뇌척수액과 말초혈액 내 알츠하이머병의 생화학적 생체표지자
Biochemical Biomarkers for Alzheimer’s Disease in Cerebrospinal Fluid and Peripheral Blood
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초록
The diagnosis of Alzheimer’s disease (AD) is still obscure even to specialists. To improve the diagnostic accuracy, to find at-risk people as early as possible, to predict the efficacy or adverse reactions of pharmacotherapy on an individual basis, to attain more reli- able results of clinical trials by recruiting better defined participants, to prove the disease-modifying ability of new candidate drugs, to establish prognosis-based therapeutic plans, and to do more, is now increasing the need for biomarkers for AD. Among AD-related biochemical markers, cerebrospinal beta-amyloid and tau have been paid the most attention since they are materials directly interfac- ing the brain interstitium and can be obtained through the lumbar puncture. Level of beta-amyloid is reduced whereas tau is increased in cerebrospinal fluid of AD patients relative to cognitively normal elderly people. Remarkably, such information has been found to help predict AD conversion of mild cognitive impairment. Despite inconsistent findings from previous studies, plasma beta-amyloid is thought to be increased before the disease onset, but show decreasing change as the disease progress. Regarding other peripheral biochemical markers, omics tools are being widely used not only to find useful biomarkers but also to generate novel hypotheses for AD pathogenesis and to lead new personalized future medicine.
Abstract
The diagnosis of Alzheimer’s disease (AD) is still obscure even to specialists. To improve the diagnostic accuracy, to find at-risk people as early as possible, to predict the efficacy or adverse reactions of pharmacotherapy on an individual basis, to attain more reli- able results of clinical trials by recruiting better defined participants, to prove the disease-modifying ability of new candidate drugs, to establish prognosis-based therapeutic plans, and to do more, is now increasing the need for biomarkers for AD. Among AD-related biochemical markers, cerebrospinal beta-amyloid and tau have been paid the most attention since they are materials directly interfac- ing the brain interstitium and can be obtained through the lumbar puncture. Level of beta-amyloid is reduced whereas tau is increased in cerebrospinal fluid of AD patients relative to cognitively normal elderly people. Remarkably, such information has been found to help predict AD conversion of mild cognitive impairment. Despite inconsistent findings from previous studies, plasma beta-amyloid is thought to be increased before the disease onset, but show decreasing change as the disease progress. Regarding other peripheral biochemical markers, omics tools are being widely used not only to find useful biomarkers but also to generate novel hypotheses for AD pathogenesis and to lead new personalized future medicine.
참고문헌 (41)
- Jack CR Jr, "Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade", Lancet Neurol, 9, pp.119~128 (2010)
- Strozyk D, "CSF Aβ 42 levels correlate with amyloid-neuropathology in a population-based autopsy study", Neurology, 60, pp.652~656 (2003)
- Hampel H, "Measurement of phosphorylated tau epitopes in the differential diagnosis of Alzheimer disease: a comparative cerebrospinal fluid study", Arch Gen Psychiatry, 1, pp.95~102 (2004)
- Hampel H, "Core biological marker candidates of Alzheimer’s disease-perspectives for diagnosis, prediction of outcome and reflection of biological activity", J Neural Transm, 111, pp.247~272 (2004)
- De Meyer G, "Diagnosis-independent Alzheimer disease biomarker signature in cognitively normal elderly people", Arch Neurol, 67, pp.949~956 (2010)
- Steinerman JR, "Laboratory biomarkers in Alzheimer’s disease", Curr Neurol Neurosci Rep, 7, pp.381~387 (2007)
- Mulugeta E, "CSF amyloid beta38 as a no-vel diagnostic marker for dementia with Lewy bodies", J Neurol Neurosurg Psychiatry, 82, pp.160~164 (2011)
- Riemenschneider M, "Tau and Aβ42 protein in CSF of patients with frontotemporal degeneration", Neurology, 58, pp.1622~1628 (2002)
- Riemenschneider M, "Phospho-tau", total tau ratio in cerebrospinal fluid discriminates Creutz-feldt-Jakob disease from other dementias, 2003, pp.8, 343~347
- McKhann GM, "The diagnosis of dementia due to Alzheimer’s disease: recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease", Alzheimers Dement, 7, pp.263~269 (2011)
- Dubois B, "Research criteria for the diagnosis of Alzheimer’s disease: revising the NINCDS-ADRDA criteria", Lancet Neurol, 6, pp.734~746 (2007)
- Siemers ER, "How can we recognize “disease modification” effects", J Nutr Health Aging, 13, pp.341~343 (2009)
