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  1. Article: Age-induced nitrative stress decreases retrograde transport of proNGF via TrkA and increases proNGF retrograde transport and neurodegeneration via p75

    Kropf, Erika / Shekari, Arman / Jaberi, Sama / Puri, Anish / Wu, Chengbiao / Fahnestock, Margaret

    Frontiers in molecular neuroscience

    2023  Volume 16, Page(s) 1241420

    Abstract: Introduction: Axonal transport of pro nerve growth factor (proNGF) is impaired in aged basal forebrain cholinergic neurons (BFCNs), which is associated with their degeneration. ProNGF is neurotrophic in the presence of its receptor tropomyosin-related ... ...

    Abstract Introduction: Axonal transport of pro nerve growth factor (proNGF) is impaired in aged basal forebrain cholinergic neurons (BFCNs), which is associated with their degeneration. ProNGF is neurotrophic in the presence of its receptor tropomyosin-related kinase A (TrkA) but induces apoptosis via the pan-neurotrophin receptor (p75
    Methods: In this study, fluorescence microscopy was used to analyze axonal transport of quantum dot labeled proNGF in rat BFCNs
    Results: Young BFCNs transported proNGF-KKE but not proNGF-Δ9-13, and proNGF transport was not different in p75
    Discussion: Together, these results indicate that age-induced nitrative stress decreases proNGF transport via TrkA while increasing proNGF transport via p75
    Language English
    Publishing date 2023-11-13
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452967-9
    ISSN 1662-5099
    ISSN 1662-5099
    DOI 10.3389/fnmol.2023.1241420
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Herpes Simplex Virus, Alzheimer's Disease and a Possible Role for Rab GTPases.

    Bearer, Elaine L / Wu, Chengbiao

    Frontiers in cell and developmental biology

    2019  Volume 7, Page(s) 134

    Abstract: Herpes simplex virus (HSV) is a common pathogen, infecting 85% of adults in the United States. After reaching the nucleus of the long-lived neuron, HSV may enter latency to persist throughout the life span. Re-activation of latent herpesviruses is ... ...

    Abstract Herpes simplex virus (HSV) is a common pathogen, infecting 85% of adults in the United States. After reaching the nucleus of the long-lived neuron, HSV may enter latency to persist throughout the life span. Re-activation of latent herpesviruses is associated with progressive cognitive impairment and Alzheimer's disease (AD). As an enveloped DNA virus, HSV exploits cellular membrane systems for its life cycle, and thereby comes in contact with the Rab family of GTPases, master regulators of intracellular membrane dynamics. Knock-down and overexpression of specific Rabs reduce HSV production. Disheveled membrane compartments could lead to AD because membrane sorting and trafficking are crucial for synaptic vesicle formation, neuronal survival signaling and Abeta production. Amyloid precursor protein (APP), a transmembrane glycoprotein, is the parent of Abeta, the major component of senile plaques in AD. Up-regulation of APP expression due to HSV is significant since excess APP interferes with Rab5 endocytic trafficking in neurons. Here, we show that purified PC12-cell endosomes transport both anterograde and retrograde when injected into the squid giant axon at rates similar to isolated HSV. Intracellular HSV co-fractionates with these endosomes, contains APP, Rab5 and TrkA, and displays a second membrane. HSV infected PC12 cells up-regulate APP expression. Whether interference with Rabs has a specific effect on HSV or indirectly affects membrane compartment dynamics co-opted by virus needs further study. Ultimately Rabs, their effectors or their membrane-binding partners may serve as handles to reduce the impact of viral re-activation on cognitive function, or even as more general-purpose anti-microbial therapies.
    Language English
    Publishing date 2019-08-07
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2019.00134
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Editorial: Using novel technologies and models to identify biomarkers and explore therapeutic strategies for neurological disorders.

    Xing, Liwei / Wu, Chengbiao / Wang, Jiaojian / Wei, Sheng / Yuan, Kai / Qin, Dongdong

    Frontiers in behavioral neuroscience

    2023  Volume 17, Page(s) 1151667

    Language English
    Publishing date 2023-03-23
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2452960-6
    ISSN 1662-5153
    ISSN 1662-5153
    DOI 10.3389/fnbeh.2023.1151667
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Novel systemic delivery of a peptide-conjugated antisense oligonucleotide to reduce α-synuclein in a mouse model of Alzheimer's disease.

