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Article ; Online: CFTR Modulators Rescue the Activity of CFTR in Colonoids Expressing the Complex Allele p.[R74W;V201M;D1270N]/dele22_24.

Kleinfelder, Karina / Somenza, Elena / Farinazzo, Alessia / Conti, Jessica / Lotti, Virginia / Latorre, Roberta Valeria / Rodella, Luca / Massella, Arianna / Tomba, Francesco / Bertini, Marina / Sorio, Claudio / Melotti, Paola

International journal of molecular sciences

2023 Volume 24, Issue 6

Abstract: An Italian, 46-year-old female patient carrying the complex allele p.[R74W;V201M;D1270N] in trans with CFTR dele22_24 was diagnosed at the Cystic Fibrosis (CF) Center of Verona as being affected by CF-pancreatic sufficient (CF-PS) in 2021. The variant ... ...

Abstract	An Italian, 46-year-old female patient carrying the complex allele p.[R74W;V201M;D1270N] in trans with CFTR dele22_24 was diagnosed at the Cystic Fibrosis (CF) Center of Verona as being affected by CF-pancreatic sufficient (CF-PS) in 2021. The variant V201M has unknown significance, while both of the other variants of this complex allele have variable clinical consequences, according to the CFTR2 database, with reported clinical benefits for treatment with ivacaftor + tezacaftor and ivacaftor + tezacaftor + elexacaftor in patients carrying the R74W-D1270N complex allele, which are currently approved (in USA, not yet in Italy). She was previously followed up by pneumologists in northern Italy because of frequent bronchitis, hemoptysis, recurrent rhinitis,
MeSH term(s)	Female ; Humans ; Middle Aged ; Cystic Fibrosis Transmembrane Conductance Regulator/genetics ; Cystic Fibrosis Transmembrane Conductance Regulator/metabolism ; Alleles ; Colforsin/therapeutic use ; Mutation ; Cystic Fibrosis/drug therapy ; Cystic Fibrosis/genetics ; Benzodioxoles/pharmacology ; Benzodioxoles/therapeutic use
Chemical Substances	Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6) ; ivacaftor (1Y740ILL1Z) ; Colforsin (1F7A44V6OU) ; Benzodioxoles ; CFTR protein, human
Language	English
Publishing date	2023-03-08
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24065199
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Article ; Online: Serum and cerebrospinal neurofilament light chain levels in patients with acquired peripheral neuropathies.

Mariotto, Sara / Farinazzo, Alessia / Magliozzi, Roberta / Alberti, Daniela / Monaco, Salvatore / Ferrari, Sergio

Journal of the peripheral nervous system : JPNS

2018 Volume 23, Issue 3, Page(s) 174–177

Abstract: Neurofilament light chain (NFL) levels reflect axonal damage in different inflammatory and neurodegenerative central nervous system conditions, in correlation with disease severity. Our aim was to determine the possible diagnostic and prognostic value of ...

Abstract	Neurofilament light chain (NFL) levels reflect axonal damage in different inflammatory and neurodegenerative central nervous system conditions, in correlation with disease severity. Our aim was to determine the possible diagnostic and prognostic value of serum and cerebrospinal fluid (CSF) NFL levels in subjects with different forms of acquired peripheral neuropathies (PN). Paired serum and CSF samples of 25 patients with acquired PN were analysed for NFL using an ultrasensitive technique (Quanterix, Simoa, Lexington, MA, USA) and compared with a group of 25 age-matched healthy subjects. Demographic, clinical, CSF and neurophysiological data were reviewed. Cases with Guillain-Barré syndrome (N = 5), multifocal motor neuropathy (N = 3), chronic inflammatory demyelinating polyneuropathy (CIDP) and variants (N = 12), anti-myelin-associated glycoprotein (MAG) neuropathy (N = 3), both CIDP and anti-MAG neuropathy (N = 1), and non-systemic vasculitic neuropathy (N = 1) were studied. NFL levels were significantly (P < 0.001) increased in patients with PN and were higher in the CSF (median: 1407 pg/mL, range: 140.2-12 661) than in serum (median: 31.52 pg/mL, range: 4.33-1178). A statistically significant correlation was observed between serum and CSF levels in cases with blood-nerve-barrier damage (r = 0.71, P < 0.01), and between serum NFL levels and disease activity at sampling (r = 0.52, P < 0.01) and at last follow-up (r = 0.53, P < 0.01) in all subjects. The increase of NFL values in both serum and CSF of patients with acquired PN and the significant correlation between serum NFL levels, disease severity and final outcome support the possible role of NFL as disease activity and prognostic biomarker also in peripheral nervous system disorders.
MeSH term(s)	Adolescent ; Adult ; Aged ; Aged, 80 and over ; Biomarkers/analysis ; Child ; Child, Preschool ; Female ; Humans ; Male ; Middle Aged ; Neurofilament Proteins/analysis ; Neurofilament Proteins/metabolism ; Peripheral Nervous System Diseases/metabolism ; Young Adult
Chemical Substances	Biomarkers ; Neurofilament Proteins ; neurofilament protein L
Language	English
Publishing date	2018-07-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1364009-4
ISSN	1529-8027 ; 1085-9489
ISSN (online)	1529-8027
ISSN	1085-9489
DOI	10.1111/jns.12279
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Article ; Online: Nanovesicles from adipose-derived mesenchymal stem cells inhibit T lymphocyte trafficking and ameliorate chronic experimental autoimmune encephalomyelitis.