- Diniz BS, "Do CSF total tau, phosphorylated tau, and beta-amyloid 42 help to predict progression of mild cognitive impairment to Alzheimer’s disease? A systematic review and meta-analysis of the literature", World J Biol Psychiatry, 9, pp.172~182 (2008)
- Visser PJ, "Prevalence and prognostic value of CSF markers of Alzheimer’s disease pathology in patients with subjective cognitive impairment or mild cognitive impairment in the DESCRIPA study: a prospective cohort study", Lancet Neurol, 8, pp.619~627 (2009)
- Mattsson N, "CSF biomarkers and incipient Alzheimer disease in patients with mild cognitive impairment", JAMA, 302, pp.385~393 (2009)
- Hampel H, "Value of CSF beta-amyloid1-42 and tau as predictors of Alzheimer’s disease in patientswith mild cognitive impairment", Mol Psychiatry, 9, pp.705~710 (2004)
- Mattsson N, "Inter-laboratory variation in cerebrospinal fluid biomarkers for Alzheimer’s disease: united we stand, divided we fall", Clin Chem Lab Med, 48, pp.603~607 (2010)
- Gomar JJ, "Utility of Combinations of Biomarkers, Cognitive Markers, and Risk Factors to Predict Conversion From Mild Cognitive Impairment to Alzheimer Disease in Patients in the Alzheimer’s Disease Neuroimaging Initiative", Arch Gen Psychiatry, 68, pp.961~969 (2011)
- Schneider LS, "Requiring an amyloid-beta1-42 biomarker for prodromal Alzheimer’s disease or mild cognitiveimpairment does not lead to more efficient clinical trials", AlzheimersDement, 6, pp.367~377 (2010)
- 42 and Alzheimer’s disease: relation to age, mortality, and risk, "Neurology", 2003, 1185~1190
- van Oijen M, "Plasma Aβ (1-40) and Aβ (1-42) and the risk of dementia: a prospective case-cohort study", Lancet Neurol, 5, pp.655~660 (2006)
- Schupf N, "Peripheral Aβ subspecies as risk biomarkers of Alzheimer’s disease", Proc Natl Acad Sci U S A, 105, pp.14052~14057 (2008)
- Blennow K, "Cerebrospinal fluid and plasma biomarkers in Alzheimer disease", Nat Rev Neurol, 6, pp.131~144 (2010)
- Song F, "Meta-Analysis of Plasma Amyloid-beta levels in Alzheimerʼs Disease", J Alzheimers Dis, 26, pp.365~375 (2011)
- Locascio JJ, "Plasma amyloid beta-protein and C-reactive protein in relation to the rate of progression of Alzheimer disease", Arch Neurol, 65, pp.776~785 (2008)
- Seshadri S, "Genome-wide analysis of genetic loci associated with Alzheimer disease", JAMA, 303, pp.1832~1840 (2010)
- Bertrand P, "Association of apolipoprotein E genotype with brain levels of apolipoprotein E and apolipoprotein J (clusterin) in Alzheimer disease", Brain Res Mol Brain Res, 33, pp.174~178 (1995)
- Choi-Miura NH, "Relationship between multifunctional protein“clusterin” and Alzheimer disease", Neurobiol Aging, 17, pp.717~722 (1996)
- Thambisetty M, "Association of plasma clusterin concentration with severity, pathology, and progression in Alzheimer disease", Arch Gen Psychiatry, 67, pp.739~748 (2010)
- Schjeide BM, "The role of clusterin, complement receptor 1, and phosphatidylinositol binding clathrin assembly protein in Alzheimer disease risk and cerebrospinal fluid biomarker levels", Arch Gen Psychiatry, 68, pp.207~213 (2011)
- Jun G, "Meta-analysis confirms CR1, CLU, and PICALM as alzheimer disease risk loci and reveals interactions with APOE genotypes", Arch Neurol, 67, pp.1473~1484 (2010)
- Lambert JC, "Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer’s disease", Nat Genet, 41, pp.1094~1099 (2009)
- Harold D, "Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer’s disease", Nat Genet, 41, pp.1088~1093 (2009)
- Schneider P, "Biological marker candidates of Alzheimer’s disease in blood, plasma, and serum", CNS Neurosci Ther, 15, pp.358~374 (2009)
- Greenberg N, "A proposed metabolic strategy for monitoring disease progression in Alzheimer’s disease", Electrophoresis, 30, pp.1235~1239 (2009)
- Salek RM, "A metabolomic study of the CRND8 transgenic mouse model of Alzheimer’s disease", Neurochem Int, 56, pp.937~947 (2010)
- Kaddurah-Daouk R, "Metabolomic changes in autopsy-confirmed Alzheimer’s disease", Alzheimers Dement, 7, pp.309~317 (2011)
- Han X, "Metabolomics in early Alzheimer’s disease: identification of altered plasma sphingolipidome using shotgun lipidomics", PLoS One, 6, pp.e21643~ (2011)
- Georganopoulou DG, "Nanoparticle-based detection in cerebral spinal fluid of a soluble pathogenic biomarker for Alzheimer’s disease", Proc Natl Acad Sci U S A, 102, pp.2273~2276 (2005)
- Geng J, "Rapid and efficient screening of Alzheimer’s disease beta-amyloid inhibitors using label-free gold nanoparticles", Mol Biosyst, 6, pp.2389~2391 (2010)
- Lee JH, "Signal enhancement of surface plasmon resonance based immunosensor using gold nanoparticle-antibody complex for beta-amyloid (1-40) detection", J Nanosci Nanotechnol, 9, pp.7155~7160 (2009)