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Article: Molecular Mechanisms of Synaptotoxicity and Neuroinflammation in Alzheimer's Disease.

Marttinen, Mikael / Takalo, Mari / Natunen, Teemu / Wittrahm, Rebekka / Gabbouj, Sami / Kemppainen, Susanna / Leinonen, Ville / Tanila, Heikki / Haapasalo, Annakaisa / Hiltunen, Mikko

Frontiers in neuroscience

2018 Volume 12, Page(s) 963

Abstract: Alzheimer's disease (AD) is the most common neurodegenerative disorder, which is clinically associated with a global cognitive decline and progressive loss of memory and reasoning. According to the prevailing amyloid cascade hypothesis of AD, increased ... ...

Abstract	Alzheimer's disease (AD) is the most common neurodegenerative disorder, which is clinically associated with a global cognitive decline and progressive loss of memory and reasoning. According to the prevailing amyloid cascade hypothesis of AD, increased soluble amyloid-β (Aβ) oligomer levels impair the synaptic functions and augment calcium dyshomeostasis, neuroinflammation, oxidative stress as well as the formation of neurofibrillary tangles at specific brain regions. Emerging new findings related to synaptic dysfunction and initial steps of neuroinflammation in AD have been able to delineate the underlying molecular mechanisms, thus reinforcing the development of new treatment strategies and biomarkers for AD beyond the conventional Aβ- and tau-targeted approaches. Particularly, the identification and further characterization of disease-associated microglia and their RNA signatures, AD-associated novel risk genes, neurotoxic astrocytes, and in the involvement of complement-dependent pathway in synaptic pruning and loss in AD have set the outstanding basis for further preclinical and clinical studies. Here, we discuss the recent development and the key findings related to the novel molecular mechanisms and targets underlying the synaptotoxicity and neuroinflammation in AD.
Language	English
Publishing date	2018-12-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2018.00963
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Article: Altered Insulin Signaling in Alzheimer's Disease Brain - Special Emphasis on PI3K-Akt Pathway.

Gabbouj, Sami / Ryhänen, Simo / Marttinen, Mikael / Wittrahm, Rebekka / Takalo, Mari / Kemppainen, Susanna / Martiskainen, Henna / Tanila, Heikki / Haapasalo, Annakaisa / Hiltunen, Mikko / Natunen, Teemu

Frontiers in neuroscience

2019 Volume 13, Page(s) 629

Abstract: Alzheimer's disease (AD) and type 2 diabetes (T2D) are both diseases with increasing prevalence in aging populations. T2D, characterized by insulin resistance and defective insulin signaling, is a common co-morbidity and a risk factor for AD, increasing ... ...

Abstract	Alzheimer's disease (AD) and type 2 diabetes (T2D) are both diseases with increasing prevalence in aging populations. T2D, characterized by insulin resistance and defective insulin signaling, is a common co-morbidity and a risk factor for AD, increasing the risk approximately two to fourfold. Insulin exerts a wide variety of effects as a growth factor as well as by regulating glucose, fatty acid, and protein metabolism. Certain lifestyle factors, physical inactivity and typical Western diet (TWD) containing high fat and high sugar are strongly associated with insulin resistance and T2D. The PI3K-Akt signaling pathway is a major mediator of effects of insulin and plays a crucial role in T2D pathogenesis. Decreased levels of phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) subunits as well as blunted Akt kinase phosphorylation have been observed in the AD brain, characterized by amyloid-β and tau pathologies. Furthermore, AD mouse models fed with TWD have shown to display altered levels of PI3K subunits. How impaired insulin-PI3K-Akt signaling in peripheral tissues or in the central nervous system (CNS) affects the development or progression of AD is currently poorly understood. Interestingly, enhancement of PI3K-Akt signaling in the CNS by intranasal insulin (IN) treatment has been shown to improve memory
Language	English
Publishing date	2019-06-18
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2019.00629
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Article ; Online: Using online game-based platforms to improve student performance and engagement in histology teaching.

