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Bengtsson, Sara
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Publications (10 of 10) Show all publications
Bengtsson, S. K., Johansson, M. & Bäckström, T. (2016). Long-term continuous allopregnanolone elevation causes memory decline and hippocampus shrinkage, in female wild-type B6 mice. Hormones and Behavior, 78, 160-167
Open this publication in new window or tab >>Long-term continuous allopregnanolone elevation causes memory decline and hippocampus shrinkage, in female wild-type B6 mice
2016 (English)In: Hormones and Behavior, ISSN 0018-506X, E-ISSN 1095-6867, Vol. 78, p. 160-167Article in journal (Refereed) Published
Abstract [en]

Chronic stress in various forms increases the risk for cognitive dysfunction, dementia and Alzheimer's disease. While the pathogenesis behind these findings is unknown, growing evidence suggests that chronic increase in neurosteroid levels, such as allopregnanolone, is part of the mechanism. We treated wild-type C57BL/6J mice with allopregnanolone for 5months, using osmotic pumps. This treatment led to moderately increased levels of allopregnanolone, equivalent to that of mild chronic stress. After an interval of no treatment for 1month, female mice showed impaired learning and memory function in the Morris water maze (MWM) in combination with diminished hippocampus weight and increased cerebellum weight, both correlating to MWM performance. Male mice showed a minor reduction in memory function and no differences in brain structure. We conclude that chronic allopregnanolone elevation can lead to cognitive dysfunction and negative brain alterations. We suggest that allopregnanolone could play a key role in the pathogenesis of stress-induced cognitive disturbances and perhaps dementia.

Keywords
Allopregnanolone, Memory and learning, Chronic stress, Mild cognitive impairment, Dementia, Brain tissue weight, GABA, Wild-type mice, C57BL/6J mice
National Category
Neurosciences Other Health Sciences
Identifiers
urn:nbn:se:umu:diva-118533 (URN)10.1016/j.yhbeh.2015.10.010 (DOI)000368962200020 ()26497250 (PubMedID)
Available from: 2016-03-22 Created: 2016-03-22 Last updated: 2018-06-07Bibliographically approved
Bengtsson, S. K. S., Nyberg, S., Hedström, H., Zingmark, E., Jonsson, B., Bäckström, T. & Bixo, M. (2015). Isoallopregnanolone antagonize allopregnanolone-induced effects on saccadic eye velocity and self-reported sedation in humans. Psychoneuroendocrinology, 52, 22-31
Open this publication in new window or tab >>Isoallopregnanolone antagonize allopregnanolone-induced effects on saccadic eye velocity and self-reported sedation in humans
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2015 (English)In: Psychoneuroendocrinology, ISSN 0306-4530, E-ISSN 1873-3360, Vol. 52, p. 22-31Article in journal (Refereed) Published
Abstract [en]

Allopregnanolone (AP) is an endogenous neurosteroid. It modulates the effect of gamma-amino-butyric acid (GABA) on the GABA type A (GABA(A)) receptor, which leads to increased receptor activity. Since the GABA-system is mainly inhibitory, increased AP activity leads to modulation of neuronal activity. In vitro studies of GABA(A) receptor activity and in vivo animal studies of sedation have shown that AP-induced effects can be inhibited by another endogenous steroid, namely isoallopregnanolone (ISO). In this study we investigated if ISO can antagonize AP-induced effects in healthy female volunteers, via measurements of saccadic eye velocity (SEV) and self-rated sedation. With a single-blind cross-over design, 12 women were studied on three separate occasions; given AP alone or AP in combination with one of two ISO doses. Congruent with previous reports, AP administration decreased SEV and induced sedation and these effects were diminished by simultaneous ISO administration. Also, the ISO effect modulation was seemingly stronger for SEV than for sedation. These effects were observed already at an ISO dose exposure that was approximately half of that of AP. In conclusion, ISO antagonized AP-induced decrease in SEV and self-reported sedation, probably in a non-competitive manner.

