liu.seSearch for publications in DiVA
Change search
Link to record
Permanent link

Direct link
BETA
Alternative names
Publications (10 of 25) Show all publications
Klionsky, D. J., Boman, A., Kågedal, K., Kurz, T., Mohseni, S., Öllinger, K. & Zughaier, S. M. (2016). Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition). Autophagy, 2(1), 1-222
Open this publication in new window or tab >>Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)
Show others...
2016 (English)In: Autophagy, ISSN 1554-8627, E-ISSN 1554-8635, Vol. 2, no 1, p. 1-222Article, review/survey (Refereed) Published
Place, publisher, year, edition, pages
Taylor & Francis, 2016
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-137050 (URN)10.1080/15548627.2015.1100356 (DOI)000373595400001 ()26799652 (PubMedID)
Note

The article contains 2467 authors of which five are affiliated with LiU and have the following author order:

Author no. 177: Andrea Boman

Author no. 968: Katarina Kågedal

Author no. 1106: Tino Kurz

Author no. 1449: Simin Mohseni

Author no. 1559: Karin Öllinger

Available from: 2017-05-02 Created: 2017-05-02 Last updated: 2019-03-14Bibliographically approved
Osman, A. A. M., Dahlin, L. B., Thomsen, N. O. B. & Mohseni, S. (2015). Autophagy in the posterior interosseous nerve of patients with type 1 and type 2 diabetes mellitus: an ultrastructural study. Diabetologia, 58(3), 625-632
Open this publication in new window or tab >>Autophagy in the posterior interosseous nerve of patients with type 1 and type 2 diabetes mellitus: an ultrastructural study
2015 (English)In: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 58, no 3, p. 625-632Article in journal (Refereed) Published
Abstract [en]

We addressed the question of whether the autophagy pathway occurs in human peripheral nerves and whether this pathway is associated with peripheral neuropathy in diabetes mellitus. By using electron microscopy, we evaluated the presence of autophagy-related structures and neuropathy in the posterior interosseous nerve of patients who had undergone carpal tunnel release and had type 1 or type 2 diabetes mellitus, and in patients with no diabetes (controls). Autophagy-related ultrastructures were observed in the samples taken from all patients of the three groups. The number of autophagy-associated structures was significantly higher (p less than 0.05) in the nerves of patients with type 1 than type 2 diabetes. Qualitative and quantitative evaluations of fascicle area, diameter of myelinated and unmyelinated nerve fibres, the density of myelinated and unmyelinated fibres and the g-ratio of myelinated fibres were performed. We found degeneration and regeneration of a few myelinated axons in controls, and a well-developed neuropathy with the loss of large myelinated axons and the presence of many small ones in patients with diabetes. The pathology in type 1 diabetes was more extensive than in type 2 diabetes. The results of this study show that the human peripheral nerves have access to the autophagy machinery, and this pathway may be regulated differently in type 1 and type 2 diabetes; insulin, presence of extensive neuropathy, and/or other factors such as duration of diabetes and HbA(1c) level may underlie this differential regulation.

Place, publisher, year, edition, pages
Springer Verlag (Germany), 2015
Keywords
Autophagy; Diabetes; Electron microscopy; Human; Neuropathy; Peripheral nerve
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-115314 (URN)10.1007/s00125-014-3477-4 (DOI)000349244100024 ()25523623 (PubMedID)
Available from: 2015-03-13 Created: 2015-03-13 Last updated: 2017-12-04
Ghofrani, S., Joghataei, M.-T., Mohseni, S., Baluchnejadmojarad, T., Bagheri, M., Khamse, S. & Roghani, M. (2015). Naringenin improves learning and memory in an Alzheimer's disease rat model: Insights into the underlying mechanisms. European Journal of Pharmacology, 764, 195-201
Open this publication in new window or tab >>Naringenin improves learning and memory in an Alzheimer's disease rat model: Insights into the underlying mechanisms
Show others...
2015 (English)In: European Journal of Pharmacology, ISSN 0014-2999, E-ISSN 1879-0712, Vol. 764, p. 195-201Article in journal (Refereed) Published
Abstract [en]