Felszeghy, Szabolcs / Pasonen-Seppänen, Sanna / Koskela, Ali / Nieminen, Petteri / Härkönen, Kai / Paldanius, Kaisa M A / Gabbouj, Sami / Ketola, Kirsi / Hiltunen, Mikko / Lundin, Mikael / Haapaniemi, Tommi / Sointu, Erkko / Bauman, Eric B / Gilbert, Gregory E / Morton, David / Mahonen, Anitta

BMC medical education

2019 Volume 19, Issue 1, Page(s) 273

Abstract: Background: Human morphology is a critical component of dental and medical graduate training. Innovations in basic science teaching methods are needed to keep up with an ever-changing landscape of technology. The purpose of this study was to investigate ...

Abstract	Background: Human morphology is a critical component of dental and medical graduate training. Innovations in basic science teaching methods are needed to keep up with an ever-changing landscape of technology. The purpose of this study was to investigate whether students in a medical and dental histology course would have better grades if they used gaming software Kahoot® and whether gamification effects on learning and enjoyment. Methods: In an effort to both evoke students' interest and expand their skill retention, an online competition using Kahoot® was implemented for first-year students in 2018 (n = 215) at the University of Eastern Finland. Additionally, closed (160/215) or open-ended (41/215) feedback questions were collected and analyzed. Results: The Kahoot® gamification program was successful and resulted in learning gains. The overall participant satisfaction using Kahoot® was high, with students (124/160) indicating that gamification increased their motivation to learn. The gaming approach seemed to enable the students to overcome individual difficulties (139/160) and to set up collaboration (107/160); furthermore, gamification promoted interest (109/160), and the respondents found the immediate feedback from senior professionals to be positive (146/160). In the open-ended survey, the students (23/41) viewed collaborative team- and gamification-based learning positively. Conclusion: This study lends support to the use of gamification in the teaching of histology and may provide a foundation for designing a gamification-integrated curriculum across healthcare disciplines.
MeSH term(s)	Academic Performance ; Curriculum ; Finland ; Games, Experimental ; Histology/education ; Humans ; Internet ; Students, Medical ; Teaching
Language	English
Publishing date	2019-07-22
Publishing country	England
Document type	Journal Article
ZDB-ID	2044473-4
ISSN	1472-6920 ; 1472-6920
ISSN (online)	1472-6920
ISSN	1472-6920
DOI	10.1186/s12909-019-1701-0
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Article ; Online: Diabetic phenotype in mouse and humans reduces the number of microglia around β-amyloid plaques.

Molecular neurodegeneration

2020 Volume 15, Issue 1, Page(s) 66

Abstract: Background: Alzheimer's disease (AD) is the most common neurodegenerative disease and type 2 diabetes (T2D) plays an important role in conferring the risk for AD. Although AD and T2D share common features, the common molecular mechanisms underlying ... ...

Abstract	Background: Alzheimer's disease (AD) is the most common neurodegenerative disease and type 2 diabetes (T2D) plays an important role in conferring the risk for AD. Although AD and T2D share common features, the common molecular mechanisms underlying these two diseases remain elusive. Methods: Mice with different AD- and/or tauopathy-linked genetic backgrounds (APPswe/PS1dE9, Tau P301L and APPswe/PS1dE9/Tau P301L) were fed for 6 months with standard diet or typical Western diet (TWD). After behavioral and metabolic assessments of the mice, the effects of TWD on global gene expression as well as dystrophic neurite and microglia pathology were elucidated. Consequently, mechanistic aspects related to autophagy, cell survival, phagocytic uptake as well as Trem2/Dap12 signaling pathway, were assessed in microglia upon modulation of PI3K-Akt signaling. To evaluate whether the mouse model-derived results translate to human patients, the effects of diabetic phenotype on microglial pathology were assessed in cortical biopsies of idiopathic normal pressure hydrocephalus (iNPH) patients encompassing β-amyloid pathology. Results: TWD led to obesity and diabetic phenotype in all mice regardless of the genetic background. TWD also exacerbated memory and learning impairment in APPswe/PS1dE9 and Tau P301L mice. Gene co-expression network analysis revealed impaired microglial responses to AD-related pathologies in APPswe/PS1dE9 and APPswe/PS1dE9/Tau P301L mice upon TWD, pointing specifically towards aberrant microglial functionality due to altered downstream signaling of Trem2 and PI3K-Akt. Accordingly, fewer microglia, which did not show morphological changes, and increased number of dystrophic neurites around β-amyloid plaques were discovered in the hippocampus of TWD mice. Mechanistic studies in mouse microglia revealed that interference of PI3K-Akt signaling significantly decreased phagocytic uptake and proinflammatory response. Moreover, increased activity of Syk-kinase upon ligand-induced activation of Trem2/Dap12 signaling was detected. Finally, characterization of microglial pathology in cortical biopsies of iNPH patients revealed a significant decrease in the number of microglia per β-amyloid plaque in obese individuals with concomitant T2D as compared to both normal weight and obese individuals without T2D. Conclusions: Collectively, these results suggest that diabetic phenotype in mice and humans mechanistically associates with abnormally reduced microglial responses to β-amyloid pathology and further suggest that AD and T2D share overlapping pathomechanisms, likely involving altered immune function in the brain.
MeSH term(s)	Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Animals ; Brain/metabolism ; Brain/pathology ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/pathology ; Humans ; Mice ; Microglia/metabolism ; Microglia/pathology ; Phenotype ; Plaque, Amyloid/pathology
Language	English
Publishing date	2020-11-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1750-1326
ISSN (online)	1750-1326
DOI	10.1186/s13024-020-00415-2
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Article ; Online: Intranasal insulin activates Akt2 signaling pathway in the hippocampus of wild-type but not in APP/PS1 Alzheimer model mice.

