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Article: Neurologic damage in hypoglycemia.

Mohseni, Simin

2014 Volume 126, Page(s) 513–532

Abstract: Hypoglycemia occurs in diabetic patients as a consequence of treatment with hypoglycemic agents, in insulinoma patients as a result of excessive insulin production, and in infants as a result of abnormal regulation of metabolism. Profound hypoglycemia ... ...

Abstract	Hypoglycemia occurs in diabetic patients as a consequence of treatment with hypoglycemic agents, in insulinoma patients as a result of excessive insulin production, and in infants as a result of abnormal regulation of metabolism. Profound hypoglycemia can cause structural and functional disturbances in both the central (CNS) and the peripheral nervous system (PNS). The brain is damaged by a short and severe episode of hypoglycemia, whereas PNS pathology appears after a mild and prolonged episode. In the CNS, damaged mitochondria, elevated intracellular Ca2(+) level, released cytochrome c to the cytosol, extensive production of superoxide, increased caspase-3 activity, release of aspartate and glutamate from presynaptic terminals, and altered biosynthetic machinery can lead to neuronal cell death in the brain. Considering the PNS, chronic hypoglycemia is associated with delayed motor and sensory conduction velocities in peripheral nerves. With respect to pathology, hypoglycemic neuropathy in the PNS is characterized by Wallerian-like axonal degeneration that starts at the nerve terminal and progresses to a more proximal part of the axon, and motor axons to the muscles may be more severely damaged than sensory axons. Since excitatory neurotransmitters primarily involve the neuron in the CNS, this "dying back" pattern of axonal damage in the PNS may involve mechanisms other than excitotoxicity.
MeSH term(s)	Animals ; Diabetes Mellitus/diagnosis ; Diabetes Mellitus/drug therapy ; Diabetes Mellitus/epidemiology ; Humans ; Hypoglycemia/chemically induced ; Hypoglycemia/diagnosis ; Hypoglycemia/epidemiology ; Hypoglycemic Agents/adverse effects ; Nervous System Diseases/chemically induced ; Nervous System Diseases/diagnosis ; Nervous System Diseases/epidemiology
Chemical Substances	Hypoglycemic Agents
Language	English
Publishing date	2014
Publishing country	Netherlands
Document type	Journal Article ; Review
ISSN	0072-9752
ISSN	0072-9752
DOI	10.1016/B978-0-444-53480-4.00036-9
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Autophagy in insulin-induced hypoglycaemic neuropathy.

Mohseni, Simin

Pathology

2011 Volume 43, Issue 3, Page(s) 254–260

Abstract: Aim: Autophagy in neurons has been linked to a growing number of pathological conditions in the CNS, but the role of this process in peripheral neuropathy has received little attention. This study aimed to determine whether autophagy is involved in ... ...

Abstract	Aim: Autophagy in neurons has been linked to a growing number of pathological conditions in the CNS, but the role of this process in peripheral neuropathy has received little attention. This study aimed to determine whether autophagy is involved in development of peripheral neuropathy in hypoglycaemic diabetic rats. Methods: The lateral plantar nerves, ventral roots, and dorsal roots of insulin-treated diabetic hypoglycaemic rats were examined for structural signs of autophagy by electron microscopy. Results: Autophagy-associated vacuoles were found in myelinated axons exhibiting early pathological changes but not in the associated Schwann cells. When the damaged axons degenerated, their associated Schwann cells gradually died and were cleared from the endoneurium by macrophages. During axonal regeneration, extensive signs of autophagy-related structures such as autophagophores appeared in regenerating axons and in the cytoplasm of the associated Schwann cells in the Band of Büngner. Conclusion: Autophagy occurs in hypoglycaemic peripheral nerves in association with axonal de- and regeneration. The extensive signs of autophagy in regenerated axons suggest that autophagy may play a role in survival of the new axons.
MeSH term(s)	Animals ; Autophagy/drug effects ; Autophagy/physiology ; Axons/drug effects ; Axons/metabolism ; Axons/ultrastructure ; Diabetes Mellitus, Experimental ; Diabetic Neuropathies/chemically induced ; Diabetic Neuropathies/metabolism ; Diabetic Neuropathies/pathology ; Female ; Hypoglycemia/chemically induced ; Hypoglycemia/metabolism ; Hypoglycemia/pathology ; Insulin/toxicity ; Microscopy, Electron, Transmission ; Nerve Fibers, Myelinated/drug effects ; Nerve Fibers, Myelinated/metabolism ; Nerve Fibers, Myelinated/ultrastructure ; Nerve Regeneration/drug effects ; Nerve Regeneration/physiology ; Peripheral Nerves/drug effects ; Peripheral Nerves/metabolism ; Peripheral Nerves/ultrastructure ; Rats ; Rats, Inbred BB ; Schwann Cells/drug effects ; Schwann Cells/metabolism ; Schwann Cells/ultrastructure
Chemical Substances	Insulin
Language	English
Publishing date	2011-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	7085-3
ISSN	1465-3931 ; 0031-3025
ISSN (online)	1465-3931
ISSN	0031-3025
DOI	10.1097/PAT.0b013e328343c992
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Article ; Online: Trans-synaptic spreading of alpha-synuclein pathology through sensory afferents leads to sensory nerve degeneration and neuropathic pain.