Keywords
Allopregnanolone, Isoallopregnanolone, Saccadic eye velocity, GABA(A) receptor, Sedation, Premenstrual dysphoric disorder
National Category
Endocrinology and Diabetes Neurosciences
Identifiers
urn:nbn:se:umu:diva-100765 (URN)10.1016/j.psyneuen.2014.10.025 (DOI)000349271000004 ()25459890 (PubMedID)
Available from: 2015-04-26 Created: 2015-03-09 Last updated: 2018-06-07Bibliographically approved
Löfgren, M., Bengtsson, S. K., Johansson, M. & Bäckström, T. (2013). Allopregnanolone promotes success in food competition in subordinate male rats. Neuropsychobiology, 68(1), 15-23
Open this publication in new window or tab >>Allopregnanolone promotes success in food competition in subordinate male rats
2013 (English)In: Neuropsychobiology, ISSN 0302-282X, E-ISSN 1423-0224, Vol. 68, no 1, p. 15-23Article in journal (Refereed) Published
Abstract [en]

Background/Aims: Allopregnanolone or 3 alpha-hydroxy-5 alpha-pregnan-20-one (AlloP) is normally sedative and anxiolytic, but can under provoking circumstances paradoxically induce aggressive behavior. Therefore, it is of particular interest to determine if there is a relationship between an anxiolytic effect and aggressive behavior following AlloP administration.

Method: Male Wistar rats were housed in triads comprising of 1 young rat (35 days) and 2 older rats (55 days), with the intent of producing a social hierarchy. The triads were sampled for total serum testosterone and submitted to a social challenge in the form of a food competition test (FCT), where the rats competed for access to drinking sweetened milk. At baseline, the younger rats were identified as subordinates. To test for the behavioral effect of AlloP, the subordinate rats were given intravenous AlloP injections of 0.5 and 1 mg/kg. To assess the optimal AlloP effect, 6 intervals (5, 10, 15, 20, 30 and 40 min) between injection and the FCT were used. In separate studies, AlloP was also given by subcutaneous and intraperitoneal administration at 10 and 17 mg/kg.

Results: AlloP (1 mg/kg, i.v.) increased drinking time and aggressive behavior in subordinate rats, with a positive correlation between these behaviors. The subcutaneous injection (17 mg/kg) also increased drinking time in subordinate animals. Serum testosterone concentration was higher in dominant compared to subordinate rats, and correlated with drinking time and weight.

Conclusions: AlloP increased drinking time and aggressive behavior, and the correlation indicates a relationship between an anxiolytic effect and aggressive behavior. Copyright (c) 2013 S. Karger AG, Basel

Keywords
Allopregnanolone, Anxiety, Behavior, Aggression, Hierarchy, Triad, Subordinate
National Category
Obstetrics, Gynecology and Reproductive Medicine
Identifiers
urn:nbn:se:umu:diva-79290 (URN)10.1159/000350478 (DOI)000321482500002 ()
Available from: 2013-08-23 Created: 2013-08-13 Last updated: 2018-06-08Bibliographically approved
Bengtsson, S. K., Johansson, M., Bäckström, T., Nitsch, R. M. & Wang, M. (2013). Brief but Chronic Increase in Allopregnanolone Cause Accelerated AD Pathology Differently in Two Mouse Models. Current Alzheimer Research, 10(1), 38-47
Open this publication in new window or tab >>Brief but Chronic Increase in Allopregnanolone Cause Accelerated AD Pathology Differently in Two Mouse Models
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2013 (English)In: Current Alzheimer Research, ISSN 1567-2050, Vol. 10, no 1, p. 38-47Article in journal (Refereed) Published
Abstract [en]

Previously, we have shown that chronic treatment with allopregnanolone (ALLO) for three months impaired learning function in the Swe/PS1 mouse model. ALLO is a neurosteroid, produced in the CNS and a GABA(A) receptor agonist. ALLO modulates the general inhibitory system in the CNS by enhancing the effect of GABA. Chronic treatment with other GABA(A) receptor active compounds, such as benzodiazepines, ethanol and medroxy-progesterone acetate has been associated to cognitive decline and/or increased risk for dementia. In this study, we sufficed with a treatment period of one month for the Swe/PS1 mouse, and included another Alzheimer's disease mouse model; the Swe/Arc model. We found that one month of chronic treatment with elevated ALLO levels within physiological range impaired learning and memory function in the Swe/Arc female and male mice. Male Swe/PS1 mice also showed marginally impaired function, while the female mice did not. Furthermore, the chronic ALLO treatment caused increased levels of soluble A beta in the Swe/PS1 mouse model while the levels were unchanged in the Swe/Arc model. Therefore, both Swe/Arc and Swe/PS1 mice showed signs of accelerated disease progression. Still, further studies are required to determine the mechanisms behind the cognitive impairment and the increased A beta-levels caused by mildly elevated ALLO-levels.