Gabbouj, Sami / Natunen, Teemu / Koivisto, Hennariikka / Jokivarsi, Kimmo / Takalo, Mari / Marttinen, Mikael / Wittrahm, Rebekka / Kemppainen, Susanna / Naderi, Reyhaneh / Posado-Fernández, Adrián / Ryhänen, Simo / Mäkinen, Petra / Paldanius, Kaisa M A / Doria, Gonçalo / Poutiainen, Pekka / Flores, Orfeu / Haapasalo, Annakaisa / Tanila, Heikki / Hiltunen, Mikko

Neurobiology of aging

2018 Volume 75, Page(s) 98–108

Abstract: Type 2 diabetes mellitus (T2DM) increases the risk for Alzheimer's disease (AD). Human AD brains show reduced glucose metabolism as measured by [18F]fluoro-2-deoxy-2-D-glucose positron emission tomography (FDG-PET). Here, we used 14-month-old wild-type ( ... ...

Abstract	Type 2 diabetes mellitus (T2DM) increases the risk for Alzheimer's disease (AD). Human AD brains show reduced glucose metabolism as measured by [18F]fluoro-2-deoxy-2-D-glucose positron emission tomography (FDG-PET). Here, we used 14-month-old wild-type (WT) and APP
MeSH term(s)	Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Animals ; Disease Models, Animal ; Hippocampus/drug effects ; Hippocampus/pathology ; Insulin/metabolism ; Memory/drug effects ; Mice ; Neurons/metabolism ; Presenilin-1/metabolism ; Proto-Oncogene Proteins c-akt/metabolism
Chemical Substances	Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Insulin ; Presenilin-1 ; Akt2 protein, mouse (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2018-11-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604505-4
ISSN	1558-1497 ; 0197-4580
ISSN (online)	1558-1497
ISSN	0197-4580
DOI	10.1016/j.neurobiolaging.2018.11.008
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Article ; Online: SEPT8 modulates β-amyloidogenic processing of APP by affecting the sorting and accumulation of BACE1.

Kurkinen, Kaisa M A / Marttinen, Mikael / Turner, Laura / Natunen, Teemu / Mäkinen, Petra / Haapalinna, Fanni / Sarajärvi, Timo / Gabbouj, Sami / Kurki, Mitja / Paananen, Jussi / Koivisto, Anne M / Rauramaa, Tuomas / Leinonen, Ville / Tanila, Heikki / Soininen, Hilkka / Lucas, Fiona R / Haapasalo, Annakaisa / Hiltunen, Mikko

Journal of cell science

2016 Volume 129, Issue 11, Page(s) 2224–2238

Abstract: Dysfunction and loss of synapses are early pathogenic events in Alzheimer's disease. A central step in the generation of toxic amyloid-β (Aβ) peptides is the cleavage of amyloid precursor protein (APP) by β-site APP-cleaving enzyme (BACE1). Here, we have ...

