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| First Name: | Taher | | Last Name: | Darreh-Shori | | Title: | Ph.D. | | Affiliation: | Karolinska Institutet | | Department: | Department of Neurobiology, Care Sciences and Society | | Street Address 1: | Division of Alzheimer Neurobiology, | | Street Address 2: | Novum, 4th Floor , Room 4F23:10 | | City: | Stockholm | | State/Province: | Stockholm | | Zip/Postal Code: | 141 86 | Country/Territory: | Sweden | | Phone: | 46-8-58583612 | | Email Address: |  |
Disclosure:
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Member reports no financial or other potential conflicts of interest. [Last Modified: 2 July 2010]
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View all comments by Taher Darreh-Shori
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Neurobiology, Chemistry/Pharmacology, Neurotransmission, Protein structure/chemistry, A-beta PP/A-beta, Molecular and Cell biology, Neuropathology, Clinical trials, Oxidative Stress, Diagnosis, Proteomics, Neuroimmunology, Stem cells, Genetics
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Research institute, University
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1. Darreh-Shori T, Forsberg A, Modiri N, Andreasen N, Blennow K, Kamil C, Ahmed H, Almkvist O, Langstrom B, Nordberg A. Differential levels of apolipoprotein E and butyrylcholinesterase show strong association with pathological signs of Alzheimer's disease in the brain in vivo. Neurobiology of aging 2010. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=20538374
2. Darreh-Shori T, Modiri N, Blennow K, Baza S, Kamil C, Ahmed H, Andreasen N, Nordberg A. The apolipoprotein E varepsilon4 allele plays pathological roles in AD through high protein expression and interaction with butyrylcholinesterase. Neurobiology of aging 2009.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=19713000
3. Darreh-Shori T, Brimijoin S, Kadir A, Almkvist O, Nordberg A. Differential CSF butyrylcholinesterase levels in Alzheimer's disease patients with the ApoE epsilon4 allele, in relation to cognitive function and cerebral glucose metabolism. Neurobiology of disease 2006;24:326-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16973370
4. Ferris S, Nordberg A, Soininen H, Darreh-Shori T, Lane R. Progression from mild cognitive impairment to Alzheimer's disease: effects of sex, butyrylcholinesterase genotype, and rivastigmine treatment. Pharmacogenetics and genomics 2009;19:635-46. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=19617863
5. Lane R, Feldman HH, Meyer J, He Y, Ferris SH, Nordberg A, Darreh-Shori T, Soininen H, Pirttila T, Farlow MR, Sfikas N, Ballard C, Greig NH. Synergistic effect of apolipoprotein E epsilon4 and butyrylcholinesterase K-variant on progression from mild cognitive impairment to Alzheimer's disease. Pharmacogenetics and genomics 2008;18:289-98. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18334913
6. Darreh-Shori T, Almkvist O, Guan ZZ, Garlind A, Strandberg B, Svensson AL, Soreq H, Hellstrom-Lindahl E, Nordberg A. Sustained cholinesterase inhibition in AD patients receiving rivastigmine for 12 months. Neurology 2002;59:563-72.
7. Darreh-Shori T, Hellstrom-Lindahl E, Flores-Flores C, Guan ZZ, Soreq H, Nordberg A. Long-lasting acetylcholinesterase splice variations in anticholinesterase-treated Alzheimer's disease patients. Journal of neurochemistry 2004;88:1102-13.
8. Darreh-Shori T, Kadir A, Almkvist O, Grut M, Wall A, Blomquist G, Eriksson B, Langstrom B, Nordberg A. Inhibition of acetylcholinesterase in CSF versus brain assessed by 11C-PMP PET in AD patients treated with galantamine. Neurobiology of aging 2008;29:168-84.
9. Darreh-Shori T, Meurling L, Pettersson T, Hugosson K, Hellstrom-Lindahl E, Andreasen N, Minthon L, Nordberg A. Changes in the activity and protein levels of CSF acetylcholinesterases in relation to cognitive function of patients with mild Alzheimer's disease following chronic donepezil treatment. J Neural Transm 2006;113:1791-801.
10. Kadir A, Darreh-Shori T, Almkvist O, Wall A, Grut M, Strandberg B, Ringheim A, Eriksson B, Blomquist G, Langstrom B, Nordberg A. PET imaging of the in vivo brain acetylcholinesterase activity and nicotine binding in galantamine-treated patients with AD. Neurobiology of aging 2008;29:1204-17.
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The lack of good and reliable disease models. |
To understand mechanism that undermine the activity and survival of cholinergic and cholinoceptive neurons and other non-excitable cells in the AD brain. |
ApoE and Amyloid-beta undermine the cholinergic system through physical interaction with cholinesterase which leads to formation of soluble BuChE/AChE-ABeta-ApoE complexes (BABA-C)with extensive ACh-hydrolyzing capacities. This would leads a gradual but consistent undermining of activity and survival of Cholinergic and cholinoceptive neurons during the AD continuum.(Darreh-Shori, T., et al. Differential levels of apolipoprotein E and butyrylcholinesterase show strong association with pathological signs of Alzheimer's disease in the brain in vivo. Neurobiology of aging (2010)). |
To isolate and show presence of the BABA-C in the AD CSF and brain homogenates. |
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