Place, publisher, year, edition, pages
Bentham Science Publishers, 2013
Keywords
Allopregnanolone, Alzheimer's disease, beta-amyloid(1-42), beta-amyloid(1-40), cognition, physiological stress, transgenic
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:umu:diva-70364 (URN)10.2174/156720513804871363 (DOI)000317271800006 ()
Available from: 2013-05-16 Created: 2013-05-14 Last updated: 2018-06-08Bibliographically approved
Bengtsson, S., Johansson, M., Bäckström, T., Nitsch, R. & Wang, M. (2013). Brief but Chronic Increase in Allopregnanolone Cause Accelerated ADPathology Differently in Two Mouse Models. Current Alzheimer Research, 10(1), 38-47
Open this publication in new window or tab >>Brief but Chronic Increase in Allopregnanolone Cause Accelerated ADPathology Differently in Two Mouse Models
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2013 (English)In: Current Alzheimer Research, ISSN 1567-2050, Vol. 10, no 1, p. 38-47Article in journal (Refereed) Published
Abstract [en]

Abstract: Previously, we have shown that chronic treatment with allopregnanolone (ALLO) for three months impaired learning function in the Swe/PS1 mouse model. ALLO is a neurosteroid, produced in the CNS and a GABAA receptor agonist. ALLO modulates the general inhibitory system in the CNS by enhancing the effect of GABA. Chronic treatment with other GABAA receptor active compounds, such as benzodiazepines, ethanol and medroxy-progesterone acetate has been associated to cognitive decline and/or increased risk for dementia. In this study, we sufficed with a treatment period of one month for the Swe/PS1 mouse, and included another Alzheimer’s disease mouse model; the Swe/Arc model. We found that one month of chronic treatment with elevated ALLO levels within physiological range impaired learning and memory function in the Swe/Arc female and male mice. Male Swe/PS1 mice also showed marginally impaired function, while the female mice did not. Furthermore, the chronic ALLO treatment caused increased levels of soluble Aβ in the Swe/PS1 mouse model while the levels were unchanged in the Swe/Arc model. Therefore, both Swe/Arc and Swe/PS1 mice showed signs of accelerated disease progression. Still, further studies are required to determine the mechanisms behind the cognitive impairment and the increased Aβ-levels caused by mildly elevated ALLO-levels. learning function in the Swe/PS1 mouse model. ALLO is a neurosteroid, produced in the CNS and a GABAA receptor agonist. ALLO modulates the general inhibitory system in the CNS by enhancing the effect of GABA. Chronic treatment with other GABAA receptor active compounds, such as benzodiazepines, ethanol and medroxy-progesterone acetate has been associated to cognitive decline and/or increased risk for dementia. In this study, we sufficed with a treatment period of one month for the Swe/PS1 mouse, and included another Alzheimer’s disease mouse model; the Swe/Arc model. We found that one month of chronic treatment with elevated ALLO levels within physiological range impaired learning and memory function in the Swe/Arc female and male mice. Male Swe/PS1 mice also showed marginally impaired function, while the female mice did not. Furthermore, the chronic ALLO treatment caused increased levels of soluble Ab in the Swe/PS1 mouse model while the levels were unchanged in the Swe/Arc model. Therefore, both Swe/Arc and Swe/PS1 mice showed signs of accelerated disease progression. Still, further studies are required to determine the mechanisms behind the cognitive impairment and the increased Aβ-levels caused by mildly elevated ALLO-levels.