Abstract	Dysfunction and loss of synapses are early pathogenic events in Alzheimer's disease. A central step in the generation of toxic amyloid-β (Aβ) peptides is the cleavage of amyloid precursor protein (APP) by β-site APP-cleaving enzyme (BACE1). Here, we have elucidated whether downregulation of septin (SEPT) protein family members, which are implicated in synaptic plasticity and vesicular trafficking, affects APP processing and Aβ generation. SEPT8 was found to reduce soluble APPβ and Aβ levels in neuronal cells through a post-translational mechanism leading to decreased levels of BACE1 protein. In the human temporal cortex, we identified alterations in the expression of specific SEPT8 transcript variants in a manner that correlated with Alzheimer's-disease-related neurofibrillary pathology. These changes were associated with altered β-secretase activity. We also discovered that the overexpression of a specific Alzheimer's-disease-associated SEPT8 transcript variant increased the levels of BACE1 and Aβ peptides in neuronal cells. These changes were related to an increased half-life of BACE1 and the localization of BACE1 in recycling endosomes. These data suggest that SEPT8 modulates β-amyloidogenic processing of APP through a mechanism affecting the intracellular sorting and accumulation of BACE1.
MeSH term(s)	Alzheimer Disease/genetics ; Alzheimer Disease/pathology ; Amyloid Precursor Protein Secretases/metabolism ; Amyloid beta-Peptides/metabolism ; Animals ; Aspartic Acid Endopeptidases/metabolism ; Cell Line, Tumor ; Down-Regulation ; Gene Expression Profiling ; HEK293 Cells ; Half-Life ; Hippocampus/pathology ; Humans ; Intracellular Space/metabolism ; Mice, Inbred C57BL ; Models, Biological ; Neurofibrillary Tangles/genetics ; Neurofibrillary Tangles/pathology ; Neurons/metabolism ; Protein Processing, Post-Translational ; Protein Stability ; Protein Transport ; RNA Interference ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Septins/genetics ; Septins/metabolism ; Temporal Lobe/metabolism ; Temporal Lobe/pathology
Chemical Substances	Amyloid beta-Peptides ; RNA, Messenger ; SEPT8 protein, mouse ; Amyloid Precursor Protein Secretases (EC 3.4.-) ; Aspartic Acid Endopeptidases (EC 3.4.23.-) ; BACE1 protein, human (EC 3.4.23.46) ; Bace1 protein, mouse (EC 3.4.23.46) ; SEPTIN8 protein, human (EC 3.6.1.-) ; Septins (EC 3.6.1.-)
Language	English
Publishing date	2016-04-15
Publishing country	England
Document type	Journal Article
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.185215
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Article ; Online: Relationship between ubiquilin-1 and BACE1 in human Alzheimer's disease and APdE9 transgenic mouse brain and cell-based models.

Natunen, Teemu / Takalo, Mari / Kemppainen, Susanna / Leskelä, Stina / Marttinen, Mikael / Kurkinen, Kaisa M A / Pursiheimo, Juha-Pekka / Sarajärvi, Timo / Viswanathan, Jayashree / Gabbouj, Sami / Solje, Eino / Tahvanainen, Eveliina / Pirttimäki, Tiina / Kurki, Mitja / Paananen, Jussi / Rauramaa, Tuomas / Miettinen, Pasi / Mäkinen, Petra / Leinonen, Ville /

Soininen, Hilkka / Airenne, Kari / Tanzi, Rudolph E / Tanila, Heikki / Haapasalo, Annakaisa / Hiltunen, Mikko

Neurobiology of disease

2016 Volume 85, Page(s) 187–205

Abstract: Accumulation of β-amyloid (Aβ) and phosphorylated tau in the brain are central events underlying Alzheimer's disease (AD) pathogenesis. Aβ is generated from amyloid precursor protein (APP) by β-site APP-cleaving enzyme 1 (BACE1) and γ-secretase-mediated ... ...

