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DocumentZinc binding to S100B affords regulation of trace metal homeostasis and excitotoxicity in the brain2018

Reference code: PT/FB
Entity holding: BIAL Foundation
Location: S. Mamede do Coronado
Title:
BIAL Foundation Archive
Start date: 1994
History:
The BIAL Foundation was created in 1994 by Laboratórios BIAL in conjunction with the Council of Rectors of Portuguese Universities. BIAL’s Foundation mission is to foster the scientific study of Man from both the physical and spiritual perspectives.
Along the years the BIAL Foundation has developed an important relationship with the scientific community, first in Portugal and after worldwide. Today it is an institution of reference which aims to stimulate new researches that may help people, promote more health and contribute to new milestones to gain access to knowledge.
Among its activities the BIAL Foundation manages the BIAL Award, created in 1984, one of the most important awards in the Health field in Europe. The BIAL Award rewards both the basic and the clinical research distinguishing works of major impact in medical research.
The BIAL Foundation also assigns Scientific Research Scholarships for the study of neurophysiological and mental health in people, arousing the interest of researchers in the areas of Psychophysiology and Parapsychology.
To date the BIAL Foundation has supported 461 projects, more than 1000 researchers, with research groups in twenty-seven countries, resulting, until April 2013, in about 600 full papers, out of which 172 published in indexed international journals with an average impact factor of 3.6 and a substantial number of citations (1665).
Since 1996 the BIAL Foundation organizes the Symposia entitled "Behind and Beyond the Brain", a Forum that gathers well renowned neurosciences speakers and the BIAL Foundation Fellows which are spread around the world.
Classified as an institution of public utility, the BIAL Foundation includes among its patrons the Portuguese President, the Portuguese Universities Rectors' Council and the Portuguese Medical Association.
URL: http://www.bial.com/pt/
Accessibility: By permission

Reference code: PT/FB/BL
Entity holding: BIAL Foundation
Title: BIAL Grants
Start date: 1994
History:
In 1994 the BIAL Foundation launched a programme of science research grants with the aim of encouraging the research into Man’s physical and mental processes, namely in fields still largely unexplored but which warrant further scientific analysis, as Psychophysiology and Parapsychology.
Since its launch, applications to the BIAL grants have been increasing. Up to now 461 projects have been supported, involving more than 1000 researchers from 27 countries.
The approved applications have benefited from grants in amounts comprised between €5,000 and €50, 000. The amount to be granted is fixed by the Scientific board according to the needs of each project.
The supported projects have originated, until April 2013, in about 600 full papers, 172 out of which were published in indexed international journals with an average impact factor of 3.6 and a substantial number of citations (1665).
Among the BIAL Foundation fellows is worth highlighting the presence of scientists from prestigious universities from the United States, United Kingdom, Australia, Russia, Germany, Japan, France, Canada, and many others.
The BIAL grants are promoted biannually.

Reference code: PT/FB/BL-2014
Location: BF-GMS
Title:
2014 Grants
Start date: 2015-01

Reference code: PT/FB/BL-2014-343
Location: BF-GMS
Title:
343 - Proteotoxic insults and synaptic dysfunction in the aging brain
Duration: 2015-06 - 2019-01
Researcher(s):
Cláudio Emanuel Moreira Gomes, Andreas Martin Grabrucker, Joana Margarida Lopes da Silva Cristóvão, Sónia Cristina Alves Dickson Leal Solano
Institution(s): FCiências.ID – Associação para a Investigação e Desenvolvimento de Ciências (Portugal); Neurocenter of Ulm University (Germany)
Contents: Contents:
Application form
Correspondence
Progress report
Final report
Articles
Author: Gomes, C.
Secondary author(s):
Grabrucker, A., Cristóvão, J., Solano, S.
Number of reproductions:
1
Keywords:
Protein homeostasis / Brain biometals / Neuroinflammation / Synaptic Biochemistry / Psychophysiology

