQC) via the clearance of damaged mitochondria. Although it is well known that the conjugation of mammalian ... ...

Abstract	PINK1-Parkin mediated mitophagy, a selective form of autophagy, represents one of the most important mechanisms in mitochondrial quality control (MQC) via the clearance of damaged mitochondria. Although it is well known that the conjugation of mammalian ATG8s (mATG8s) to phosphatidylethanolamine (PE) is a key step in autophagy, its role in mitophagy remains controversial. In this study, we clarify the role of the mATG8-conjugation system in mitophagy by generating knockouts of the mATG8-conjugation machinery. Unexpectedly, we show that mitochondria could still be cleared in the absence of the mATG8-conjugation system, in a process independent of lysosomal degradation. Instead, mitochondria are cleared via extracellular release through a secretory autophagy pathway, in a process we define as Autophagic Secretion of Mitochondria (ASM). Functionally, increased ASM promotes the activation of the innate immune cGAS-STING pathway in recipient cells. Overall, this study reveals ASM as a mechanism in MQC when the cellular mATG8-conjugation machinery is dysfunctional and highlights the critical role of mATG8 lipidation in suppressing inflammatory responses.
MeSH term(s)	Animals ; Autophagy ; Biological Transport ; Lysosomes/metabolism ; Mammals ; Mitochondria/metabolism ; Mitophagy
Language	English
Publishing date	2022-06-28
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/s41467-022-31213-7
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Article ; Online: Ooplasmic flow cooperates with transport and anchorage in

Lu, Wen / Lakonishok, Margot / Serpinskaya, Anna S / Kirchenbüechler, David / Ling, Shuo-Chien / Gelfand, Vladimir I

The Journal of cell biology

2018 Volume 217, Issue 10, Page(s) 3497–3511

Abstract: The posterior determination of ... ...

Abstract	The posterior determination of the
MeSH term(s)	Animals ; Biological Transport, Active/physiology ; Cytoplasm/genetics ; Cytoplasm/metabolism ; Drosophila Proteins/genetics ; Drosophila Proteins/metabolism ; Drosophila melanogaster ; Kinesins/genetics ; Kinesins/metabolism ; Microtubules/genetics ; Microtubules/metabolism ; Oocytes/cytology ; Oocytes/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism
Chemical Substances	Drosophila Proteins ; RNA, Messenger ; RNA-Binding Proteins ; osk protein, Drosophila ; stau protein, Drosophila (139568-71-1) ; Kinesins (EC 3.6.4.4)
Language	English
Publishing date	2018-07-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	218154-x
ISSN	1540-8140 ; 0021-9525
ISSN (online)	1540-8140
ISSN	0021-9525
DOI	10.1083/jcb.201709174
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