Place, publisher, year, edition, pages
Bentham Science Publishers, 2013
Keywords
Alzheimer's disease, beta-amyloid proteins, allopregnanolone, chronic stress, transgenic mouse models, synaptophysin, amyloid plaques
National Category
Neurosciences
Research subject
Obstetrics and Gynaecology; Neurology; Medical Pharmacology; Geriatrics
Identifiers
urn:nbn:se:umu:diva-66571 (URN)
Funder
Swedish Research Council, 4x-11198
Available from: 2013-02-28 Created: 2013-02-25 Last updated: 2018-06-08Bibliographically approved
Bengtsson, S. (2013). Stress steroids as accelerators of Alzheimer's disease.: Effects of chronically elevated levels of allopregnanolone in transgenic AD models.. (Doctoral dissertation). Umeå: Umeå universitet
Open this publication in new window or tab >>Stress steroids as accelerators of Alzheimer's disease.: Effects of chronically elevated levels of allopregnanolone in transgenic AD models.
2013 (English)Doctoral thesis, comprehensive summary (Other academic)
Alternative title[sv]
Accelererar stressteroider Alzheimers sjukdom? : Effekter av kroniskt förhöjda allopregnanolonnivåer i transgena AD modeller.
Abstract [en]

Background Alzheimer’s disease (AD) and dementia are devastating con­ditions not only for the affected patients but also for their families.  The economical costs for the society are tremendous. Mid-life psychological stress, psychosocial stress and post-traumatic stress disorder cause cognitive dysfunction and lead to increased risk for dementia. However, the mecha­nisms behind stress-induced AD and dementia are not known. AD is char­acterized by solid amyloid plaques in the CNS. However, over the last decade it has been concluded that the levels of soluble beta-amyloid (Aβ) correlate to cognitive performance while plaques often do not. The soluble Aβ accu­mulate intracellularly and disturb the synaptic function. Interestingly, the levels of intracellular Aβ depend on neuronal activity. Previous studies have shown that decreased neuronal activity cause increased intracellular levels of Aβ and cognitive decline. Stress steroids produced in the brain, e.g. allopreg­nanolone, enhance the activity of the GABAergic system, i.e. the main in­hibitory system of the brain. Consequently, allopregnanolone affects neu­ronal activity. Therefore, it is possible that elevated levels of allopreg­nanolone (due to e.g. stress) cause increased intracellular levels of Aβ. This could be a mechanism behind stress-induced AD. The purpose of this thesis was to investigate if elevation of allopregnanolone is a possible link in the mechanism behind stress-induced AD by investigating the effects of chroni­cally elevated levels of allopregnanolone in transgenic mouse models for AD.

Methods Swe/PS1 and Swe/Arc mice (transgenic models for AD) were treated chronically with elevated allopregnanolone levels, comparable to those at mild stress. After an interval of no treatment, the mice were tested for learning and memory performance in the Morris water maze. The brain tissue of the mice was then analyzed for disease markers, i.e. soluble and insoluble Aβ40 and Aβ42 using enzyme-linked immunosorbent assay, and amyloid plaques using immunohistochemistry and Congo red staining tech­nique. The brain tissue was also analyzed for a marker of synaptic function, i.e. synaptophysin.

Results Chronic treatment of allopregnanolone caused impaired learning performance in both the Swe/PS1 and the Swe/Arc mouse models. The Swe/PS1 mice had increased levels of soluble Aβ in both hippocampus and cortex. Interestingly, the levels of soluble Aβ were unchanged in the Swe/Arc mice. Three months of allopregnanolone treatment in the Swe/PS1 mouse model caused decreased plaque size, predominantly in hippocampus. It may be concluded that chronic allopregnanolone elevation caused smaller but more abundant congophilic plaques as both total plaque area and number of plaques were increased in mice with poor learning ability. Additional spots for accumulation of Aβ, predominantly the more toxic Aβ42, and thus addi­tional starting points for plaque production could be a part of the mechanism behind stress-induced Alzheimer’s disease.

Conclusions The conclusion of this thesis is that chronic elevation of allo­pregnanolon accelerated the development of Alzheimer’s disease in the Swe/PS1 and the Swe/Arc transgenic mouse models. Allopregnanolone may be an important link in the mechanism behind stress-induced AD. However, further studies are required to grasp the extent of its pathological influence.