Reference code: PT/FB/BL-2014-343.03
Location: BF-GMS
Title:
Zinc binding to S100B affords regulation of trace metal homeostasis and excitotoxicity in the brain
Publication year: 2018
URL:
https://www.frontiersin.org/articles/10.3389/fnmol.2017.00456/full
Abstract/Results: ABSTRACT:
Neuronal metal ions such as zinc are essential for brain function. In particular synaptic processes are tightly related to metal and protein homeostasis, for example through extracellular metal-binding proteins. One such protein is neuronal S100B, a calcium and zinc binding damage-associated molecular pattern (DAMP), whose chronic upregulation is associated with aging, Alzheimer’s disease (AD), motor neuron disease and traumatic brain injury (TBI). Despite gained insights on the structure of S100B, it remains unclear how its calcium and zinc binding properties regulate its function on cellular level. Here we report a novel role of S100B in trace metal homeostasis, in particular the regulation of zinc levels in the brain. Our results show that S100B at increased extracellular levels is not toxic, persists at high levels, and is taken up into neurons, as shown by cell culture and biochemical analysis. Combining protein bioimaging and zinc quantitation, along with a zinc-binding impaired S100B variant, we conclude that S100B effectively scavenges zinc ions through specific binding, resulting in a redistribution of the intracellular zinc pool. Our results indicate that scavenging of zinc by increased levels of S100B affects calcium levels in vitro. Thereby S100B is able to mediate the cross talk between calcium and zinc homeostasis. Further, we investigated a possible new neuro-protective role of S100B in excitotoxicity via its effects on calcium and zinc homeostasis. Exposure of cells to zinc-S100B but not the zinc-binding impaired S100B results in an inhibition of excitotoxicity. We conclude that in addition to its known functions, S100B acts as sensor and regulator of elevated zinc levels in the brain and this metal-buffering activity is tied to a neuroprotective role.
Accessibility: Document exists in file
Language:
eng
Author:
Hagmeyer, S.
Secondary author(s):
Cristóvão, J. S., Mulvihill, J. E., Boeckers, T. M., Gomes, C. M., Grabrucker, A. M.
Document type:
Article
Number of reproductions:
1
Reference:
Hagmeyer, S., Cristóvão, J. S., Mulvihill, J. E., Boeckers, T., Gomes, C., & Grabrucker, A. (2018). Zinc Binding to S100B Affords Regulation of Trace Metal Homeostasis and Excitotoxicity in the Brain. Frontiers in Molecular Neuroscience, 10: 456. https://doi.org/10.3389/fnmol.2017.00456
2-year Impact Factor: 3.720|2018
Times cited: 32|2025-09-17
Indexed document: Yes
Quartile: Q2
Keywords: Zn / Zinc / S100B / DAMP / Synapse / Calcium / Excitotoxicity / Zinc sensor

Zinc binding to S100B affords regulation of trace metal homeostasis and excitotoxicity in the brain

Zinc binding to S100B affords regulation of trace metal homeostasis and excitotoxicity in the brain
DocumentThe neuronal S100B protein is a calcium-tuned suppressor of amyloid-b aggregation2018

Reference code: PT/FB
Entity holding: BIAL Foundation
Location: S. Mamede do Coronado
Title:
BIAL Foundation Archive
Start date: 1994
History:
The BIAL Foundation was created in 1994 by Laboratórios BIAL in conjunction with the Council of Rectors of Portuguese Universities. BIAL’s Foundation mission is to foster the scientific study of Man from both the physical and spiritual perspectives.
Along the years the BIAL Foundation has developed an important relationship with the scientific community, first in Portugal and after worldwide. Today it is an institution of reference which aims to stimulate new researches that may help people, promote more health and contribute to new milestones to gain access to knowledge.
Among its activities the BIAL Foundation manages the BIAL Award, created in 1984, one of the most important awards in the Health field in Europe. The BIAL Award rewards both the basic and the clinical research distinguishing works of major impact in medical research.
The BIAL Foundation also assigns Scientific Research Scholarships for the study of neurophysiological and mental health in people, arousing the interest of researchers in the areas of Psychophysiology and Parapsychology.
To date the BIAL Foundation has supported 461 projects, more than 1000 researchers, with research groups in twenty-seven countries, resulting, until April 2013, in about 600 full papers, out of which 172 published in indexed international journals with an average impact factor of 3.6 and a substantial number of citations (1665).
Since 1996 the BIAL Foundation organizes the Symposia entitled "Behind and Beyond the Brain", a Forum that gathers well renowned neurosciences speakers and the BIAL Foundation Fellows which are spread around the world.
Classified as an institution of public utility, the BIAL Foundation includes among its patrons the Portuguese President, the Portuguese Universities Rectors' Council and the Portuguese Medical Association.
URL: http://www.bial.com/pt/
Accessibility: By permission

