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Home: Community: Researcher Profiles
Researcher Profile

RESEARCHER INFORMATION
First Name:Jin-Jing
Last Name:Pei
Title:Associate Professor
Advanced Degrees:PhD, MD
Affiliation:Karolinska Institutet
Department:Neurotec
Street Address 1:Novum plan 5
Street Address 2:Geriatric-lab
State/Province:Stockholm
Zip/Postal Code:14157
Country/Territory:Sweden
Phone:46-8-58583649
Fax:46-8-58583880
Email Address: 
Disclosure:
(view policy) 
 
View all comments by Jin-Jing Pei
Clinical Interests:
Alzheimer Disease, Polyglutamine Disorders (Huntington's, etc.), Prion Diseases, Aging Process, Tauopathies, Parkinson Disease, Neurodevelopmental Disorders (Down syndrome, etc.), Stroke and Trauma, Neuromuscular Disorders (ALS, etc.)
Research Focus:
Diagnosis, Signal transduction, Brain imaging, Neuropathology, Chemistry/Pharmacology, Proteomics, A-beta PP/A-beta, Molecular and Cell biology, Drug screening, Tau/Cytoskeleton, Genetics, Microscopy, Neurobiology, Bioinformatics/Statistics, Oxidative Stress, Protein structure/chemistry, Electrophysiology, Animal Models, Apoptosis/Cell cycle, Neurotransmission, Stem cells
Work Sector(s):
Medical hospital, Research institute, University
Web Sites:
Lab: http://www.neurotec.ki.se/ExpGer/jinjing.htm
Top Papers
1.Jin-Jing Pei, Toshihisa Tanaka, Yunn-Chyn Tung, Eva Braak, Khalid Iqbal, and Inge Grundke-Iqbal. Glycogen synthase kinase-3: Distribution, Levels and Activity of Glycogen Synthase Kinase-3 in the Alzheimer Disease Brain. Journal of Neuropathology and Experimental Neurology 56 (1997): 70-78.
2.Jin-Jing Pei*, Eva Braak, Heiko Braak, Inge Grundke-Iqbal, Khalid Iqbal, Bengt Winblad and Richard F. Cowburn. Distribution of active glycogen synthase kinase 3b (GSK-3b) in brains staged for Alzheimer’s disease neurofibrillary changes. Journal of Neuropathology and Experimental Neurology 58 (1999): 1010-1019.
3.Jin-Jing Pei, Cheng-Xin Gong, Wen-Lin An, Bengt Winblad, Richard F. Cowburn, Inge Grundke-Iqbal, Khalid Iqbal. Okadaic acid-induced inhibition of protein phosphatase 2A produces activation of mitogen-activated protein kinases ERK1/2, MEK1/2 and p70 S6 similar to that in Alzheimer’s disease. American Journal of Pathology 163 (2003): 845-58.
4.Jin-Jing Pei*, Sabiha Khatoon, Wen-Lin An, Maria Nordlinder, Toshihisa Tanaka, Heiko Braak, Ichiro Tsujio, Masatoshi Takeda, Irina Alafuzoff, Bengt Winblad, Richard Cowburn, Inge Grundke-Iqbal, Khalid Iqbal. Role of protein kinase B in Alzheimer's neurofibrillary degeneration. Acta Neuropathologica 105 (2003): 381-392.
5.Wen-Lin An, Richard F Cowburn, Lin Li, Heiko Braak, Irina Alafuzoff, Khalid Iqbal, Inge-Grundke Iqbal, Bengt Winblad, Jin-Jing Pei*. Up-regulation of phosphorylated/activated p70 S6 kinase and its relationship to neurofibrillary pathology in Alzheimer’s disease. American Journal of Pathology 163 2003): 591-607.
6.Wen-Lin An, Cecilia Bjorkdahl, Rong Liu, Richard F Cowburn, Bengt Winblad, Jin-Jing Pei*. Mechanism of zinc-induced phosphorylation of p70 S6 kinase and glycogen synthase kinase 3b in SH-SY5Y neuroblastoma cells. J Neurochem 92 (2005): 1104-1115.
7.Cecilia Bjorkdahl, Magnus Sjögren, Bengt Winblad B, Jin-Jing Pei*. Zinc induces neurofilament phosphorylation independent of p70 S6 kinase in N2a cells. NeuroReport 16 (2005): 591-595.
8.Xu Li, Irina Alafuzoff, Hilkka Soininen, Bengt Winblad, Jin-Jing Pei*. Levels of mTOR and its downstream targets 4E-BP1, eEF2, and eEF2 kinase in relationships with tau in Alzheimer’s disease brain. FEBS Journal 272 (2005):4211-20.
9.Jin-Jing Pei*, Wen-Lin An, Xin-Wen Zhou, Takeshi Nishimura, Jan Norberg, Eirkur Benedikz, Jürgen Götz, Bengt Winblad. P70 S6 kinase mediates tau phosphorylation and synthesis. FEBS Lett. 580 (2006):107-14.
10.Xinwen Zhou, Xu Li, Cecilia Bjorkdahl, Magnus J Sjogren, Irina Alafuzoff, Hilkka Soininen, Inge Grundke-Iqbal, Khalid Iqbal, Bengt Winblad, Jin-Jing Pei*. Assessments of the accumulation severities of amyloid ß-protein and hyperphosphorylated tau in the medial temporal cortex of control and Alzheimer's brains. Neurobiology of Disease (in press).
What is the greatest void to date in our knowledge of Alzheimer's Disease?
no cure
If resources were not limited, what research projects would you pursue?
Animal models based on the targets we have characterized
What is your leading hypothesis?
Upregulation of protein kinases such as GSK-3 play a key role in tau tangle formation

De-regulation of mTOR /p70 S6 kinase signalling plays a dual role in tau tangle formation: tau synthesis and phosphorylation
What piece of missing evidence would help prove it?
animal models

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