Alzheimer's disease (AD) is one of the prevalent neurological disorders of the central nervous system hallmarked by increased beta-amyloid (Aβ) deposition and ensuing learning and memory deficit. In the present study, the beneficial effect of naringenin on improvement of learning and memory was evaluated in an Alzheimer's disease rat model. The Aβ-injected rats showed a lower alternation score in Y-maze task, impairment of retention and recall capability in passive avoidance test, and lower correct choices and higher errors in radial arm maze (RAM) task as compared to sham group in addition to enhanced oxidative stress and apoptosis. Naringenin, but not a combination of naringenin and fulvestrant (an estrogenic receptor antagonist) significantly improved the performance of Aβ-injected rats in passive avoidance and RAM tasks. Naringenin pretreatment of Aβ-injected rats also lowered hippocampal malondialdehyde (MDA) with no significant effect on nitrite and superoxide dismutase (SOD) activity in addition to lowering apoptosis. These results suggest naringenin pretreatment attenuates Aβ-induced impairment of learning and memory through mitigation of lipid peroxidation and apoptosis and its beneficial effect is somewhat mediated via estrogenic pathway.

Keywords
Naringenin, Alzheimer’s disease, Beta-Amyloid, Learning and Memory, Oxidative stress, Apoptosis
National Category
Neurosciences
Identifiers
urn:nbn:se:liu:diva-120716 (URN)10.1016/j.ejphar.2015.07.001 (DOI)000362987800024 ()26148826 (PubMedID)
Note

Funding agencies: Cellular and Molecular Research Center at Iran University of Medical Sciences (Tehran) [2011.37]; Linkoping University (Linkoping, Sweden)

Available from: 2015-09-08 Created: 2015-08-24 Last updated: 2018-01-11Bibliographically approved
Bagheri, M., Rezakhani, A., Roghani, M., Joghataei, M. T. & Mohseni, S. (2015). Protocol for Three-dimensional Confocal Morphometric Analysis of Astrocytes. Journal of Visualized Experiments (106), e53113
Open this publication in new window or tab >>Protocol for Three-dimensional Confocal Morphometric Analysis of Astrocytes
Show others...
2015 (English)In: Journal of Visualized Experiments, ISSN 1940-087X, E-ISSN 1940-087X, no 106, p. e53113-Article in journal (Refereed) Published
Abstract [en]

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 mu m(2)). 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 beta(1-40) (A beta(1-40)) 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.

Place, publisher, year, edition, pages
JOURNAL OF VISUALIZED EXPERIMENTS, 2015
Keywords
Neuroscience; Issue 106; Amyloid beta; Astrocyte size; Confocal microscope; Surface area; Three-dimensional morphometry; Volume
National Category
Medical Image Processing
Identifiers
urn:nbn:se:liu:diva-125167 (URN)10.3791/53113 (DOI)000368574400013 ()26709729 (PubMedID)
Note

Funding Agencies|County Council of Ostergotland, (Sweden); Cellular and Molecular Research Center at Iran University of Medical Sciences (Tehran, Iran)

Available from: 2016-02-15 Created: 2016-02-15 Last updated: 2017-11-30
Mohseni, S. (2014). Neurologic damage in hypoglycemia.. In: Handbook of Clinical Neurology: (pp. 513-32). Elsevier, 126
Open this publication in new window or tab >>Neurologic damage in hypoglycemia.
2014 (English)In: Handbook of Clinical Neurology, Elsevier, 2014, Vol. 126, p. 513-32Chapter in book (Refereed)
Abstract [en]

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.

Place, publisher, year, edition, pages
Elsevier, 2014
Series
Handbook of Clinical Neurology, ISSN 0072-9752 ; 126
National Category
Neurosciences
Identifiers
urn:nbn:se:liu:diva-116360 (URN)10.1016/B978-0-444-53480-4.00036-9 (DOI)25410242 (PubMedID)978-0-444-53480-4 (ISBN)
Available from: 2015-03-26 Created: 2015-03-26 Last updated: 2018-01-11
Bagheri, M., Rezakhani, A., Nyström, S., Turkina, M., Roghani, M., Hammarström, P. & Mohseni, S. (2013). Amyloid Beta1-40-Induced Astrogliosis and the Effect of Genistein Treatment in Rat: A Three-Dimensional Confocal Morphometric and Proteomic Study. PLoS ONE, 8(10)
Open this publication in new window or tab >>Amyloid Beta1-40-Induced Astrogliosis and the Effect of Genistein Treatment in Rat: A Three-Dimensional Confocal Morphometric and Proteomic Study
Show others...
2013 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 8, no 10Article in journal (Refereed) Published
Abstract [en]