Reference code: PT/FB/BL
Entity holding: BIAL Foundation
Title: BIAL Grants
Start date: 1994
History:
In 1994 the BIAL Foundation launched a programme of science research grants with the aim of encouraging the research into Man’s physical and mental processes, namely in fields still largely unexplored but which warrant further scientific analysis, as Psychophysiology and Parapsychology.
Since its launch, applications to the BIAL grants have been increasing. Up to now 461 projects have been supported, involving more than 1000 researchers from 27 countries.
The approved applications have benefited from grants in amounts comprised between €5,000 and €50, 000. The amount to be granted is fixed by the Scientific board according to the needs of each project.
The supported projects have originated, until April 2013, in about 600 full papers, 172 out of which were published in indexed international journals with an average impact factor of 3.6 and a substantial number of citations (1665).
Among the BIAL Foundation fellows is worth highlighting the presence of scientists from prestigious universities from the United States, United Kingdom, Australia, Russia, Germany, Japan, France, Canada, and many others.
The BIAL grants are promoted biannually.

Reference code: PT/FB/BL-2014
Location: BF-GMS
Title:
2014 Grants
Start date: 2015-01

Reference code: PT/FB/BL-2014-343
Location: BF-GMS
Title:
343 - Proteotoxic insults and synaptic dysfunction in the aging brain
Duration: 2015-06 - 2019-01
Researcher(s):
Cláudio Emanuel Moreira Gomes, Andreas Martin Grabrucker, Joana Margarida Lopes da Silva Cristóvão, Sónia Cristina Alves Dickson Leal Solano
Institution(s): FCiências.ID – Associação para a Investigação e Desenvolvimento de Ciências (Portugal); Neurocenter of Ulm University (Germany)
Contents: Contents:
Application form
Correspondence
Progress report
Final report
Articles
Author: Gomes, C.
Secondary author(s):
Grabrucker, A., Cristóvão, J., Solano, S.
Number of reproductions:
1
Keywords:
Protein homeostasis / Brain biometals / Neuroinflammation / Synaptic Biochemistry / Psychophysiology