    Leitão, André D G / Ahammad, Rijwan U / Spencer, Brian / Wu, Chengbiao / Masliah, Eliezer / Rissman, Robert A

    Neurobiology of disease

    2023  Volume 186, Page(s) 106285

    Abstract: Neurodegenerative disorders of aging are characterized by the progressive accumulation of proteins such as α-synuclein (α-syn) and amyloid beta (Aβ). Misfolded and aggregated α-syn has been implicated in neurological disorders such as Parkinson's disease, ...

    Abstract Neurodegenerative disorders of aging are characterized by the progressive accumulation of proteins such as α-synuclein (α-syn) and amyloid beta (Aβ). Misfolded and aggregated α-syn has been implicated in neurological disorders such as Parkinson's disease, and Dementia with Lewy Bodies, but less so in Alzheimer's Disease (AD), despite the fact that accumulation of α-syn has been confirmed in over 50% of postmortem brains neuropathologically diagnosed with AD. To date, no therapeutic strategy has effectively or consistently downregulated α-syn in AD. Here we tested the hypothesis that by using a systemically-delivered peptide (ApoB
    MeSH term(s) Animals ; Mice ; Oligonucleotides, Antisense/pharmacology ; alpha-Synuclein/genetics ; Alzheimer Disease/drug therapy ; Amyloid beta-Peptides ; Apolipoproteins B ; Disease Models, Animal
    Chemical Substances Oligonucleotides, Antisense ; alpha-Synuclein ; Amyloid beta-Peptides ; Apolipoproteins B
    Language English
    Publishing date 2023-09-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1211786-9
    ISSN 1095-953X ; 0969-9961
    ISSN (online) 1095-953X
    ISSN 0969-9961
    DOI 10.1016/j.nbd.2023.106285
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4444: 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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  5. Article ; Online: Impacts of H

    Barber, Sophia / Gomez-Godinez, Veronica / Young, Joy / Wei, Abigail / Chen, Sarah / Snissarenko, Anna / Chan, Sze Sze / Wu, Chengbiao / Shi, Linda

    Journal of biophotonics

    2024  Volume 17, Issue 3, Page(s) e202300370

    Abstract: Axonal degeneration is a key component of neurodegenerative diseases such as Huntington's disease (HD), Alzheimer's disease, and amyotrophic lateral sclerosis. Nicotinamide, an NAD+ precursor, has long since been implicated in axonal protection and ... ...

    Abstract Axonal degeneration is a key component of neurodegenerative diseases such as Huntington's disease (HD), Alzheimer's disease, and amyotrophic lateral sclerosis. Nicotinamide, an NAD+ precursor, has long since been implicated in axonal protection and reduction of degeneration. However, studies on nicotinamide (NAm) supplementation in humans indicate that NAm has no protective effect. Sterile alpha and toll/interleukin receptor motif-containing protein 1 (SARM1) regulates several cell responses to axonal damage and has been implicated in promoting neuronal degeneration. SARM1 inhibition seems to result in protection from neuronal degeneration while hydrogen peroxide has been implicated in oxidative stress and axonal degeneration. The effects of laser-induced axonal damage in wild-type and HD dorsal root ganglion cells treated with NAm, hydrogen peroxide (H
    MeSH term(s) Animals ; Mice ; Humans ; Hydrogen Peroxide ; Niacinamide ; Huntington Disease ; Mice, Knockout ; Neurons/metabolism ; Cytoskeletal Proteins/metabolism ; Armadillo Domain Proteins/genetics ; Armadillo Domain Proteins/metabolism
    Chemical Substances Hydrogen Peroxide (BBX060AN9V) ; Niacinamide (25X51I8RD4) ; SARM1 protein, human ; Cytoskeletal Proteins ; Armadillo Domain Proteins ; SARM1 protein, mouse
    Language English
    Publishing date 2024-01-07
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 2390063-5
    ISSN 1864-0648 ; 1864-063X
    ISSN (online) 1864-0648
    ISSN 1864-063X
    DOI 10.1002/jbio.202300370
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6723: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  6. Article: Ras and Rab Interactor 3: From Cellular Mechanisms to Human Diseases.

    Shen, Ruinan / Murphy, Caitlin J / Xu, Xiaowen / Hu, Mingzheng / Ding, Jianqing / Wu, Chengbiao

    Frontiers in cell and developmental biology

    2022  Volume 10, Page(s) 824961

    Abstract: Ras and Rab interactor 3 (RIN3) functions as a Guanine nucleotide Exchange Factor (GEF) for some members of the Rab family of small GTPase. By promoting the activation of Rab5, RIN3 plays an important role in regulating endocytosis and endocytic ... ...

