Low cerebrospinal fluid concentration of mitochondrial DNA in preclinical Alzheimer disease
Objective To identify a novel biochemical marker that precedes clinical symptoms in Alzheimer disease (AD). Methods Using quantitative polymerase chain reaction techniques, we measured circulating cell‐free mitochondrial DNA (mtDNA) in cerebrospinal fluid (CSF) from study participants, selected from...
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| Published in | Annals of neurology Vol. 74; no. 5; pp. 655 - 668 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Blackwell Publishing Ltd
01.11.2013
Wiley Subscription Services, Inc |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Objective
To identify a novel biochemical marker that precedes clinical symptoms in Alzheimer disease (AD).
Methods
Using quantitative polymerase chain reaction techniques, we measured circulating cell‐free mitochondrial DNA (mtDNA) in cerebrospinal fluid (CSF) from study participants, selected from a cohort of 282 subjects, who were classified according to their concentrations of amyloid β1–42, total tau, and phosphorylated tau and by the presence or absence of dementia, into asymptomatic subjects at risk of AD, symptomatic patients diagnosed with sporadic AD, presymptomatic subjects carrying pathogenic PSEN1 mutations, and patients diagnosed with frontotemporal lobar degeneration (FTLD). We performed equivalent studies in a separate validation cohort of sporadic AD and FTLD patients. In addition, we measured mtDNA copy number in cultured cortical neurons from mutant amyloid precursor protein/presenilin1 (APP/PS1) transgenic mice.
Results
Asymptomatic patients at risk of AD and symptomatic AD patients, but not FTLD patients, exhibit a significant decrease in circulating cell‐free mtDNA in the CSF. These observations were confirmed in the validation cohort. In addition, presymptomatic subjects carrying pathogenic PSEN1 gene mutations show low mtDNA content in CSF before the appearance of AD‐related biomarkers in CSF. Moreover, mtDNA content in CSF discriminates with high sensitivity and specificity AD patients from either controls or patients with FTLD. Furthermore, cultured cortical neurons from APP/PS1 transgenic mice have fewer mtDNA copies before the appearance of altered synaptic markers.
Interpretation
Low content of mtDNA in CSF may be a novel biomarker for the early detection of preclinical AD. These findings support the hypothesis that mtDNA depletion is a characteristic pathophysiological factor of neurodegeneration in AD. Ann Neurol 2013;74:655–668 |
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| AbstractList | Objective To identify a novel biochemical marker that precedes clinical symptoms in Alzheimer disease (AD). Methods Using quantitative polymerase chain reaction techniques, we measured circulating cell-free mitochondrial DNA (mtDNA) in cerebrospinal fluid (CSF) from study participants, selected from a cohort of 282 subjects, who were classified according to their concentrations of amyloid [beta] sub(1-42), total tau, and phosphorylated tau and by the presence or absence of dementia, into asymptomatic subjects at risk of AD, symptomatic patients diagnosed with sporadic AD, presymptomatic subjects carrying pathogenic PSEN1 mutations, and patients diagnosed with frontotemporal lobar degeneration (FTLD). We performed equivalent studies in a separate validation cohort of sporadic AD and FTLD patients. In addition, we measured mtDNA copy number in cultured cortical neurons from mutant amyloid precursor protein/presenilin1 (APP/PS1) transgenic mice. Results Asymptomatic patients at risk of AD and symptomatic AD patients, but not FTLD patients, exhibit a significant decrease in circulating cell-free mtDNA in the CSF. These observations were confirmed in the validation cohort. In addition, presymptomatic subjects carrying pathogenic PSEN1 gene mutations show low mtDNA content in CSF before the appearance of AD-related biomarkers in CSF. Moreover, mtDNA content in CSF discriminates with high sensitivity and specificity AD patients from either controls or patients with FTLD. Furthermore, cultured cortical neurons from APP/PS1 transgenic mice have fewer mtDNA copies before the appearance of altered synaptic markers. Interpretation Low content of mtDNA in CSF may be a novel biomarker for the early detection of preclinical AD. These findings support the hypothesis that mtDNA depletion is a characteristic pathophysiological factor of neurodegeneration in AD. Ann Neurol 2013; 74:655-668 Objective To identify a novel biochemical marker that precedes clinical symptoms in Alzheimer disease (AD). Methods Using quantitative polymerase chain reaction techniques, we measured circulating cell-free mitochondrial DNA (mtDNA) in cerebrospinal fluid (CSF) from study participants, selected from a cohort of 282 