Astrocytes are highly involved in regulation and homeostasis of the extracellular environment in the healthy brain. In pathological conditions, these cells play a major role in the inflammatory response seen in CNS tissues, which is called reactive astrogliosis and includes hypertrophy and proliferation of astrocytes. Here, we performed 3D confocal microscopy to evaluate the morphological response of reactive astrocytes positive for glial fibrillary acidic protein (GFAP) in rats, to the presence of Aβ1–40 in the rat brain before and after treatment with genistein. In 50 astrocytes per animal, we measured the volume and surface area for the nucleus, cell body, the entire cell, the tissue covered by single astrocytes and quantified the number and length of branches, the density of the astrocytes and the intensity of GFAP immunoreactivity. Injecting Aβ1–40 into the brain of rats caused astrogliosis indicated by increased values for all measured parameters. Mass spectrometric analysis of hippocampal tissue in Aβ1–40-injected brain showed decreased amounts of tubulins, enolases and myelin basic protein, and increased amounts of dihydropyrimidinase-related protein 2. In Aβ1–40-injected rats pretreated with genistein, GFAP intensity was decreased to the sham-operated group level, and Aβ1–40-induced astrogliosis was significantly ameliorated.

Place, publisher, year, edition, pages
Public Library of Science, 2013
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-101388 (URN)10.1371/journal.pone.0076526 (DOI)000325810900075 ()
Note

Funding Agencies|County Council of Ostergotland (Sweden)||Linkoping University||Cellular and Molecular Research Center||Tehran University of Medical Sciences (Tehran, Iran)||

Available from: 2013-11-22 Created: 2013-11-21 Last updated: 2018-04-25
Bagheri, M., Roghani, M., Joghataei, M.-T. & Mohseni, S. (2012). Genistein inhibits aggregation of exogenous amyloid-beta(1-40) and alleviates astrogliosis in the hippocampus of rats. Brain Research, 1429, 145-154
Open this publication in new window or tab >>Genistein inhibits aggregation of exogenous amyloid-beta(1-40) and alleviates astrogliosis in the hippocampus of rats
2012 (English)In: Brain Research, ISSN 0006-8993, E-ISSN 1872-6240, Vol. 1429, p. 145-154Article in journal (Refereed) Published
Abstract [en]

We addressed the question of whether injection of Amyloid beta (Aβ)(1-40) in the rat brain is associated with pathology in the hippocampus, and if genistein has any protective effect against the neuronal damage caused by Aβ(1-40). Genistein is a plant-derived compound with a structure similar to that of the female sex hormone estrogen and it was recently shown that pretreatment with a single dose of genistein ameliorated learning and memory deficits in an (Aβ)(1-40) rat model of Alzheimer's disease. Here, we report that injection of the amyloid peptide into the hippocampus of rats led to formation of Aβ(1-40) positive aggregates close to the lateral blade of the dentate gyrus (DGlb). We also observed the following in the hippocampus: extensive cell death in the DGlb (P<0.0001), CA1 (P=0.03), and CA3 (P=0.002); an increased number of iNOS-expressing cells (P=0.01) and gliosis. Genistein given to rats by gavage 1h before injection of Aβ(1-40) inhibited the formation of Aβ(1-40) positive aggregates in the brain tissue and led to increased number of nNOS(+) (P=0.0001) cells in the hippocampus compared to sham-operated genistein-treated controls. Treatment with genistein also alleviated the extensive astrogliosis that occurred in Aβ(1-40)-injected hippocampus to a level similar to that observed in sham-operated rats. We conclude that the neurons in the DGlb are most sensitive to Aβ(1-40), and a single dose of genistein can ameliorate Aβ(1-40) induced pathology.

Place, publisher, year, edition, pages
Elsevier, 2012
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-72775 (URN)10.1016/j.brainres.2011.10.020 (DOI)000300268200016 ()22079317 (PubMedID)
Note
funding agencies|Cellular and Molecular Research Center at Tehran University of Medical Sciences (Tehran)||Linkoping University (Linkoping, Sweden)||County Council of Ostergotland||Available from: 2011-12-07 Created: 2011-12-07 Last updated: 2017-12-08Bibliographically approved
Klionsky, D. J., Abdalla, F. C., Abeliovich, H., Abraham, R. T., Acevedo-Arozena, A., Adeli, K., . . . Zuckerbraun, B. (2012). Guidelines for the use and interpretation of assays for monitoring autophagy. Autophagy, 8(4), 445-544
Open this publication in new window or tab >>Guidelines for the use and interpretation of assays for monitoring autophagy
Show others...
2012 (English)In: Autophagy, ISSN 1554-8627, Vol. 8, no 4, p. 445-544Article, review/survey (Refereed) Published
Abstract [en]

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.