Abstract	Accumulation of β-amyloid (Aβ) and phosphorylated tau in the brain are central events underlying Alzheimer's disease (AD) pathogenesis. Aβ is generated from amyloid precursor protein (APP) by β-site APP-cleaving enzyme 1 (BACE1) and γ-secretase-mediated cleavages. Ubiquilin-1, a ubiquitin-like protein, genetically associates with AD and affects APP trafficking, processing and degradation. Here, we have investigated ubiquilin-1 expression in human brain in relation to AD-related neurofibrillary pathology and the effects of ubiquilin-1 overexpression on BACE1, tau, neuroinflammation, and neuronal viability in vitro in co-cultures of mouse embryonic primary cortical neurons and microglial cells under acute neuroinflammation as well as neuronal cell lines, and in vivo in the brain of APdE9 transgenic mice at the early phase of the development of Aβ pathology. Ubiquilin-1 expression was decreased in human temporal cortex in relation to the early stages of AD-related neurofibrillary pathology (Braak stages 0-II vs. III-IV). There was a trend towards a positive correlation between ubiquilin-1 and BACE1 protein levels. Consistent with this, ubiquilin-1 overexpression in the neuron-microglia co-cultures with or without the induction of neuroinflammation resulted in a significant increase in endogenously expressed BACE1 levels. Sustained ubiquilin-1 overexpression in the brain of APdE9 mice resulted in a moderate, but insignificant increase in endogenous BACE1 levels and activity, coinciding with increased levels of soluble Aβ40 and Aβ42. BACE1 levels were also significantly increased in neuronal cells co-overexpressing ubiquilin-1 and BACE1. Ubiquilin-1 overexpression led to the stabilization of BACE1 protein levels, potentially through a mechanism involving decreased degradation in the lysosomal compartment. Ubiquilin-1 overexpression did not significantly affect the neuroinflammation response, but decreased neuronal viability in the neuron-microglia co-cultures under neuroinflammation. Taken together, these results suggest that ubiquilin-1 may mechanistically participate in AD molecular pathogenesis by affecting BACE1 and thereby APP processing and Aβ accumulation.
MeSH term(s)	Adaptor Proteins, Vesicular Transport/metabolism ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid Precursor Protein Secretases/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/genetics ; Amyloid beta-Protein Precursor/metabolism ; Animals ; Aspartic Acid Endopeptidases/metabolism ; Brain/metabolism ; Brain/pathology ; Carrier Proteins/metabolism ; Cell Cycle Proteins/metabolism ; Cell Line, Tumor ; Cell Survival/physiology ; Coculture Techniques ; Humans ; Mice, Inbred C57BL ; Mice, Transgenic ; Microglia/metabolism ; Microglia/pathology ; Neurons/metabolism ; Neurons/pathology ; Peptide Fragments/metabolism ; tau Proteins/metabolism
Chemical Substances	APP protein, human ; Adaptor Proteins, Vesicular Transport ; Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Carrier Proteins ; Cell Cycle Proteins ; MAPT protein, human ; Peptide Fragments ; UBQLN1 protein, human ; UBQLN1 protein, mouse ; amyloid beta-protein (1-40) ; amyloid beta-protein (1-42) ; tau Proteins ; Amyloid Precursor Protein Secretases (EC 3.4.-) ; Aspartic Acid Endopeptidases (EC 3.4.23.-) ; BACE1 protein, human (EC 3.4.23.46) ; Bace1 protein, mouse (EC 3.4.23.46)
Language	English
Publishing date	2016-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2015.11.005
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Article: Molecular Mechanisms of Synaptotoxicity and Neuroinflammation in Alzheimer's Disease.

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Article: Altered Insulin Signaling in Alzheimer's Disease Brain - Special Emphasis on PI3K-Akt Pathway.

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Article ; Online: Using online game-based platforms to improve student performance and engagement in histology teaching.

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Article ; Online: Diabetic phenotype in mouse and humans reduces the number of microglia around β-amyloid plaques.

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Article ; Online: Intranasal insulin activates Akt2 signaling pathway in the hippocampus of wild-type but not in APP/PS1 Alzheimer model mice.

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Article ; Online: SEPT8 modulates β-amyloidogenic processing of APP by affecting the sorting and accumulation of BACE1.

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Article ; Online: Relationship between ubiquilin-1 and BACE1 in human Alzheimer's disease and APdE9 transgenic mouse brain and cell-based models.

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