دورية أكاديمية
أعرض في EDS

Alzheimer disease-related presenilin-1 variants exert distinct effects on monoamine oxidase-A activity in vitro.

التفاصيل البيبلوغرافية
العنوان: Alzheimer disease-related presenilin-1 variants exert distinct effects on monoamine oxidase-A activity in vitro.
المؤلفون: Pennington PR; Cell Signalling Laboratory, Department of Psychiatry, University of Saskatchewan, B45 HSB, 107 Wiggins Rd, Saskatoon, SK, S7N 5E5, Canada., Wei Z, Rui L, Doig JA, Graham B, Kuski K, Gabriel GG, Mousseau DD
المصدر: Journal of neural transmission (Vienna, Austria : 1996) [J Neural Transm (Vienna)] 2011 Jul; Vol. 118 (7), pp. 987-95. Date of Electronic Publication: 2011 Mar 04.
نوع المنشور: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Springer-Verlag Country of Publication: Austria NLM ID: 9702341 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1435-1463 (Electronic) Linking ISSN: 03009564 NLM ISO Abbreviation: J Neural Transm (Vienna) Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Wien ; New York : Springer-Verlag, 1996-
مواضيع طبية MeSH: Genetic Variation*, Alzheimer Disease/*enzymology , Depressive Disorder/*enzymology , Monoamine Oxidase/*metabolism , Neurons/*enzymology , Presenilin-1/*genetics, Alzheimer Disease/genetics ; Alzheimer Disease/pathology ; Animals ; Cell Line, Transformed ; Cell Line, Tumor ; Depressive Disorder/genetics ; Depressive Disorder/pathology ; HEK293 Cells ; Humans ; Mice ; Neuroblastoma/enzymology ; Neuroblastoma/pathology ; Neurons/cytology ; Presenilin-1/physiology
مستخلص: Monoamine oxidase-A (MAO-A) has been associated with both depression and Alzheimer disease (AD). Recently, carriers of AD-related presenilin-1 (PS-1) alleles have been found to be at higher risk for developing clinical depression. We chose to examine whether PS-1 could influence MAO-A function in vitro. Overexpression of selected AD-related PS-1 variants (wildtype, Y115H, ΔEx9 and M146V) in mouse hippocampal HT-22 cells affects MAO-A catalytic activity in a variant-specific manner. The ability of the PS-1 substrate-competitor DAPT to induce MAO-A activity in cells expressing either PS-1 wildtype or PS-1(M146V) suggests the potential for a direct influence of PS-1 on MAO-A function. In support of this, we were able to co-immunoprecipitate MAO-A with FLAG-tagged PS-1 wildtype and M146V proteins. This potential for a direct protein-protein interaction between PS-1 and MAO-A is not specific for HT-22 cells as we were also able to co-immunoprecipitate MAO-A with FLAG-PS-1 variants in N2a mouse neuroblastoma cells and in HEK293 human embryonic kidney cells. Finally, we demonstrate that the two PS-1 variants reported to be associated with an increased incidence of clinical depression [e.g., A431E and L235V] both induce MAO-A activity in HT-22 cells. A direct influence of PS-1 variants on MAO-A function could provide an explanation for the changes in monoaminergic tone observed in several neurodegenerative processes including AD. The ability to induce MAO-A catalytic activity with a PS-1/γ-secretase inhibitor should also be considered when designing secretase inhibitor-based therapeutics.