Ferreira, Nelson / Gonçalves, Nádia Pereira / Jan, Asad / Jensen, Nanna Møller / van der Laan, Amelia / Mohseni, Simin / Vægter, Christian Bjerggaard / Jensen, Poul Henning

Acta neuropathologica communications

2021 Volume 9, Issue 1, Page(s) 31

Abstract: Pain is a common non-motor symptom of Parkinson's disease (PD), with current limited knowledge of its pathophysiology. Here, we show that peripheral inoculation of mouse alpha-synuclein (α-Syn) pre-formed fibrils, in a transgenic mouse model of PD, ... ...

Abstract	Pain is a common non-motor symptom of Parkinson's disease (PD), with current limited knowledge of its pathophysiology. Here, we show that peripheral inoculation of mouse alpha-synuclein (α-Syn) pre-formed fibrils, in a transgenic mouse model of PD, elicited retrograde trans-synaptic spreading of α-Syn pathology (pSer129) across sensory neurons and dorsal nerve roots, reaching central pain processing regions, including the spinal dorsal horn and the projections of the anterolateral system in the central nervous system (CNS). Pathological peripheral to CNS propagation of α-Syn aggregates along interconnected neuronal populations within sensory afferents, was concomitant with impaired nociceptive response, reflected by mechanical allodynia, reduced nerve conduction velocities (sensory and motor) and degeneration of small- and medium-sized myelinated fibers. Our findings show a link between the transneuronal propagation of α-Syn pathology with sensory neuron dysfunction and neuropathic impairment, suggesting promising avenues of investigation into the mechanisms underlying pain in PD.
MeSH term(s)	Animals ; Disease Models, Animal ; Female ; Mice ; Mice, Transgenic ; Microscopy, Electron, Transmission ; Neuralgia/etiology ; Neuralgia/physiopathology ; Parkinson Disease/physiopathology ; Retrograde Degeneration/pathology ; Retrograde Degeneration/physiopathology ; Sensory Receptor Cells/metabolism ; Sensory Receptor Cells/pathology ; Sensory Receptor Cells/ultrastructure ; Synaptic Transmission ; Synucleinopathies/pathology ; Synucleinopathies/physiopathology ; alpha-Synuclein/metabolism
Chemical Substances	Snca protein, mouse ; alpha-Synuclein
Language	English
Publishing date	2021-02-25
Publishing country	England
Document type	Journal Article ; 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/s40478-021-01131-8
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Article: Sortilin Modulates Schwann Cell Signaling and Remak Bundle Regeneration Following Nerve Injury.

Ulrichsen, Maj / Gonçalves, Nádia P / Mohseni, Simin / Hjæresen, Simone / Lisle, Thomas L / Molgaard, Simon / Madsen, Niels K / Andersen, Olav M / Svenningsen, Åsa F / Glerup, Simon / Nykjær, Anders / Vægter, Christian B

Frontiers in cellular neuroscience

2022 Volume 16, Page(s) 856734

Abstract: Peripheral nerve regeneration relies on the ability of Schwann cells to support the regrowth of damaged axons. Schwann cells re-differentiate when reestablishing contact with the sprouting axons, with large fibers becoming remyelinated and small ... ...