Reference code: PT/FB/BL-2014-343.04
Location: BF-GMS
Title:
The neuronal S100B protein is a calcium-tuned suppressor of amyloid-b aggregation
Publication year: 2018
URL:
http://advances.sciencemag.org/content/4/6/eaaq1702.full
Abstract/Results: ABSTRACT:
Amyloid-ß (Aß) aggregation and neuroinflammation are consistent features in Alzheimer’s disease (AD) and strong candidates for the initiation of neurodegeneration. S100B is one of the most abundant proinflammatory proteins that is chronically up-regulated in AD and is found associated with senile plaques. This recognized biomarker for brain distress may, thus, play roles in amyloid aggregation which remain to be determined. We report a novel role for the neuronal S100B protein as suppressor of Aß42 aggregation and toxicity. We determined the structural details of the interaction between monomeric Aß42 and S100B, which is favored by calcium binding to S100B, possibly involving conformational switching of disordered Aß42 into an a-helical conformer, which locks aggregation. From nuclear magnetic resonance experiments, we show that this dynamic interaction occurs at a promiscuous peptide-binding region within the interfacial cleft of the S100B homodimer. This physical interaction is coupled to a functional role in the inhibition of Aß42 aggregation and toxicity and is tuned by calcium binding to S100B. S100B delays the onset of Aß42 aggregation by interacting with Aß42 monomers inhibiting primary nucleation, and the calcium-bound state substantially affects secondary nucleation by inhibiting fibril surface–catalyzed reactions through S100B binding to growing Aß42 oligomers and fibrils. S100B protects cells from Aß42-mediated toxicity, rescuing cell viability and decreasing apoptosis induced by Aß42 in cell cultures. Together, our findings suggest that molecular targeting of S100B could be translated into development of novel approaches to ameliorate AD neurodegeneration.
Accessibility: Document exists in file
Copyright/Reproduction:
By permission
Language:
eng
Author:
Cristóvão, J. S.
Secondary author(s):
Morris, V. K., Cardoso, I., Leal, S., Martínez, J., Botelho, H. M., Göbl, C., David, R., Kierdorf, K., Alemi, M., Madl, T., Fritz, G., Reif, B., Gomes, C. M.
Document type:
Article
Number of reproductions:
1
Reference:
Cristóvão, J. S., Morris, V. K., Cardoso, I., Leal, S., Martínez, J., Botelho, H. M., Göbl, C., David, R., Kierdorf, K., Alemi, M., Madl, T., Fritz, G., Reif, B., & Gomes, C. M. (2018). The neuronal S100B protein is a calcium-tuned suppressor of amyloid-B aggregation. Science Advances, 4(6), eaaq1702. https://doi.org/10.1126/sciadv.aaq1702
2-year Impact Factor: 12.804|2018
Times cited: 51|2025-09-17
Indexed document: Yes
Quartile: Q1
Keywords: S100B / Calcium

The neuronal S100B protein is a calcium-tuned suppressor of amyloid-b aggregation

The neuronal S100B protein is a calcium-tuned suppressor of amyloid-b aggregation
DocumentDistribution and relative abundance of S100 proteins in the brain of the APP23 Alzheimer's Disease model mice2019

Reference code: PT/FB
Entity holding: BIAL Foundation
Location: S. Mamede do Coronado
Title:
BIAL Foundation Archive
Start date: 1994
History:
The BIAL Foundation was created in 1994 by Laboratórios BIAL in conjunction with the Council of Rectors of Portuguese Universities. BIAL’s Foundation mission is to foster the scientific study of Man from both the physical and spiritual perspectives.
Along the years the BIAL Foundation has developed an important relationship with the scientific community, first in Portugal and after worldwide. Today it is an institution of reference which aims to stimulate new researches that may help people, promote more health and contribute to new milestones to gain access to knowledge.
Among its activities the BIAL Foundation manages the BIAL Award, created in 1984, one of the most important awards in the Health field in Europe. The BIAL Award rewards both the basic and the clinical research distinguishing works of major impact in medical research.
The BIAL Foundation also assigns Scientific Research Scholarships for the study of neurophysiological and mental health in people, arousing the interest of researchers in the areas of Psychophysiology and Parapsychology.
To date the BIAL Foundation has supported 461 projects, more than 1000 researchers, with research groups in twenty-seven countries, resulting, until April 2013, in about 600 full papers, out of which 172 published in indexed international journals with an average impact factor of 3.6 and a substantial number of citations (1665).
Since 1996 the BIAL Foundation organizes the Symposia entitled "Behind and Beyond the Brain", a Forum that gathers well renowned neurosciences speakers and the BIAL Foundation Fellows which are spread around the world.
Classified as an institution of public utility, the BIAL Foundation includes among its patrons the Portuguese President, the Portuguese Universities Rectors' Council and the Portuguese Medical Association.
URL: http://www.bial.com/pt/
Accessibility: By permission