References: Proc Natl Acad Sci U S A. 2007 Jan 9;104(2):403-9. (PMID: 17197420)
Behav Brain Res. 2007 Mar 12;178(1):18-28. (PMID: 17229472)
Biochem Biophys Res Commun. 2002 Jul 19;295(3):766-70. (PMID: 12099705)
Neurosci Lett. 2002 Jul 19;327(2):79-82. (PMID: 12098640)
Neurobiol Aging. 2007 Mar;28(3):327-35. (PMID: 16574280)
Biochem Biophys Res Commun. 2003 Jan 31;301(1):119-26. (PMID: 12535650)
Neurology. 2008 Apr 8;70(15):1258-64. (PMID: 18391157)
J Neural Transm Park Dis Dement Sect. 1992;4(3):227-40. (PMID: 1627256)
J Biol Chem. 2001 Apr 13;276(15):11539-44. (PMID: 11278803)
J Biol Chem. 2009 Feb 20;284(8):4749-53. (PMID: 18845536)
Psychopharmacology (Berl). 1992;106 Suppl:S137-9. (PMID: 1546130)
Cell Signal. 2009 Jan;21(1):161-8. (PMID: 18951975)
Neuroscience. 1994 Sep;62(1):15-30. (PMID: 7816197)
J Alzheimers Dis. 2010;20 Suppl 2:S499-512. (PMID: 20413847)
Izv Akad Nauk Ser Biol. 2003 Sep-Oct;(5):542-6. (PMID: 14735783)
J Biol Chem. 2004 Dec 3;279(49):51654-60. (PMID: 15456764)
Arch Gen Psychiatry. 2006 Nov;63(11):1209-16. (PMID: 17088501)
Brain Res. 2007 Sep 5;1167:13-9. (PMID: 17692293)
Brain Res. 2002 Sep 13;949(1-2):105-11. (PMID: 12213305)
EMBO Rep. 2001 Sep;2(9):835-41. (PMID: 11520861)
Nat Neurosci. 2006 Nov;9(11):1354-5. (PMID: 17066063)
Prog Neurobiol. 2010 Aug;91(4):362-75. (PMID: 20441786)
Neurology. 1987 Oct;37(10):1630-3. (PMID: 3658170)
Life Sci. 2009 Jul 31;85(5-6):262-8. (PMID: 19539632)
J Neurol Neurosurg Psychiatry. 2004 Dec;75(12):1662-6. (PMID: 15548477)
Neurobiol Aging. 2005 Apr;26(4):429-38. (PMID: 15653171)
Nat Med. 2006 Nov;12(11):1241-3. (PMID: 17088888)
J Biol Chem. 1997 Nov 7;272(45):28415-22. (PMID: 9353300)
Acta Neuropathol. 1966 Mar 4;6(2):181-7. (PMID: 5963288)
J Neural Transm (Vienna). 2003 Jul;110(7):789-801. (PMID: 12811639)
Neurosci Lett. 1986 Mar 14;64(3):247-52. (PMID: 3960404)
Hum Mol Genet. 2006 May 1;15(9):1437-49. (PMID: 16551656)
J Neurol Neurosurg Psychiatry. 2004 Mar;75(3):500-2. (PMID: 14966176)
J Biol Chem. 2009 Feb 20;284(8):4755-9. (PMID: 18957434)
J Affect Disord. 2009 Sep;117(1-2):24-9. (PMID: 19138799)
Science. 2009 Jul 24;325(5939):403-4. (PMID: 19628848)
Nat Med. 1999 Jan;5(1):101-6. (PMID: 9883847)
Can J Neurol Sci. 2001 Feb;28 Suppl 1:S83-95. (PMID: 11237316)
J Mol Neurosci. 2005;27(2):213-7. (PMID: 16186632)
J Neurosci. 2008 Dec 17;28(51):13805-14. (PMID: 19091971)
Ann Neurol. 1988 Aug;24(2):233-42. (PMID: 3178178)
J Neuropathol Exp Neurol. 1984 Jul;43(4):359-68. (PMID: 6737007)
Neurotoxicology. 2004 Jan;25(1-2):101-15. (PMID: 14697885)
Eur J Pharmacol. 2010 Jan 10;626(1):64-71. (PMID: 19837057)
J Neurochem. 2009 Oct;111(1):101-10. (PMID: 19650872)
Ann Neurol. 2001 Jan;49(1):53-66. (PMID: 11198297)
Neurobiol Dis. 2004 Aug;16(3):572-80. (PMID: 15262269)
Dementia. 1993 Jan-Feb;4(1):1-15. (PMID: 8358501)
Nat Cell Biol. 2000 Apr;2(4):205-11. (PMID: 10783238)
J Biol Chem. 2006 May 26;281(21):14670-6. (PMID: 16569643)
FEBS Lett. 2003 Aug 28;550(1-3):30-4. (PMID: 12935881)
BMC Neurosci. 2007 Sep 16;8:73. (PMID: 17868476)
J Biol Chem. 2005 Sep 9;280(36):31537-47. (PMID: 16014629)
Neuron. 1996 Nov;17(5):1023-30. (PMID: 8938133)
J Neurochem. 1984 Aug;43(2):388-93. (PMID: 6204013)
Neuropathol Appl Neurobiol. 2000 Dec;26(6):553-67. (PMID: 11123722)
Neurology. 1999 Dec 10;53(9):1998-2002. (PMID: 10599771)
J Am Geriatr Soc. 1986 Aug;34(8):561-4. (PMID: 3722676)
Neuron. 1996 Jul;17(1):181-90. (PMID: 8755489)
Int Psychogeriatr. 2003 Dec;15(4):337-49. (PMID: 15000414)
معلومات مُعتمدة: Canada Canadian Institutes of Health Research
المشرفين على المادة: 0 (Presenilin-1)
EC 1.4.3.4 (Monoamine Oxidase)
تواريخ الأحداث: Date Created: 20110305 Date Completed: 20120522 Latest Revision: 20211020
رمز التحديث: 20231215
DOI: 10.1007/s00702-011-0616-7
PMID: 21373759
قاعدة البيانات: MEDLINE
الوصف
تدمد:1435-1463
DOI:10.1007/s00702-011-0616-7