Abstract	Peripheral nerve regeneration relies on the ability of Schwann cells to support the regrowth of damaged axons. Schwann cells re-differentiate when reestablishing contact with the sprouting axons, with large fibers becoming remyelinated and small nociceptive fibers ensheathed and collected into Remak bundles. We have previously described how the receptor sortilin facilitates neurotrophin signaling in peripheral neurons
Language	English
Publishing date	2022-05-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2022.856734
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Article ; Online: Schwann cell p75 neurotrophin receptor modulates small fiber degeneration in diabetic neuropathy.

Gonçalves, Nádia P / Jager, Sara E / Richner, Mette / Murray, Simon S / Mohseni, Simin / Jensen, Troels S / Vaegter, Christian B

Glia

2020 Volume 68, Issue 12, Page(s) 2725–2743

Abstract: Diabetic neuropathy has an incidence as high as 50% of diabetic patients and is characterized by damage to neurons, Schwann cells and blood vessels within the peripheral nervous system. The low-affinity neurotrophin receptor p75 ( ... ...

Abstract	Diabetic neuropathy has an incidence as high as 50% of diabetic patients and is characterized by damage to neurons, Schwann cells and blood vessels within the peripheral nervous system. The low-affinity neurotrophin receptor p75 (p75
MeSH term(s)	Animals ; Axons ; Diabetic Neuropathies ; Humans ; Mice ; Receptor, Nerve Growth Factor ; Receptors, Nerve Growth Factor/genetics ; Schwann Cells ; Sciatic Nerve
Chemical Substances	Receptor, Nerve Growth Factor ; Receptors, Nerve Growth Factor
Language	English
Publishing date	2020-07-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.23881
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Zs.A 2345: Show issues

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Article ; Online: Antioxidant properties of a human neuropeptide and its protective effect on free radical-induced DNA damage.

Mohseni, Simin / Emtenani, Shirin / Emtenani, Shamsi / Asoodeh, Ahmad

Journal of peptide science : an official publication of the European Peptide Society

2014 Volume 20, Issue 6, Page(s) 429–437

Abstract: Human catestatin CgA352-372 (SL21) is an endogenous neuropeptide with multiple biological functions. The present study aimed to evaluate the antioxidant, antibacterial, cytotoxic, and DNA damage protective effects of SL21 neuropeptide. SL21 neuropeptide ... ...

Abstract	Human catestatin CgA352-372 (SL21) is an endogenous neuropeptide with multiple biological functions. The present study aimed to evaluate the antioxidant, antibacterial, cytotoxic, and DNA damage protective effects of SL21 neuropeptide. SL21 neuropeptide generated from the C-terminus of chromogranin A (CgA) was synthesized by solid-phase method. Synthetic peptide was subjected to various in vitro antioxidant assays including the scavenging of 1,1-diphenyl-2-pycryl-hydrazyl (DPPH), 2,2-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS(·+) ), and hydroxyl free radicals, metal ion chelation, inhibition of lipid peroxidation, and reducing power. Moreover, protective effect of SL21 on H2 O2 -induced DNA damage was analyzed using pTZ57/RT plasmid. Methylthiazoltetrazolium assay was also performed to study the cytotoxic effect of SL21 neuropeptide on human peripheral blood mononuclear cells. Furthermore, antibacterial and hemolysis assays were conducted. The results demonstrated high activities of SL21 in scavenging free radicals (DPPH, ABTS(·+) , and hydroxyl), chelating of Cu(2+) /Fe(2+) metal ions, reducing power, and inhibition of lipid peroxidation in a concentration-dependent manner. SL21 neuropeptide revealed a protective effect on DNA damage caused by hydroxyl radicals. Interestingly, the peptide exhibited no significant cytotoxicity towards peripheral blood mononuclear cells. Furthermore, SL21 peptide displayed antimicrobial activity against Staphylococcus aureus and Pseudomonas aeruginosa without any hemolytic activity on human red blood cells. Conclusively, the present study established SL21 (catestatin) as a novel antioxidative peptide that could further be investigated for its potential use as a pharmaceutical agent.
MeSH term(s)	Anti-Bacterial Agents/chemical synthesis ; Anti-Bacterial Agents/chemistry ; Anti-Bacterial Agents/pharmacology ; Antioxidants/chemical synthesis ; Antioxidants/chemistry ; Antioxidants/pharmacology ; Chromogranin A/chemistry ; DNA Damage ; Dose-Response Relationship, Drug ; Free Radicals/chemistry ; Free Radicals/metabolism ; Humans ; Hydrogen Peroxide/chemistry ; Hydrogen Peroxide/metabolism ; Leukocytes, Mononuclear ; Microbial Sensitivity Tests ; Neuropeptides/chemical synthesis ; Neuropeptides/chemistry ; Neuropeptides/pharmacology ; Pseudomonas aeruginosa/drug effects ; Staphylococcus aureus/drug effects ; Structure-Activity Relationship
Chemical Substances	Anti-Bacterial Agents ; Antioxidants ; Chromogranin A ; Free Radicals ; Neuropeptides ; Hydrogen Peroxide (BBX060AN9V)
Language	English
Publishing date	2014-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1234416-3
ISSN	1099-1387 ; 1075-2617
ISSN (online)	1099-1387
ISSN	1075-2617
DOI	10.1002/psc.2634
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Zs.A 6200: Show issues