Reference code: PT/FB/BL
Entity holding: BIAL Foundation
Title: BIAL Grants
Start date: 1994
History:
In 1994 the BIAL Foundation launched a programme of science research grants with the aim of encouraging the research into Man’s physical and mental processes, namely in fields still largely unexplored but which warrant further scientific analysis, as Psychophysiology and Parapsychology.
Since its launch, applications to the BIAL grants have been increasing. Up to now 461 projects have been supported, involving more than 1000 researchers from 27 countries.
The approved applications have benefited from grants in amounts comprised between €5,000 and €50, 000. The amount to be granted is fixed by the Scientific board according to the needs of each project.
The supported projects have originated, until April 2013, in about 600 full papers, 172 out of which were published in indexed international journals with an average impact factor of 3.6 and a substantial number of citations (1665).
Among the BIAL Foundation fellows is worth highlighting the presence of scientists from prestigious universities from the United States, United Kingdom, Australia, Russia, Germany, Japan, France, Canada, and many others.
The BIAL grants are promoted biannually.

Reference code: PT/FB/BL-2014
Location: BF-GMS
Title:
2014 Grants
Start date: 2015-01

Reference code: PT/FB/BL-2014-343
Location: BF-GMS
Title:
343 - Proteotoxic insults and synaptic dysfunction in the aging brain
Duration: 2015-06 - 2019-01
Researcher(s):
Cláudio Emanuel Moreira Gomes, Andreas Martin Grabrucker, Joana Margarida Lopes da Silva Cristóvão, Sónia Cristina Alves Dickson Leal Solano
Institution(s): FCiências.ID – Associação para a Investigação e Desenvolvimento de Ciências (Portugal); Neurocenter of Ulm University (Germany)
Contents: Contents:
Application form
Correspondence
Progress report
Final report
Articles
Author: Gomes, C.
Secondary author(s):
Grabrucker, A., Cristóvão, J., Solano, S.
Number of reproductions:
1
Keywords:
Protein homeostasis / Brain biometals / Neuroinflammation / Synaptic Biochemistry / Psychophysiology

Reference code: PT/FB/BL-2014-343.14
Location: BF-GMS
Title:
Distribution and relative abundance of S100 proteins in the brain of the APP23 Alzheimer's Disease model mice
Publication year: 2019
URL:
https://www.frontiersin.org/articles/10.3389/fnins.2019.00640/full
Abstract/Results: ABSTRACT:
Increasing evidence links proteins of the S100 family to the pathogenesis of Alzheimer's disease (AD). S100 proteins are EF-hand calcium-binding proteins with intra- and extracellular functions related to regulation of proliferation, differentiation, apoptosis, and trace metal homeostasis, and are important modulators of inflammatory responses. For example, S100A6, S100A8, and S100B expression levels were found increased in inflammatory diseases, but also neurodegenerative disorders, and S100A8/A9 complexes may provide a mechanistic link between amyloid-beta (A beta) plaque formation and neuroinflammation. On the other hand, S100B, a proinflammatory protein that is chronically up-regulated in AD and whose elevation precedes plaque formation, was recently shown to suppress A beta aggregation. Here, we report expression of S100A6 and S100B in astrocytes and less so in neurons, and low level of expression of S100A8 in both neurons and glial cells in vitro. In vivo, S100A8 expression is almost absent in the brain of aged wildtype mice, while S100A6 and S100B are expressed in all brain regions and most prominently in the cortex and cerebellum. S100B seems to be enriched in Purkinje cells of the cerebellum. In contrast, in the brain of APP23 mice, a mouse model for Alzheimer's disease, S100B, S100A6, and S100A8 show co-localization with A beta plaques, compatible with astrocyte activation, and the expression level of S100A8 is increased in neural cells. While S100A6 and S100B are enriched in the periphery of plaques where less fibrillar is found, S100A8 is more intense within the center of the inclusion. In vitro assays show that, similarly to S100B, S100A6, and S100A8 also delay A beta aggregation suggesting a regulatory action over protein aggregation. We posit that elevated expression levels and overlapping spatial distribution of brain S100 proteins and plaques translates functional relationships between these inflammatory mediators and AD pathophysiology processes that uncover important molecular mechanisms linking the aggregation and neuroinflammation cascades.
Accessibility: Document exists in file
Language:
eng
Author:
Hagmeyer, S.
Secondary author(s):
Romão, M. A., Cristóvão, J. S., Vilella, A., Zoli, M., Gomes, C. M., Grabrucker, A. M.
Document type:
Article
Number of reproductions:
1
Reference:
Hagmeyer, S., Romão, M. A., Cristóvão, J. S., Vilella, A., Zoli, M., Gomes, C. M., & Grabrucker, A. M. (2019). Distribution and relative abundance of S100 proteins in the brain of the APP23 Alzheimer's disease model mice. Frontiers in Neuroscience, 13: 640. https://doi.org/10.3389/fnins.2019.00640
2-year Impact Factor: 3.707|2019
Times cited: 32|2025-09-17
Indexed document: Yes
Quartile: Q2
Keywords: S100A8 / S100A6 / S100B / Amyloid beta / Cerebellum / Aggregates / Zinc