Place, publisher, year, edition, pages
Umeå: Umeå universitet, 2013. p. 66
Series
Umeå University medical dissertations, ISSN 0346-6612 ; 1553
Keywords
Allopregnanolone, Alzheimer's disease, beta-amyloid, synaptophysin, chronic stress, Morris water maze
National Category
Neurosciences
Research subject
Obstetrics and Gynaecology; Medical Pharmacology; Neurology; Geriatrics; medical behavioral science
Identifiers
urn:nbn:se:umu:diva-66572 (URN)978-91-7459-565-9 (ISBN)
Public defence
2013-03-22, Hörsal Betula, Norrlands Universitetssjukhus, Byggnad 6M, Umeå, 09:00 (Swedish)
Opponent
Supervisors
Available from: 2013-03-01 Created: 2013-02-25 Last updated: 2018-06-08Bibliographically approved
Bengtsson, S. K., Johansson, M., Bäckström, T. & Wang, M. (2012). Chronic Allopregnanolone Treatment Accelerates Alzheimer's Disease Development in A beta PP(Swe)PSEN1(Delta E9) Mice. Journal of Alzheimer's Disease, 31(1), 71-84
Open this publication in new window or tab >>Chronic Allopregnanolone Treatment Accelerates Alzheimer's Disease Development in A beta PP(Swe)PSEN1(Delta E9) Mice
2012 (English)In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 31, no 1, p. 71-84Article in journal (Refereed) Published
Abstract [en]

The endogenous neurosteroid allopregnanolone alters neuronal excitability via modulation of the GABA(A) receptor and causes decreased neurotransmission. In Alzheimer's disease (AD), neurotransmission seems to alter the levels of toxic intracellular amyloid-beta (A beta) oligomers, which are implicated in AD pathogenesis and cause cognitive decline. Inhibition of synaptic activity has been shown to increase levels of intracellular A beta. Allopregnanolone at endogenous stress levels inhibits synaptic activity and could have similar effects. By using a transgenic A beta PP(Swe)PSEN1(Delta E9) mouse model for AD, we observed that chronic allopregnanolone treatment for three months with stress levels of allopregnanolone impaired learning in the Morris water maze. The learning impairment was seen one month after the end of treatment. Chronic allopregnanolone treatment also led to increased levels of soluble A beta in the brain, which could be a sign of advanced pathogenesis. Since the learning and memory of wild-type mice was not affected by the treatment, we propose that chronic allopregnanolone treatment accelerates the pathogenesis of AD. However, further studies are required in order to determine the underlying mechanism.

Keywords
Allopregnanolone, Alzheimer's disease, amyloid-beta, amyloid-beta(1-40), amyloid-beta(1-42), cognition, physiological stress
National Category
Neurosciences
Identifiers
urn:nbn:se:umu:diva-57556 (URN)10.3233/JAD-2012-120268 (DOI)000306122900009 ()
Available from: 2012-08-13 Created: 2012-08-06 Last updated: 2018-06-08Bibliographically approved
Bäckström, T., Haage, D., Löfgren, M., Johansson, I. M., Strömberg, J., Nyberg, S., . . . Bengtsson, S. K. (2011). Paradoxical effects of GABA-A modulators may explain sex steroid induced negative mood symptoms in some persons. Neuroscience, 191(Special issue), 46-54
Open this publication in new window or tab >>Paradoxical effects of GABA-A modulators may explain sex steroid induced negative mood symptoms in some persons
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2011 (English)In: Neuroscience, ISSN 0306-4522, E-ISSN 1873-7544, Vol. 191, no Special issue, p. 46-54Article, review/survey (Refereed) Published
Abstract [en]

Some women have negative mood symptoms, caused by progestagens in hormonal contraceptives or sequential hormone therapy or by progesterone in the luteal phase of the menstrual cycle, which may be attributed to metabolites acting on the GABA-A receptor. The GABA system is the major inhibitory system in the adult CNS and most positive modulators of the GABA-A receptor (benzodiazepines, barbiturates, alcohol, GABA steroids), induce inhibitory (e.g. anesthetic, sedative, anticonvulsant, anxiolytic) effects. However, some individuals have adverse effects (seizures, increased pain, anxiety, irritability, aggression) upon exposure. Positive GABA-A receptor modulators induce strong paradoxical effects including negative mood in 3%-8% of those exposed, while up to 25% have moderate symptoms. The effect is biphasic: low concentrations induce an adverse anxiogenic effect while higher concentrations decrease this effect and show inhibitory, calming properties. The prevalence of premenstrual dysphoric disorder (PMDD) is also 3%-8% among women in fertile ages, and up to 25% have more moderate symptoms of premenstrual syndrome (PMS). Patients with PMDD have severe luteal phase-related symptoms and show changes in GABA-A receptor sensitivity and GABA concentrations. Findings suggest that negative mood symptoms in women with PMDD are caused by the paradoxical effect of allopregnanolone mediated via the GABA-A receptor, which may be explained by one or more of three hypotheses regarding the paradoxical effect of GABA steroids on behavior: (1) under certain conditions, such as puberty, the relative fraction of certain GABA-A receptor subtypes may be altered, and at those subtypes the GABA steroids may act as negative modulators in contrast to their usual role as positive modulators; (2) in certain brain areas of vulnerable women the transmembrane C1(-) gradient may be altered by factors such as estrogens that favor excitability; (3) inhibition of inhibitory neurons may promote disinhibition, and hence excitability. This article is part of a Special Issue entitled: Neuroactive Steroids: Focus on Human Brain. (C) 2011 Published by Elsevier Ltd on behalf of IBRO.