Farinazzo, Alessia / Angiari, Stefano / Turano, Ermanna / Bistaffa, Edoardo / Dusi, Silvia / Ruggieri, Serena / Bonafede, Roberta / Mariotti, Raffaella / Constantin, Gabriela / Bonetti, Bruno

Scientific reports

2018 Volume 8, Issue 1, Page(s) 7473

Abstract: Cell based-therapies represent promising strategies for the treatment of neurological diseases. We have previously shown that adipose stem cells (ASC) ameliorate chronic experimental autoimmune encephalomyelitis (EAE). Recent evidence indicates that most ...

Abstract	Cell based-therapies represent promising strategies for the treatment of neurological diseases. We have previously shown that adipose stem cells (ASC) ameliorate chronic experimental autoimmune encephalomyelitis (EAE). Recent evidence indicates that most ASC paracrine effects are mediated by extracellular vesicles, i.e. micro- and nanovesicles (MVs and NVs). We show that preventive intravenous administration of NVs isolated from ASC (ASC-NVs) before disease onset significantly reduces the severity of EAE and decreases spinal cord inflammation and demyelination, whereas therapeutic treatment with ASC-NVs does not ameliorate established EAE. This treatment marginally inhibits antigen-specific T cell activation, while reducing microglial activation and demyelination in the spinal cord. Importantly, ASC-NVs inhibited integrin-dependent adhesion of encephalitogenic T cells in vitro, with no effect on adhesion molecule expression. In addition, intravital microscopy showed that encephalitogenic T cells treated with ASC NVs display a significantly reduced rolling and firm adhesion in inflamed spinal cord vessels compared to untreated cells. Our results show that ASC-NVs ameliorate EAE pathogenesis mainly by inhibiting T cell extravasation in the inflamed CNS, suggesting that NVs may represent a novel therapeutic approach in neuro-inflammatory diseases, enabling the safe administration of ASC effector factors.
MeSH term(s)	Adipose Tissue/cytology ; Animals ; Cell Movement/immunology ; Cells, Cultured ; Chronic Disease ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Encephalomyelitis, Autoimmune, Experimental/therapy ; Extracellular Vesicles/physiology ; Extracellular Vesicles/transplantation ; Mesenchymal Stem Cell Transplantation/methods ; Mesenchymal Stem Cells/cytology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; T-Lymphocytes/pathology ; T-Lymphocytes/physiology
Language	English
Publishing date	2018-05-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-25676-2
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Article ; Online: Murine adipose-derived mesenchymal stromal cell vesicles: in vitro clues for neuroprotective and neuroregenerative approaches.

Farinazzo, Alessia / Turano, Ermanna / Marconi, Silvia / Bistaffa, Edoardo / Bazzoli, Elena / Bonetti, Bruno

Cytotherapy

2015 Volume 17, Issue 5, Page(s) 571–578

Abstract: Background aims: Adipose-derived mesenchymal stromal cells (ASC) are known to promote neuroprotection and neuroregeneration in vitro and in vivo. These biological effects are probably mediated by paracrine mechanisms. In recent years, nanovesicles (NV) ... ...

