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Anna Matton

Assistant professor

Postal address : Department of Neurobiology, Care Sciences and Society (NVS), H1, Division of Neurogeriatrics, Novum Pl 5 14157 Huddinge, Sweden

About me

My background is in biomedicine (Lund University) and my research focus lie within the field of neuroscience. After accomplishing my PhD on Parkinson disease mechanisms from Karolinska Institutet and National Institute of Health (USA) I started my postdoc switching to studies on the molecular mechanisms of Alzheimer disease. Since 2015, I’m part of Miia Kivipelto’s research group and Angel Cedazo-Minguez’s group. The goal of my research is to understand more on the molecular basis of prevention and risk in Alzheimer disease.

Research description

Alzheimer disease is a devastating disorder with a steadily increasing number of affected. A number of risk factors for Alzheimer disease have been identified and preventive interventions in dementia is an important step to delay disease onset and disease progression. My goal is to gain more understanding of the biology behind prevention and risk for Alzheimer disease. By investigating how genes and environment affect the brain at a molecular level, we can pinpoint the target molecules and in the future develop more individualized therapies and preventive interventions. Specifically I'm studying cellular mechanisms related to ApoE genotype and cholesterol metabolism and utilize a combination of clinical samples (brain, CSF, blood) transgenic models and cell lines.  

Publications

Modulation of the endoplasmic reticulum-mitochondria interface in Alzheimer's disease and related models
Hedskog L, Pinho Cm, Filadi R, Rönnbäck A, Hertwig L, Wiehager B, et al
Proceedings of the National Academy of Sciences of the United States of America 2013;110(19):7916-21

The pathogenic aβ43 is enriched in familial and sporadic Alzheimer disease
Sandebring A, Welander H, Winblad B, Graff C, Tjernberg Lo
PloS one 2013;8(2):e55847-

Identification of two novel synaptic γ-secretase associated proteins that affect amyloid β-peptide levels without altering Notch processing
Frykman S, Teranishi Y, Hur Jy, Sandebring A, Yamamoto Ng, Ancarcrona M, et al
Neurochemistry international 2012;61(1):108-18

Thioredoxin-80 is a product of alpha-secretase cleavage that inhibits amyloid-beta aggregation and is decreased in Alzheimer's disease brain
Gil-bea F, Akterin S, Persson T, Mateos L, Sandebring A, Avila-cariño J, et al
EMBO molecular medicine 2012;4(10):1097-111

DJ-1 acts in parallel to the PINK1/parkin pathway to control mitochondrial function and autophagy
Thomas Kj, Mccoy Mk, Blackinton J, Beilina A, Van Der Brug M, Sandebring A, et al
HUMAN MOLECULAR GENETICS 2011;20(1):40-50

Mitochondrial alterations in PINK1 deficient cells are influenced by calcineurin-dependent dephosphorylation of dynamin-related protein 1
Sandebring A, Thomas Kj, Beilina A, Van Der Brug M, Cleland Mm, Ahmad R, et al
PloS one 2009;4(5):e5701-

Parkin deficiency disrupts calcium homeostasis by modulating phospholipase C signalling
Sandebring A, Dehvari N, Perez-manso M, Thomas Kj, Karpilovski E, Cookson Mr, et al
FEBS JOURNAL 2009;276(18):5041-52

Parkin-mediated ubiquitination regulates phospholipase C-gamma 1
Dehvari N, Sandebring A, Flores-morales A, Mateos L, Chuan Yc, Goldberg Ms, et al
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE 2009;13(9B):3061-8

Altered mitochondrial dynamics caused by loss of PTEN-induced kinase 1 function, associated with recessive parkinsonism, are reversed by downregulation of Dynamin-related protein 1
Thomas Kj, Sandebring A, Beilina A, Van Der Brug M, Cleland Mm, Zambrano I, et al
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS 2008;:S55-S55

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