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Article ; Online: Lactate damages primary hippocampal neurons in vitro.

Sepehr, Arian / Mohseni, Simin

Cell biology international

2009 Volume 34, Issue 1, Page(s) 61–65

Abstract: In the present study, rat primary cultures were used to study the effect of lactate on the survival of hippocampal neurons in the presence or absence of glucose. Our results showed no extensive cell damage under glucose-free conditions compared with ... ...

Abstract	In the present study, rat primary cultures were used to study the effect of lactate on the survival of hippocampal neurons in the presence or absence of glucose. Our results showed no extensive cell damage under glucose-free conditions compared with glucose-rich conditions. Addition of 10 and 50 mM lactate to glucose-free and glucose-rich media increased the cell damage significantly, as observed by morphology and lactate dehydrogenase activity. The results of the present study suggest that primary neurons in vitro are not sensitive to glucose deficiency and the presence of lactate damages the neurons in a concentration-dependent manner.
MeSH term(s)	Animals ; Cells, Cultured ; Embryo, Mammalian/cytology ; Glucose/pharmacology ; Hippocampus/cytology ; Lactate Dehydrogenases/metabolism ; Lactates/toxicity ; Neurons/cytology ; Neurons/drug effects ; Neurons/metabolism ; Rats
Chemical Substances	Lactates ; Lactate Dehydrogenases (EC 1.1.-) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2009-12-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1143453-3
ISSN	1095-8355 ; 1065-6995
ISSN (online)	1095-8355
ISSN	1065-6995
DOI	10.1042/CBI20090132
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Article ; Online: Study of Autophagy and Microangiopathy in Sural Nerves of Patients with Chronic Idiopathic Axonal Polyneuropathy.

Samuelsson, Kristin / Osman, Ayman A M / Angeria, Maria / Risling, Mårten / Mohseni, Simin / Press, Rayomand

PloS one

2016 Volume 11, Issue 9, Page(s) e0163427

Abstract: Twenty-five percent of polyneuropathies are idiopathic. Microangiopathy has been suggested to be a possible pathogenic cause of chronic idiopathic axonal polyneuropathy (CIAP). Dysfunction of the autophagy pathway has been implicated as a marker of ... ...

Abstract	Twenty-five percent of polyneuropathies are idiopathic. Microangiopathy has been suggested to be a possible pathogenic cause of chronic idiopathic axonal polyneuropathy (CIAP). Dysfunction of the autophagy pathway has been implicated as a marker of neurodegeneration in the central nervous system, but the autophagy process is not explored in the peripheral nervous system. In the current study, we examined the presence of microangiopathy and autophagy-related structures in sural nerve biopsies of 10 patients with CIAP, 11 controls with inflammatory neuropathy and 10 controls without sensory polyneuropathy. We did not find any significant difference in endoneurial microangiopathic markers in patients with CIAP compared to normal controls, though we did find a correlation between basal lamina area thickness and age. Unexpectedly, we found a significantly larger basal lamina area thickness in patients with vasculitic neuropathy. Furthermore, we found a significantly higher density of endoneurial autophagy-related structures, particularly in patients with CIAP but also in patients with inflammatory neuropathy, compared to normal controls. It is unclear if the alteration in the autophagy pathway is a consequence or a cause of the neuropathy. Our results do not support the hypothesis that CIAP is primarily caused by a microangiopathic process in endoneurial blood vessels in peripheral nerves. The significantly higher density of autophagy structures in sural nerves obtained from patients with CIAP and inflammatory neuropathy vs. controls indicates the involvement of this pathway in neuropathy, particularly in CIAP, since the increase in density of autophagy-related structures was more pronounced in patients with CIAP than those with inflammatory neuropathy. To our knowledge this is the first report investigating signs of autophagy process in peripheral nerves in patients with CIAP and inflammatory neuropathy.
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0163427
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Article: Protocol for three-dimensional confocal morphometric analysis of astrocytes