Abstract	Background aims: Adipose-derived mesenchymal stromal cells (ASC) are known to promote neuroprotection and neuroregeneration in vitro and in vivo. These biological effects are probably mediated by paracrine mechanisms. In recent years, nanovesicles (NV) and microvesicles (MV) have been shown to play a major role in cell-to-cell communication. We tested the efficacy of NV and MV obtained from ASC in mediating neuroprotection and neuroregeneration in vitro. Methods: We exposed neuronal cells (both cell line and primary cultures) to oxidative stress in the presence or not of NV or MV. Results: In this experimental setting, we found that low doses of NV or MV protected neurons from apoptotic cell death. We then assessed the neuroregenerative effect of NV/MV in cerebellar slice cultures demyelinated with lysophosphatidylcholine. We observed that low but not higher doses of NV and MV increased the process of remyelination and activated nestin-positive oligodendroglial precursors. Conclusions: Taken together, our data in vitro support the relevance of ASC vesicles as a source of protecting and regenerating factors that might modulate the microenvironment in neuro-inflammatory as well as in neurodegenerative disorders. The present findings may suggest that stromal cell-derived vesicles might represent a potential therapeutic tool, enabling the safe administration of stromal cell effector factors, avoiding the cellular counterpart.
MeSH term(s)	Adipose Tissue/cytology ; Animals ; Cell Line, Tumor ; Cell-Derived Microparticles/classification ; Cell-Derived Microparticles/metabolism ; Cell-Derived Microparticles/ultrastructure ; Electrophoresis, Polyacrylamide Gel ; Humans ; Mesenchymal Stromal Cells/cytology ; Mice, Inbred C57BL ; Nerve Regeneration/drug effects ; Neurons/drug effects ; Neurons/metabolism ; Neuroprotective Agents/pharmacology
Chemical Substances	Neuroprotective Agents
Language	English
Publishing date	2015-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2039821-9
ISSN	1477-2566 ; 1465-3249
ISSN (online)	1477-2566
ISSN	1465-3249
DOI	10.1016/j.jcyt.2015.01.005
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Article ; Online: In silico

Kleinfelder, Karina / Lotti, Virginia / Eramo, Adriana / Amato, Felice / Lo Cicero, Stefania / Castelli, Germana / Spadaro, Francesca / Farinazzo, Alessia / Dell'Orco, Daniele / Preato, Sara / Conti, Jessica / Rodella, Luca / Tomba, Francesco / Cerofolini, Angelo / Baldisseri, Elena / Bertini, Marina / Volpi, Sonia / Villella, Valeria Rachela / Esposito, Speranza /

Zollo, Immacolata / Castaldo, Giuseppe / Laudanna, Carlo / Sorsher, Eric J / Hong, Jeong / Joshi, Disha / Cutting, Garry / Lucarelli, Marco / Melotti, Paola / Sorio, Claudio

iScience

2023 Volume 26, Issue 11, Page(s) 108180

Abstract: Mutation targeted therapy in cystic fibrosis (CF) is still not eligible for all CF subjects, especially for cases carrying rare variants such as the CFTR genotype W57G/A234D (c.169T>G/c.701C>A). We ... ...

Abstract	Mutation targeted therapy in cystic fibrosis (CF) is still not eligible for all CF subjects, especially for cases carrying rare variants such as the CFTR genotype W57G/A234D (c.169T>G/c.701C>A). We performed
Language	English
Publishing date	2023-10-12
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.108180
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Article ; Online: Mycobacterium avium subspecies paratuberculosis and myelin basic protein specific epitopes are highly recognized by sera from patients with Neuromyelitis optica spectrum disorder.

Bo, Marco / Niegowska, Magdalena / Arru, Giannina / Sechi, Elia / Mariotto, Sara / Mancinelli, Chiara / Farinazzo, Alessia / Alberti, Daniela / Gajofatto, Alberto / Ferrari, Sergio / Capra, Ruggero / Monaco, Salvatore / Sechi, GianPietro / Sechi, Leonardo A

Journal of neuroimmunology

2018 Volume 318, Page(s) 97–102

Abstract: Epstein-Barr virus (EBV) is the main environmental agent associated to neuromyelitis optica spectrum disorder (NMOSD). Following to studies reporting an increased prevalence of antibodies against peptides derived from Mycobacterium avium subsp. ... ...