    Abstract Ras and Rab interactor 3 (RIN3) functions as a Guanine nucleotide Exchange Factor (GEF) for some members of the Rab family of small GTPase. By promoting the activation of Rab5, RIN3 plays an important role in regulating endocytosis and endocytic trafficking. In addition, RIN3 activates Ras, another small GTPase, that controls multiple signaling pathways to regulate cellular function. Increasing evidence suggests that dysregulation of RIN3 activity may contribute to the pathogenesis of several disease conditions ranging from Paget's Disease of the Bone (PDB), Alzheimer's Disease (AD), Chronic Obstructive Pulmonary Disease (COPD) and to obesity. Recent genome-wide association studies (GWAS) identified variants in the
    Language English
    Publishing date 2022-03-14
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2022.824961
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Isolation and Culturing of Rat Primary Embryonic Basal Forebrain Cholinergic Neurons (BFCNs).

    Xu, Wei / Wu, Chengbiao

    Bio-protocol

    2017  Volume 7, Issue 14, Page(s) e2413

    Abstract: The basal forebrain is located close to the medial and ventral surfaces of the cerebral hemispheres that develop from the sub-pallium. It regulates multiple processes including attention, learning, memory and sleep. Dysfunction and degeneration of basal ... ...

    Abstract The basal forebrain is located close to the medial and ventral surfaces of the cerebral hemispheres that develop from the sub-pallium. It regulates multiple processes including attention, learning, memory and sleep. Dysfunction and degeneration of basal forebrain cholinergic neurons (BFCNs) are believed to be involved in many disorders of the brain such as Alzheimer's disease (AD), schizophrenia, sleep disorders and drug abuse ( Mobley
    Language English
    Publishing date 2017-07-20
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2833269-6
    ISSN 2331-8325 ; 2331-8325
    ISSN (online) 2331-8325
    ISSN 2331-8325
    DOI 10.21769/BioProtoc.2413
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Charcot Marie Tooth 2B Peripheral Sensory Neuropathy: How Rab7 Mutations Impact NGF Signaling?

    Liu, Harry / Wu, Chengbiao

    International journal of molecular sciences

    2017  Volume 18, Issue 2

    Abstract: Charcot-Marie-Tooth 2B peripheral sensory neuropathy (CMT2B) is a debilitating autosomal dominant hereditary sensory neuropathy. Patients with this disease lose pain sensation and frequently need amputation. Axonal dysfunction and degeneration of ... ...

    Abstract Charcot-Marie-Tooth 2B peripheral sensory neuropathy (CMT2B) is a debilitating autosomal dominant hereditary sensory neuropathy. Patients with this disease lose pain sensation and frequently need amputation. Axonal dysfunction and degeneration of peripheral sensory neurons is a major clinical manifestation of CMT2B. However, the cellular and molecular pathogenic mechanisms remain undefined. CMT2B is caused by missense point mutations (L129F, K157N, N161T/I, V162M) in Rab7 GTPase. Strong evidence suggests that the Rab7 mutation(s) enhances the cellular levels of activated Rab7 proteins, thus resulting in increased lysosomal activity and autophagy. As a consequence, trafficking and signaling of neurotrophic factors such as nerve growth factor (NGF) in the long axons of peripheral sensory neurons are particularly vulnerable to premature degradation. A "gain of toxicity" model has, thus, been proposed based on these observations. However, studies of fly photo-sensory neurons indicate that the Rab7 mutation(s) causes a "loss of function", resulting in haploinsufficiency. In the review, we summarize experimental evidence for both hypotheses. We argue that better models (rodent animals and human neurons) of CMT2B are needed to precisely define the disease mechanisms.
    MeSH term(s) Axons/metabolism ; Charcot-Marie-Tooth Disease/genetics ; Charcot-Marie-Tooth Disease/metabolism ; Genetic Association Studies ; Humans ; Muramidase/metabolism ; Mutation ; Nerve Growth Factor/metabolism ; Signal Transduction ; rab GTP-Binding Proteins/chemistry ; rab GTP-Binding Proteins/genetics ; rab GTP-Binding Proteins/metabolism
    Chemical Substances rab7 protein (152989-05-4) ; Nerve Growth Factor (9061-61-4) ; Muramidase (EC 3.2.1.17) ; rab GTP-Binding Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2017-02-04
    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/ijms18020324
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Hippocampal Reduction of α-Synuclein via RNA Interference Improves Neuropathology in Alzheimer's Disease Mice.