Bagheri, Maryam / Rezakhani, Arjang / Roghani, Mehrdad / Joghataei, Mohammad T / Mohseni, Simin

Journal of visualized experiments. 2015 Dec. 11, , no. 106

2015

Abstract: As glial cells in the brain, astrocytes have diverse functional roles in the central nervous system. In the presence of harmful stimuli, astrocytes modify their functional and structural properties, a condition called reactive astrogliosis. Here, a ... ...

Abstract	As glial cells in the brain, astrocytes have diverse functional roles in the central nervous system. In the presence of harmful stimuli, astrocytes modify their functional and structural properties, a condition called reactive astrogliosis. Here, a protocol for assessment of the morphological properties of astrocytes is presented. This protocol includes quantification of 12 different parameters i.e. the surface area and volume of the tissue covered by an astrocyte (astrocyte territory), the entire astrocyte including branches, cell body, and nucleus, as well as total length and number of branches, the intensity of fluorescence immunoreactivity of antibodies used for astrocyte detection, and astrocyte density (number/1,000 μm2). For this purpose three-dimensional (3D) confocal microscopic images were created, and 3D image analysis software such as Volocity 6.3 was used for measurements. Rat brain tissue exposed to amyloid beta1-40 (Aβ1-40) with or without a therapeutic intervention was used to present the method. This protocol can also be used for 3D morphometric analysis of other cells from either in vivo or in vitro conditions.
Keywords	amyloid ; antibodies ; astrocytes ; brain ; computer software ; fluorescence ; image analysis ; morphometry ; rats ; surface area ; therapeutics
Language	English
Dates of publication	2015-1211
Size	p. e53113.
Publishing place	Journal of Visualized Experiments
Document type	Article
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/53113
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Three-dimensional architecture of human diabetic peripheral nerves revealed by X-ray phase contrast holographic nanotomography.

Dahlin, Lars B / Rix, Kristian R / Dahl, Vedrana A / Dahl, Anders B / Jensen, Janus N / Cloetens, Peter / Pacureanu, Alexandra / Mohseni, Simin / Thomsen, Niels O B / Bech, Martin

Scientific reports

2020 Volume 10, Issue 1, Page(s) 7592

Abstract: A deeper knowledge of the architecture of the peripheral nerve with three-dimensional (3D) imaging of the nerve tissue at the sub-cellular scale may contribute to unravel the pathophysiology of neuropathy. Here we demonstrate the feasibility of X-ray ... ...

Abstract	A deeper knowledge of the architecture of the peripheral nerve with three-dimensional (3D) imaging of the nerve tissue at the sub-cellular scale may contribute to unravel the pathophysiology of neuropathy. Here we demonstrate the feasibility of X-ray phase contrast holographic nanotomography to enable 3D imaging of nerves at high resolution, while covering a relatively large tissue volume. We show various subcomponents of human peripheral nerves in biopsies from patients with type 1 and 2 diabetes and in a healthy subject. Together with well-organized, parallel myelinated nerve fibres we show regenerative clusters with twisted nerve fibres, a sprouted axon from a node of Ranvier and other specific details. A novel 3D construction (with movie created) of a node of Ranvier with end segment of a degenerated axon and sprout of a regenerated one is captured. Many of these architectural elements are not described in the literature. Thus, X-ray phase contrast holographic nanotomography enables identifying specific morphological structures in 3D in peripheral nerve biopsies from a healthy subject and from patients with type 1 and 2 diabetes.
MeSH term(s)	Aged ; Case-Control Studies ; Diabetes Mellitus, Type 1/complications ; Diabetes Mellitus, Type 2/complications ; Diabetic Neuropathies/diagnostic imaging ; Diabetic Neuropathies/pathology ; Female ; Holography/methods ; Humans ; Image Processing, Computer-Assisted ; Male ; Microscopy ; Middle Aged ; Nanotechnology ; Peripheral Nerves/diagnostic imaging ; Peripheral Nerves/pathology ; X-Ray Microtomography/methods
Language	English
Publishing date	2020-05-05
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/s41598-020-64430-5
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