subjects, who were classified according to their concentrations of amyloid [beta]1-42, total tau, and phosphorylated tau and by the presence or absence of dementia, into asymptomatic subjects at risk of AD, symptomatic patients diagnosed with sporadic AD, presymptomatic subjects carrying pathogenic PSEN1 mutations, and patients diagnosed with frontotemporal lobar degeneration (FTLD). We performed equivalent studies in a separate validation cohort of sporadic AD and FTLD patients. In addition, we measured mtDNA copy number in cultured cortical neurons from mutant amyloid precursor protein/presenilin1 (APP/PS1) transgenic mice. Results Asymptomatic patients at risk of AD and symptomatic AD patients, but not FTLD patients, exhibit a significant decrease in circulating cell-free mtDNA in the CSF. These observations were confirmed in the validation cohort. In addition, presymptomatic subjects carrying pathogenic PSEN1 gene mutations show low mtDNA content in CSF before the appearance of AD-related biomarkers in CSF. Moreover, mtDNA content in CSF discriminates with high sensitivity and specificity AD patients from either controls or patients with FTLD. Furthermore, cultured cortical neurons from APP/PS1 transgenic mice have fewer mtDNA copies before the appearance of altered synaptic markers. Interpretation Low content of mtDNA in CSF may be a novel biomarker for the early detection of preclinical AD. These findings support the hypothesis that mtDNA depletion is a characteristic pathophysiological factor of neurodegeneration in AD. Ann Neurol 2013;74:655-668 [PUBLICATION ABSTRACT] To identify a novel biochemical marker that precedes clinical symptoms in Alzheimer disease (AD).OBJECTIVETo identify a novel biochemical marker that precedes clinical symptoms in Alzheimer disease (AD).Using quantitative polymerase chain reaction techniques, we measured circulating cell-free mitochondrial DNA (mtDNA) in cerebrospinal fluid (CSF) from study participants, selected from a cohort of 282 subjects, who were classified according to their concentrations of amyloid β1-42, total tau, and phosphorylated tau and by the presence or absence of dementia, into asymptomatic subjects at risk of AD, symptomatic patients diagnosed with sporadic AD, presymptomatic subjects carrying pathogenic PSEN1 mutations, and patients diagnosed with frontotemporal lobar degeneration (FTLD). We performed equivalent studies in a separate validation cohort of sporadic AD and FTLD patients. In addition, we measured mtDNA copy number in cultured cortical neurons from mutant amyloid precursor protein/presenilin1 (APP/PS1) transgenic mice.METHODSUsing quantitative polymerase chain reaction techniques, we measured circulating cell-free mitochondrial DNA (mtDNA) in cerebrospinal fluid (CSF) from study participants, selected from a cohort of 282 subjects, who were classified according to their concentrations of amyloid β1-42, total tau, and phosphorylated tau and by the presence or absence of dementia, into asymptomatic subjects at risk of AD, symptomatic patients diagnosed with sporadic AD, presymptomatic subjects carrying pathogenic PSEN1 mutations, and patients diagnosed with frontotemporal lobar degeneration (FTLD). We performed equivalent studies in a separate validation cohort of sporadic AD and FTLD patients. In addition, we measured mtDNA copy number in cultured cortical neurons from mutant amyloid precursor protein/presenilin1 (APP/PS1) transgenic mice.Asymptomatic patients at risk of AD and symptomatic AD patients, but not FTLD patients, exhibit a significant decrease in circulating cell-free mtDNA in the CSF. These observations were confirmed in the validation cohort. In addition, presymptomatic subjects carrying pathogenic PSEN1 gene mutations show low mtDNA content in CSF before the appearance of AD-related biomarkers in CSF. Moreover, mtDNA content in CSF discriminates with high sensitivity and specificity AD patients from either controls or patients with FTLD. Furthermore, cultured cortical neurons from APP/PS1 transgenic mice have fewer mtDNA copies before the appearance of altered synaptic markers.RESULTSAsymptomatic patients at risk of AD and symptomatic AD patients, but not FTLD patients, exhibit a significant decrease in circulating cell-free mtDNA in the CSF. These observations were confirmed in the validation cohort. In addition, presymptomatic subjects carrying pathogenic PSEN1 gene mutations show low mtDNA content in CSF before the appearance of AD-related biomarkers in CSF. Moreover, mtDNA content in CSF discriminates with high sensitivity and specificity AD patients from either controls or patients with FTLD. Furthermore, cultured cortical neurons from APP/PS1 transgenic mice have fewer mtDNA copies before the appearance of altered synaptic markers.Low content of mtDNA in CSF may be a novel biomarker for the early