Distribution and relative abundance of S100 proteins in the brain of the APP23 Alzheimer's Disease model mice

Distribution and relative abundance of S100 proteins in the brain of the APP23 Alzheimer's Disease model mice
DocumentS100B dysregulation during brain development affects synaptic SHANK protein networks via alteration of zinc homeostasis2021

Reference code: PT/FB
Entity holding: BIAL Foundation
Location: S. Mamede do Coronado
Title:
BIAL Foundation Archive
Start date: 1994
History:
The BIAL Foundation was created in 1994 by Laboratórios BIAL in conjunction with the Council of Rectors of Portuguese Universities. BIAL’s Foundation mission is to foster the scientific study of Man from both the physical and spiritual perspectives.
Along the years the BIAL Foundation has developed an important relationship with the scientific community, first in Portugal and after worldwide. Today it is an institution of reference which aims to stimulate new researches that may help people, promote more health and contribute to new milestones to gain access to knowledge.
Among its activities the BIAL Foundation manages the BIAL Award, created in 1984, one of the most important awards in the Health field in Europe. The BIAL Award rewards both the basic and the clinical research distinguishing works of major impact in medical research.
The BIAL Foundation also assigns Scientific Research Scholarships for the study of neurophysiological and mental health in people, arousing the interest of researchers in the areas of Psychophysiology and Parapsychology.
To date the BIAL Foundation has supported 461 projects, more than 1000 researchers, with research groups in twenty-seven countries, resulting, until April 2013, in about 600 full papers, out of which 172 published in indexed international journals with an average impact factor of 3.6 and a substantial number of citations (1665).
Since 1996 the BIAL Foundation organizes the Symposia entitled "Behind and Beyond the Brain", a Forum that gathers well renowned neurosciences speakers and the BIAL Foundation Fellows which are spread around the world.
Classified as an institution of public utility, the BIAL Foundation includes among its patrons the Portuguese President, the Portuguese Universities Rectors' Council and the Portuguese Medical Association.
URL: http://www.bial.com/pt/
Accessibility: By permission

Reference code: PT/FB/BL
Entity holding: BIAL Foundation
Title: BIAL Grants
Start date: 1994
History:
In 1994 the BIAL Foundation launched a programme of science research grants with the aim of encouraging the research into Man’s physical and mental processes, namely in fields still largely unexplored but which warrant further scientific analysis, as Psychophysiology and Parapsychology.
Since its launch, applications to the BIAL grants have been increasing. Up to now 461 projects have been supported, involving more than 1000 researchers from 27 countries.
The approved applications have benefited from grants in amounts comprised between €5,000 and €50, 000. The amount to be granted is fixed by the Scientific board according to the needs of each project.
The supported projects have originated, until April 2013, in about 600 full papers, 172 out of which were published in indexed international journals with an average impact factor of 3.6 and a substantial number of citations (1665).
Among the BIAL Foundation fellows is worth highlighting the presence of scientists from prestigious universities from the United States, United Kingdom, Australia, Russia, Germany, Japan, France, Canada, and many others.
The BIAL grants are promoted biannually.