Abstract	Epstein-Barr virus (EBV) is the main environmental agent associated to neuromyelitis optica spectrum disorder (NMOSD). Following to studies reporting an increased prevalence of antibodies against peptides derived from Mycobacterium avium subsp. paratuberculosis (MAP) homologous to EBV and human epitopes (MBP
MeSH term(s)	Adult ; Antibodies, Bacterial/immunology ; Antigens, Bacterial/immunology ; Autoantibodies/immunology ; Autoantigens/immunology ; Epitopes/immunology ; Female ; Humans ; Interferon Regulatory Factors/immunology ; Male ; Middle Aged ; Mycobacterium avium subsp. paratuberculosis/immunology ; Myelin Basic Protein/immunology ; Neuromyelitis Optica/immunology
Chemical Substances	Antibodies, Bacterial ; Antigens, Bacterial ; Autoantibodies ; Autoantigens ; Epitopes ; IRF5 protein, human ; Interferon Regulatory Factors ; Myelin Basic Protein
Language	English
Publishing date	2018-02-28
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	8335-5
ISSN	1872-8421 ; 0165-5728
ISSN (online)	1872-8421
ISSN	0165-5728
DOI	10.1016/j.jneuroim.2018.02.013
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Zs.A 1646: Show issues

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Article: Antibody response against HERV-W env surface peptides differentiates multiple sclerosis and neuromyelitis optica spectrum disorder.

Arru, Giannina / Sechi, Elia / Mariotto, Sara / Farinazzo, Alessia / Mancinelli, Chiara / Alberti, Daniela / Ferrari, Sergio / Gajofatto, Alberto / Capra, Ruggero / Monaco, Salvatore / Deiana, Giovanni A / Caggiu, Elisa / Mameli, Giuseppe / Sechi, Leonardo A / Sechi, Gian Pietro

Multiple sclerosis journal - experimental, translational and clinical

2017 Volume 3, Issue 4, Page(s) 2055217317742425

Abstract: Background: A specific humoral immune response against HERV-W envelope surface (env-su) glycoprotein antigens has been reported in serum of patients with multiple sclerosis (MS). However, it has not been evaluated to date in patients with neuromyelitis ... ...

Abstract	Background: A specific humoral immune response against HERV-W envelope surface (env-su) glycoprotein antigens has been reported in serum of patients with multiple sclerosis (MS). However, it has not been evaluated to date in patients with neuromyelitis optica spectrum disorder (NMOSD). Objective: The objective of this paper is to investigate whether antibody (Ab) response against HERV-W env-su antigenic peptides differs between NMOSD and MS. Methods: Serum samples were collected from 36 patients with NMOSD, 36 patients with MS and 36 healthy control individuals (HCs). An indirect ELISA was set up to detect specific Abs against HERV-W env-su peptides. Results: Our data showed that two antigenic peptides, particularly HERV-Wenv Conclusion: Increased circulating serum levels of these HERV-W Abs may be suitable as additional biomarkers to better differentiate MS from NMOSD.
Language	English
Publishing date	2017-11-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2841884-0
ISSN	2055-2173 ; 2055-2173
ISSN (online)	2055-2173
ISSN	2055-2173
DOI	10.1177/2055217317742425
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Article ; Online: Allelic origin of protease-sensitive and protease-resistant prion protein isoforms in Gerstmann-Sträussler-Scheinker disease with the P102L mutation.

Monaco, Salvatore / Fiorini, Michele / Farinazzo, Alessia / Ferrari, Sergio / Gelati, Matteo / Piccardo, Pedro / Zanusso, Gianluigi / Ghetti, Bernardino

PloS one

2012 Volume 7, Issue 2, Page(s) e32382

Abstract: Gerstmann-Sträussler-Scheinker (GSS) disease is a dominantly inherited prion disease associated with point mutations in the Prion Protein gene. The most frequent mutation associated with GSS involves a proline-to-leucine substitution at residue 102 of ... ...