Place, publisher, year, edition, pages
Landes Bioscience, 2012
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-82027 (URN)10.4161/auto.19496 (DOI)000305403400002 ()22966490 (PubMedID)
Available from: 2012-09-28 Created: 2012-09-28 Last updated: 2017-01-16
Mohseni, S. (2011). Autophagy in insulin-induced hypoglycaemic neuropathy. PATHOLOGY, 43(3), 254-260
Open this publication in new window or tab >>Autophagy in insulin-induced hypoglycaemic neuropathy
2011 (English)In: PATHOLOGY, ISSN 0031-3025, Vol. 43, no 3, p. 254-260Article in journal (Refereed) Published
Abstract [en]

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 Bungner. 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.

Place, publisher, year, edition, pages
LIPPINCOTT WILLIAMS and WILKINS, 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA, 2011
Keywords
Autophagy, diabetes, electron microscopy, hypoglycaemia, peripheral neuropathy
National Category
Engineering and Technology
Identifiers
urn:nbn:se:liu:diva-67707 (URN)10.1097/PAT.0b013e328343c992 (DOI)000289034100009 ()
Available from: 2011-04-26 Created: 2011-04-26 Last updated: 2016-02-29
Bagheri, M., Joghataei, M.-T., Mohseni, S. & Roghani, M. (2011). Genistein ameliorates learning and memory deficits in amyloid beta((1-40)) rat model of Alzheimers disease. Neurobiology of Learning and Memory, 95(3), 270-276
Open this publication in new window or tab >>Genistein ameliorates learning and memory deficits in amyloid beta((1-40)) rat model of Alzheimers disease
2011 (English)In: Neurobiology of Learning and Memory, ISSN 1074-7427, E-ISSN 1095-9564, Vol. 95, no 3, p. 270-276Article in journal (Refereed) Published
Abstract [en]

Alzheimers disease (AD) is a debilitating neurodegenerative disorder characterized by increased beta-amyloid (A beta) deposition and neuronal dysfunction leading to impaired learning and recall. Ageing, heredity, and induced oxidative stress are among proposed risk factors. The increased frequency of the disease in women also suggests a role for estrogen in development of AD. In the present study, effects of the phytoestrogen genistein (10 mg/kg) on learning and memory impairments was assessed in intrahippocampal A beta((1-40))-injected rats. The estrogen receptor antagonist fulvestrant was injected intracerebroventricularly in a group of A beta-lesioned rats. The A beta-injected animals exhibited the following: lower spontaneous alternation score in Y-maze tasks, impaired retention and recall capability in the passive avoidance test, and fewer correct choices and more errors in the RAM task. Genistein, but not genistein and fulvestrant, significantly improved most of these parameters. Measurements of oxidative stress markers in hippocampal tissue of A beta-injected rats showed an elevation of malondialdehyde (MDA) and nitrite content, and a reduction of superoxide dismutase (SOD) activity. Genistein significantly attenuated the increased MDA content but did not affect the nitrite content or SOD activity. These results indicate that genistein pretreatment ameliorates A beta-induced impairment of short-term spatial memory in rats through an estrogenic pathway and by inducing attenuation of oxidative stress.

Place, publisher, year, edition, pages
Elsevier Science B.V., Amsterdam, 2011
Keywords
Alzheimers disease, Beta-amyloid, Genistein, Learning and memory
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-67550 (URN)10.1016/j.nlm.2010.12.001 (DOI)000288774300006 ()
Note
Original Publication: Maryam Bagheri, Mohammad-Taghi Joghataei, Simin Mohseni and Mehrdad Roghani, Genistein ameliorates learning and memory deficits in amyloid beta((1-40)) rat model of Alzheimers disease, 2011, NEUROBIOLOGY OF LEARNING AND MEMORY, (95), 3, 270-276. http://dx.doi.org/10.1016/j.nlm.2010.12.001 Copyright: Elsevier Science B.V., Amsterdam http://www.elsevier.com/Available from: 2011-04-18 Created: 2011-04-18 Last updated: 2017-12-11Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-1342-369X

Search in DiVA

Show all publications