Reference code: PT/FB/BL-2014
Location: BF-GMS
Title:
2014 Grants
Start date: 2015-01

Reference code: PT/FB/BL-2014-343
Location: BF-GMS
Title:
343 - Proteotoxic insults and synaptic dysfunction in the aging brain
Duration: 2015-06 - 2019-01
Researcher(s):
Cláudio Emanuel Moreira Gomes, Andreas Martin Grabrucker, Joana Margarida Lopes da Silva Cristóvão, Sónia Cristina Alves Dickson Leal Solano
Institution(s): FCiências.ID – Associação para a Investigação e Desenvolvimento de Ciências (Portugal); Neurocenter of Ulm University (Germany)
Contents: Contents:
Application form
Correspondence
Progress report
Final report
Articles
Author: Gomes, C.
Secondary author(s):
Grabrucker, A., Cristóvão, J., Solano, S.
Number of reproductions:
1
Keywords:
Protein homeostasis / Brain biometals / Neuroinflammation / Synaptic Biochemistry / Psychophysiology

Reference code: PT/FB/BL-2014-343.19
Location: BF-GMS
Title:
S100B dysregulation during brain development affects synaptic SHANK protein networks via alteration of zinc homeostasis
Publication year: 2021
URL:
https://www.nature.com/articles/s41398-021-01694-z
Abstract/Results: ABSTRACT:
Autism Spectrum Disorders (ASD) are caused by a combination of genetic predisposition and nongenetic factors. Among the nongenetic factors, maternal immune system activation and zinc deficiency have been proposed. Intriguingly, as a genetic factor, copy-number variations in S100B, a pro-inflammatory damage-associated molecular pattern (DAMP), have been associated with ASD, and increased serum S100B has been found in ASD. Interestingly, it has been shown that increased S100B levels affect zinc homeostasis in vitro. Thus, here, we investigated the influence of increased S100B levels in vitro and in vivo during pregnancy in mice regarding zinc availability, the zinc-sensitive SHANK protein networks associated with ASD, and behavioral outcomes. We observed that S100B affects the synaptic SHANK2 and SHANK3 levels in a zinc-dependent manner, especially early in neuronal development. Animals exposed to high S100B levels in utero similarly show reduced levels of free zinc and SHANK2 in the brain. On the behavioral level, these mice display hyperactivity, increased stereotypic and abnormal social behaviors, and cognitive impairment. Pro-inflammatory factors and zinc-signaling alterations converge on the synaptic level revealing a common pathomechanism that may mechanistically explain a large share of ASD cases.
Accessibility: Document exists in file
Language:
eng
Author:
Daini, E.
Secondary author(s):
Hagmeyer, S., De Benedictis, C. A., Cristóvão, J. S., Bodria, M., Ross, A. M., Raab, A., Boeckers, T. M., Feldmann, J., Gomes, C. M., Zoli, M., Vilella, A., Grabrucker, A. M.
Document type:
Article
Number of reproductions:
1
Reference:
Daini, E., Hagmeyer, S., De Benedictis, C. A., Cristóvão, J. S., Bodria, M., Ross, A. M., Raab, A., Boeckers, T. M., Feldmann, J., Gomes, C. M., Zoli, M., Vilella, A., & Grabrucker, A. M. (2021). S100B dysregulation during brain development affects synaptic SHANK protein networks via alteration of zinc homeostasis. Translational Psychiatry, 11(1), 562. https://doi.org/10.1038/s41398-021-01694-z
2-year Impact Factor: 7.989|2021
Times cited: 10|2025-09-20
Indexed document: Yes
Quartile: Q1
Keywords: Autism spectrum disorder (ASD) / S100B / Zinc

S100B dysregulation during brain development affects synaptic SHANK protein networks via alteration of zinc homeostasis

S100B dysregulation during brain development affects synaptic SHANK protein networks via alteration of zinc homeostasis