Abstract	Gerstmann-Sträussler-Scheinker (GSS) disease is a dominantly inherited prion disease associated with point mutations in the Prion Protein gene. The most frequent mutation associated with GSS involves a proline-to-leucine substitution at residue 102 of the prion protein, and is characterized by marked variability at clinical, pathological and molecular levels. Previous investigations of GSS P102L have shown that disease-associated pathological prion protein, or PrP(Sc), consists of two main conformers, which under exogenous proteolysis generates a core fragment of 21 kDa and an internal fragment of 8 kDa. Both conformers are detected in subjects with spongiform degeneration, whereas only the 8 kDa fragment is recovered in cases lacking spongiosis. Several studies have reported an exclusive derivation of protease-resistant PrP(Sc) isoforms from the mutated allele; however, more recently, the propagation of protease-resistant wild-type PrP(Sc) has been described. Here we analyze the molecular and pathological phenotype of six GSS P102L cases characterized by the presence of 21 and 8 kDa PrP fragments and two subjects with only the 8 kDa PrP fragment. Using sensitive protein separation techniques and Western blots with antibodies differentially recognizing wild-type and mutant PrP we observed a range of PrP(Sc) allelic conformers, either resistant or sensitive to protease treatment in all investigated subjects. Additionally, tissue deposition of protease-sensitive wild-type PrP(Sc) molecules was seen by conventional PrP immunohistochemistry and paraffin-embedded tissue blot. Our findings enlarge the spectrum of conformational allelic PrP(Sc) quasispecies propagating in GSS P102L thus providing a molecular support to the spectrum of disease phenotypes, and, in addition, impact the diagnostic role of PrP immunohistochemistry in prion diseases.
MeSH term(s)	Adult ; Aged ; Alleles ; Centrifugation, Density Gradient ; Female ; Gerstmann-Straussler-Scheinker Disease/genetics ; Gerstmann-Straussler-Scheinker Disease/metabolism ; Humans ; Immunohistochemistry/methods ; Isoelectric Focusing ; Male ; Middle Aged ; Models, Genetic ; Peptide Hydrolases/metabolism ; Phenotype ; Point Mutation ; Positron-Emission Tomography/methods ; PrPSc Proteins/genetics ; Protein Conformation ; Proteolysis ; Sucrose/chemistry
Chemical Substances	PrPSc Proteins ; Sucrose (57-50-1) ; Peptide Hydrolases (EC 3.4.-)
Language	English
Publishing date	2012-02-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0032382
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Article ; Online: Human adipose-derived mesenchymal stem cells systemically injected promote peripheral nerve regeneration in the mouse model of sciatic crush.

Marconi, Silvia / Castiglione, Giusy / Turano, Ermanna / Bissolotti, Guido / Angiari, Stefano / Farinazzo, Alessia / Constantin, Gabriela / Bedogni, Giorgio / Bedogni, Alberto / Bonetti, Bruno

Tissue engineering. Part A

2012 Volume 18, Issue 11-12, Page(s) 1264–1272

Abstract: Mesenchymal stem cells (MSCs) represent a promising therapeutic approach in nerve tissue engineering. To date, the local implantation of MSC in injured nerves has been the only route of administration used. In case of multiple sites of injury, the ... ...

