Hostname: page-component-586b7cd67f-t7fkt Total loading time: 0 Render date: 2024-11-28T00:48:40.881Z Has data issue: false hasContentIssue false
  • English
  • Français

Unchanged rat brain amyloid precursor protein levels after exposure to benzodiazepines in vivo

Published online by Cambridge University Press:  12 June 2006

J. Kálmán ,
M. Palotás ,
M. Pákáski ,
M. Hugyecz ,
Z. Janka  and
A. Palotás
J. Kálmán
Affiliation:
University of Szeged, Department of Psychiatry, Szeged, Hungary
M. Palotás
Affiliation:
University of Szeged, Department of Psychiatry, Szeged, Hungary University of Szeged, Department of Anesthesiology and Intensive Therapy, Szeged, Hungary
M. Pákáski
Affiliation:
University of Szeged, Department of Psychiatry, Szeged, Hungary
M. Hugyecz
Affiliation:
University of Szeged, Department of Psychiatry, Szeged, Hungary
Z. Janka
Affiliation:
University of Szeged, Department of Psychiatry, Szeged, Hungary
A. Palotás
Affiliation:
University of Szeged, Department of Psychiatry, Szeged, Hungary University of Szeged, Department of Center for Cardiology, Division of Cardiac Surgery, Albert Szent-Györgyi Medical and Pharmaceutical Center, Szeged, Hungary
Get access

Abstract

Summary

Background and objective: Recent studies emphasize a positive correlation between (cardiac) surgical interventions and increased risk for developing Alzheimer's disease in the late postoperative period. Since amyloid precursor protein and its neurotoxic derivatives play key roles in the development of Alzheimer's dementia, the impact of several agents used in the intra- and perioperative period is examined. Method: Amyloid precursor protein concentrations were assessed by semi-quantitative Western-immunoblot in brains of rats following intraperitoneal treatment with diazepam and midazolam. Results: There were no significant changes in the amyloid precursor protein concentrations. Conclusion: Both diazepam and midazolam are considered to be relatively safe with respect to amyloid precursor protein metabolism.

Keywords

ANAESTHESIA GENERALBENZODIAZEPINES, diazepam, midazolamALZHEIMER DISEASEAMYLOID BETA-PROTEIN PRECURSORPOSTOPERATIVE PERIOD, cognitive dysfunction
Type
Original Article
Information
European Journal of Anaesthesiology , Volume 23 , Issue 9 , September 2006 , pp. 772 - 775
Copyright
2006 European Society of Anaesthesiology

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Roach GW, Kanchuger M, Mangano CMet al. Adverse cerebral outcomes after coronary bypass surgery. Multicenter study of perioperative ischemia research group and the ischemia research and education foundation investigators. New Engl J Med 1996; 335: 1857–1863.Google Scholar
Mullges W, Berg D, Schmidtke A, Weinacker B, Toyka KV. Early natural course of transient encephalopathy after coronary artery bypass grafting. Crit Care Med 2000; 28: 1808–1811.Google Scholar
Bohnen NI, Warner MA, Kokmen E, Beard CM, Kurland LT. Alzheimer's disease and cumulative exposure to anesthesia: a case-control study. J Am Geriatr Soc 1994; 42: 198–201.Google Scholar
Breteler MM, van Duijn CM, Chandra Vet al. Medical history and the risk of Alzheimer's disease: a collaborative re-analysis of case-control studies. EURODEM risk factors research group. Int J Epidemiol 1991; 20: S36–S42.Google Scholar
Gasparini M, Vanacore N, Schiaffini Cet al. A case-control study on Alzheimer's disease and exposure to anesthesia. Neurol Sci 2002; 23: 11–14.Google Scholar
Brown WR, Moody DM, Tytell M, Ghazi-Birry HS, Challa VR. Microembolic brain injuries from cardiac surgery: are they seeds of future Alzheimer's disease? Ann N Y Acad Sci 1997; 826: 386–389.Google Scholar
Newman MF, Kirchner JL, Phillips-Bute Bet al. Longitudinal assessment of neurocognitive function after coronary artery bypass surgery. N Engl J Med 2001; 344: 395–402.Google Scholar
Selnes OA, Royall RM, Grega MA, Borowicz JrLM, Quaskey S, McKhann GM. Cognitive changes 5 years after coronary artery bypass grafting is there evidence of late decline? Arch Neurol 2001; 58: 598–604.Google Scholar
Selkoe DJ, Abraham CR, Podlisny MB, Duffy LK. Isolation of low-molecular-weight proteins from amyloid plaque fibers in Alzheimer's disease. J Neurochem 1986; 46: 1820–1834.Google Scholar
Stephenson DT, Rash K, Clemens JA. Amyloid precursor protein accumulates in regions of neurodegeneration following focal cerebral ischemia in the rat. Brain Res 1992; 593: 128–135.Google Scholar
Hess HH, Lees MB, Derr JE. A linear Lowry–Folin assay for both water-soluble and sodium dodecyl sulfate-solubilized proteins. Ann Biochem 1978; 85: 295–300.Google Scholar
Farr SA, Uezu K, Flood JF, Morley JE. Septohippocampal drug interactions in post-trial memory processing. Brain Res 1999; 847: 221–230.Google Scholar
Fastbom J, Forsell Y, Winblad B. Benzodiazepines may have protective effects against Alzheimer disease. Alzheimer Dis Assoc Disord 1998; 12: 14–17.Google Scholar
Lowe SL, Francis PT, Procter AW, Palmer AM, Davison AN, Bowen DM. Gamma-aminobutyric acid concentration in brain tissue at two stages of Alzheimer's disease. Brain 1988; 111: 785–799.Google Scholar
Rossor MN, Garrett NJ, Johnson AL, Mountjoy CQ, Roth M, Iversen LL. A post-mortem study of the cholinergic and GABA systems in senile dementia. Brain 1982; 105: 313–330.Google Scholar
Churcher I, Ashton K, Butcher JWet al. A new series of potent benzodiazepine γ-secretase inhibitors. Bioorg Med Chem Lett 2003; 13: 179–183.Google Scholar
Lund C, Hol PK, Lundblad Ret al. Comparison of cerebral embolization during off-pump and on-pump coronary artery bypass surgery. Ann Thorac Surg 2003; 76: 765–770.Google Scholar
Russell D. Cerebral microemboli and cognitive impairment. J. Neurol Sci 2002; 203–204, 211–214.Google Scholar
Palotás A, Bogáts G, Babik Bet al. Coronary artery bypass surgery provokes Alzheimer's disease-like changes in the cerebrospinal fluid. 2005 (submitted).Google Scholar
Kálmán J, Juhász A, Bogáts G, Babik B, Ramanóczy Á, Janka Z, Penke B, Palotás A. Elevated levels of inflammatory biomarkers in the cerebrospinal fluid after coronary artery bypass surgery are predictors of cognitive decline. Neurochem Int 2006; 48 (3): 177–180.Google Scholar