    Leitão, André D G / Spencer, Brian / Sarsoza, Floyd / Ngolab, Jennifer / Amalraj, Jessica / Masliah, Eliezer / Wu, Chengbiao / Rissman, Robert A

    Journal of Alzheimer's disease : JAD

    2023  Volume 95, Issue 1, Page(s) 349–361

    Abstract: Background: Alzheimer's disease (AD) cases are often characterized by the pathological accumulation of α-synuclein (α-syn) in addition to amyloid-β (Aβ) and tau hallmarks. The role of α-syn has been extensively studied in synucleinopathy disorders, but ... ...

    Abstract Background: Alzheimer's disease (AD) cases are often characterized by the pathological accumulation of α-synuclein (α-syn) in addition to amyloid-β (Aβ) and tau hallmarks. The role of α-syn has been extensively studied in synucleinopathy disorders, but less so in AD. Recent studies have shown that α-syn may also play a role in AD and its downregulation may be protective against the toxic effects of Aβ accumulation.
    Objective: We hypothesized that selectively knocking down α-syn via RNA interference improves the neuropathological and biochemical findings in AD mice.
    Methods: Here we used amyloid precursor protein transgenic (APP-Tg) mice to model AD and explore pathologic and behavioral phenotypes with knockdown of α-syn using RNA interference. We selectively reduced α-syn levels by stereotaxic bilateral injection of either LV-shRNA α-syn or LV-shRNA-luc (control) into the hippocampus of AD mice.
    Results: We found that downregulation of α-syn results in significant reduction in the number of Aβ plaques. In addition, mice treated with LV-shRNA α-syn had amelioration of abnormal microglial activation (Iba1) and astrocytosis (GFAP) phenotypes in AD mice.
    Conclusion: Our data suggests a novel link between Aβ and α-syn pathology as well as a new therapeutic angle for targeting AD.
    MeSH term(s) Mice ; Animals ; Alzheimer Disease/pathology ; alpha-Synuclein/genetics ; alpha-Synuclein/metabolism ; RNA Interference ; Amyloid beta-Protein Precursor/genetics ; Amyloid beta-Peptides/metabolism ; Mice, Transgenic ; Hippocampus/pathology ; Plaque, Amyloid/pathology ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; tau Proteins/metabolism ; Disease Models, Animal
    Chemical Substances alpha-Synuclein ; Amyloid beta-Protein Precursor ; Amyloid beta-Peptides ; RNA, Small Interfering ; tau Proteins
    Language English
    Publishing date 2023-07-28
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1440127-7
    ISSN 1875-8908 ; 1387-2877
    ISSN (online) 1875-8908
    ISSN 1387-2877
    DOI 10.3233/JAD-230232
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6084: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  10. Article: Uncoupling neurotrophic function from nociception of nerve growth factor: what can be learned from a rare human disease?

    Sung, Kijung / Yang, Wanlin / Wu, Chengbiao

    Neural regeneration research

    2019  Volume 14, Issue 4, Page(s) 570–573

    Abstract: Nerve growth factor (NGF) is a powerful trophic factor that provides essential support for the survival and differentiation of sympathetic and sensory neurons during development. However, NGF also activates nociceptors contributing significantly to ... ...

    Abstract Nerve growth factor (NGF) is a powerful trophic factor that provides essential support for the survival and differentiation of sympathetic and sensory neurons during development. However, NGF also activates nociceptors contributing significantly to inflammatory pain and neuropathic pain after tissue injury. As such anti-NGF based therapies represent a promising strategy for pain management. Because of dose-dependent serious side effects such as back pain, injection site hyperalgesia, clinical trials of using NGF to treat various disorders such as diabetic neuropathies, chemotherapy-induced and human immunodeficiency virus-associated peripheral neuropathies were all discontinued. Thus far, worldwide clinical applications of NGF in treating patients are very limited except in China. Hereditary sensory autonomic neuropathy type V (HSAN V) is an extremely rare disease. Genetic analyses have revealed that HSAN V is associated with autosomal recessive mutations in NGF. One of the mutations occurred at the 100
    Language English
    Publishing date 2019-01-15
    Publishing country India
    Document type Journal Article ; Review
    ZDB-ID 2388460-5
    ISSN 1876-7958 ; 1673-5374
    ISSN (online) 1876-7958
    ISSN 1673-5374
    DOI 10.4103/1673-5374.247442
    Database MEDical Literature Analysis and Retrieval System OnLINE

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