Abstract	Mesenchymal stem cells (MSCs) represent a promising therapeutic approach in nerve tissue engineering. To date, the local implantation of MSC in injured nerves has been the only route of administration used. In case of multiple sites of injury, the systemic administration of cells capable of reaching damaged nerves would be advisable. In this regard, we found that an intravenous administration of adipose-derived MSC (ASC) 1 week after sciatic nerve crush injury, a murine model of acute axonal damage, significantly accelerated the functional recovery. Sciatic nerves from ASC-treated mice showed the presence of a restricted number of undifferentiated ASC together with a significant improvement in fiber sprouting and the reduction of inflammatory infiltrates for up to 3 weeks. Besides the immune modulatory effect, our results show that ASC may contribute to peripheral nerve regeneration because of their ability to produce in culture neuroprotective factors such as insulin-like growth factor I, brain-derived neurotrophic factor, or basic fibroblast growth factor. In addition to this production in vitro, we interestingly found that the concentration of glial-derived neurotrophic factor (GDNF) was significantly increased in the sciatic nerves in mice treated with ASC. Since no detectable levels of GDNF were observed in ASC cultures, we hypothesize that ASC induced the local production of GDNF by Schwann cells. In conclusion, we show that systemically injected ASC have a clear therapeutic potential in an acute model of axonal damage. Among the possible mechanisms promoting nerve regeneration, our results rule out a process of trans-differentiation and rather suggest the relevance of a bystander effect, including the production of in situ molecules, which, directly or indirectly through a cross-talk with local glial cells, may modulate the local environment with the down-regulation of inflammation and the promotion of axonal regeneration.
MeSH term(s)	Adipose Tissue/cytology ; Animals ; Disease Models, Animal ; Female ; Humans ; Inflammation/pathology ; Injections ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stromal Cells/cytology ; Mice ; Mice, Inbred C57BL ; Motor Activity ; Nerve Crush ; Nerve Growth Factors/metabolism ; Nerve Regeneration/physiology ; Neurogenesis ; Recovery of Function ; Sciatic Nerve/pathology ; Sciatic Nerve/physiopathology
Chemical Substances	Nerve Growth Factors
Language	English
Publishing date	2012-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2420582-5
ISSN	1937-335X ; 1937-3341
ISSN (online)	1937-335X
ISSN	1937-3341
DOI	10.1089/ten.TEA.2011.0491
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Article ; Online: Neurotoxicity and synaptic plasticity impairment of N-acetylglucosamine polymers: implications for Alzheimer's disease.

Turano, Ermanna / Busetto, Giuseppe / Marconi, Silvia / Guzzo, Flavia / Farinazzo, Alessia / Commisso, Mauro / Bistaffa, Edoardo / Angiari, Stefano / Musumeci, Salvatore / Sotgiu, Stefano / Bonetti, Bruno

Neurobiology of aging

2015 Volume 36, Issue 5, Page(s) 1780–1791

Abstract: We assessed whether polymers of N-acetylglucosamine (GlcNAc) have any pathogenetic role in Alzheimer's disease (AD). First, by using specific dyes, we found deposits of polymers of GlcNAc in sporadic but not in familial AD. We found that neurons and ... ...

Abstract	We assessed whether polymers of N-acetylglucosamine (GlcNAc) have any pathogenetic role in Alzheimer's disease (AD). First, by using specific dyes, we found deposits of polymers of GlcNAc in sporadic but not in familial AD. We found that neurons and microglia exposed to GlcNAc and uridine diphosphate (UDP)-GlcNAc are able to form GlcNAc polymers, which display a significant neurotoxicity in vitro. Moreover, the exposure of organotypic hippocampal cultures to the same compounds led to synaptic impairment with decreased levels of syntaxin and synaptophysin. In addition, acute hippocampal slices treated with GlcNAc/UDP-GlcNAc showed a clear reduction of long-term potentiation of excitatory synapses. Finally, we demonstrated that microglial cells are able to phagocytose chitin particles and, when exposed to GlcNAc/UDP-GlcNAc, show cellular activation and intracellular deposition of GlcNAc polymers that are eventually released in the extracellular space. Taken together, our results indicate that both microglia and neurons produce GlcNAc polymers, which trigger neurotoxicity both directly and through microglia activation. GlcNAc polymer-driven neurotoxicity offers novel pathogenic insights in sporadic AD and new therapeutic options.
MeSH term(s)	Acetylglucosamine/metabolism ; Acetylglucosamine/toxicity ; Aged ; Aged, 80 and over ; Alzheimer Disease/etiology ; Animals ; Cells, Cultured ; Female ; Hippocampus/cytology ; Humans ; Long-Term Potentiation/drug effects ; Male ; Mice ; Microglia/metabolism ; Middle Aged ; Neuronal Plasticity/drug effects ; Neurons/metabolism ; Polymers ; Qa-SNARE Proteins/metabolism ; Synaptophysin/metabolism
Chemical Substances	Polymers ; Qa-SNARE Proteins ; Synaptophysin ; Acetylglucosamine (V956696549)
Language	English
Publishing date	2015-05
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.2014.12.033
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