Place, publisher, year, edition, pages
Oxford: , 2011
Keywords
premenstrual syndrome, GABA-A receptor, paradoxical, GABA-steroid, neurosteroid
National Category
Neurology Neurosciences
Identifiers
urn:nbn:se:umu:diva-49248 (URN)10.1016/j.neuroscience.2011.03.061 (DOI)000295749300006 ()
Available from: 2011-11-09 Created: 2011-11-04 Last updated: 2018-06-08Bibliographically approved
Bengtsson, S., Lundgren, P., Gouissem, S., Johansson, M., Bäckström, T. & Wang, M.Chronic allopregnanolone elevation cause altered plaque production in Swe/PS1 mice.
Open this publication in new window or tab >>Chronic allopregnanolone elevation cause altered plaque production in Swe/PS1 mice
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(English)Manuscript (preprint) (Other academic)
Abstract [en]

Abstract. We have previously shown that chronic elevation of the neurosteroid allopregnanolone caused learning dysfunction and increased levels of soluble Aβ in the Swe/PS1 mouse model. The mechanism behind these findings is however unknown. We further investigated the brain tissue of these mice to identify any effects on congophilic plaque burden, Aβ42-specific plaque burden and synaptic function. We found a significant reduction in the average size of the congophilic core of neuritic plaques after chronic allopregnanolone treatment compared to vehicle. This seems to be caused by an altered plaque production, leading to more abundant, but smaller neuritic plaques. We may also have detected a decrease in the amount of synaptophysin, and thus synaptic function among the same mice. However, the long interval between the end of treatment and tissue collection possibly allowed time for recovery and only minor differences were noted. We found that the natural relationship between levels of insoluble Aβ, congophilic and Aβ42-specific plaque load was disrupted after chronically elevated allopregnanolone levels. Furthermore, the levels of syn-aptophysin and insoluble Aβ became more important in the relationship to learning and memory. The causality of these factors is still unknown and further studies are required to fully understand the effect of neurosteroids on AD development.

Keywords
Alzheimer's disease, allopregnanolone, neuroendocrinology, GABA, beta-amyloid, synaptophysin, chronic stress
National Category
Neurosciences
Research subject
Obstetrics and Gynaecology; Medical Pharmacology; medical behavioral science; Neurology
Identifiers
urn:nbn:se:umu:diva-66574 (URN)
Funder
Swedish Research Council, 4x-11198
Available from: 2013-02-28 Created: 2013-02-25 Last updated: 2018-06-08Bibliographically approved
Wang, C., Iashchishyn, I., Nyström, S., Klementieva, O., Kara, J., Bengtsson, S., . . . Morozova-Roche, L.S100A9-driven amyloid-neuroinflammatory cascade in traumatic brain injury as a risk factor for Alzheimer’s disease.
Open this publication in new window or tab >>S100A9-driven amyloid-neuroinflammatory cascade in traumatic brain injury as a risk factor for Alzheimer’s disease
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(English)Manuscript (preprint) (Other academic)
Keywords
Traumatic brain injury, Alzheimer’s disease, Aβ, S100A9, Amyloid, Cytotoxicity; Neuroinflammation
National Category
Other Medical Sciences not elsewhere specified
Research subject
Medical Biochemistry
Identifiers
urn:nbn:se:umu:diva-125077 (URN)
External cooperation:
Projects
Role of pro-inflammatory S100A9 protein in amyloid-neuroinflammatory cascade in Alzheimer’s disease and traumatic brain injury
Available from: 2016-09-05 Created: 2016-09-05 Last updated: 2018-06-07
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