detection of preclinical AD. These findings support the hypothesis that mtDNA depletion is a characteristic pathophysiological factor of neurodegeneration in AD.INTERPRETATIONLow content of mtDNA in CSF may be a novel biomarker for the early detection of preclinical AD. These findings support the hypothesis that mtDNA depletion is a characteristic pathophysiological factor of neurodegeneration in AD. Objective To identify a novel biochemical marker that precedes clinical symptoms in Alzheimer disease (AD). Methods Using quantitative polymerase chain reaction techniques, we measured circulating cell‐free mitochondrial DNA (mtDNA) in cerebrospinal fluid (CSF) from study participants, selected from a cohort of 282 subjects, who were classified according to their concentrations of amyloid β1–42, total tau, and phosphorylated tau and by the presence or absence of dementia, into asymptomatic subjects at risk of AD, symptomatic patients diagnosed with sporadic AD, presymptomatic subjects carrying pathogenic PSEN1 mutations, and patients diagnosed with frontotemporal lobar degeneration (FTLD). We performed equivalent studies in a separate validation cohort of sporadic AD and FTLD patients. In addition, we measured mtDNA copy number in cultured cortical neurons from mutant amyloid precursor protein/presenilin1 (APP/PS1) transgenic mice. Results Asymptomatic patients at risk of AD and symptomatic AD patients, but not FTLD patients, exhibit a significant decrease in circulating cell‐free mtDNA in the CSF. These observations were confirmed in the validation cohort. In addition, presymptomatic subjects carrying pathogenic PSEN1 gene mutations show low mtDNA content in CSF before the appearance of AD‐related biomarkers in CSF. Moreover, mtDNA content in CSF discriminates with high sensitivity and specificity AD patients from either controls or patients with FTLD. Furthermore, cultured cortical neurons from APP/PS1 transgenic mice have fewer mtDNA copies before the appearance of altered synaptic markers. Interpretation Low content of mtDNA in CSF may be a novel biomarker for the early detection of preclinical AD. These findings support the hypothesis that mtDNA depletion is a characteristic pathophysiological factor of neurodegeneration in AD. Ann Neurol 2013;74:655–668 To identify a novel biochemical marker that precedes clinical symptoms in Alzheimer disease (AD). Using quantitative polymerase chain reaction techniques, we measured circulating cell-free mitochondrial DNA (mtDNA) in cerebrospinal fluid (CSF) from study participants, selected from a cohort of 282 subjects, who were classified according to their concentrations of amyloid β1-42, total tau, and phosphorylated tau and by the presence or absence of dementia, into asymptomatic subjects at risk of AD, symptomatic patients diagnosed with sporadic AD, presymptomatic subjects carrying pathogenic PSEN1 mutations, and patients diagnosed with frontotemporal lobar degeneration (FTLD). We performed equivalent studies in a separate validation cohort of sporadic AD and FTLD patients. In addition, we measured mtDNA copy number in cultured cortical neurons from mutant amyloid precursor protein/presenilin1 (APP/PS1) transgenic mice. Asymptomatic patients at risk of AD and symptomatic AD patients, but not FTLD patients, exhibit a significant decrease in circulating cell-free mtDNA in the CSF. These observations were confirmed in the validation cohort. In addition, presymptomatic subjects carrying pathogenic PSEN1 gene mutations show low mtDNA content in CSF before the appearance of AD-related biomarkers in CSF. Moreover, mtDNA content in CSF discriminates with high sensitivity and specificity AD patients from either controls or patients with FTLD. Furthermore, cultured cortical neurons from APP/PS1 transgenic mice have fewer mtDNA copies before the appearance of altered synaptic markers. Low content of mtDNA in CSF may be a novel biomarker for the early detection of preclinical AD. These findings support the hypothesis that mtDNA depletion is a characteristic pathophysiological factor of neurodegeneration in AD. |
| Author | Sanchez-Valle, Raquel Llado, Albert Serra, Nuria Podlesniy, Petar Figueiro-Silva, Joana Antonell, Anna Lleo, Alberto Trullas, Ramon Molinuevo, Jose Luis Alcolea, Daniel |
| Author_xml | – sequence: 1 givenname: Petar surname: Podlesniy fullname: Podlesniy, Petar organization: Neurobiology Unit, Instituto de Investigaciones Biomedicas de Barcelona, Consejo Superior de Investigaciones Cientificas, CSIC, Barcelona, Spain – sequence: 2 givenname: Joana surname: Figueiro-Silva fullname: Figueiro-Silva, Joana organization: Neurobiology Unit, Instituto de Investigaciones Biomedicas de Barcelona, Consejo Superior de Investigaciones Cientificas, CSIC, Barcelona, Spain – sequence: 3 givenname: Albert surname: Llado fullname: Llado, Albert organization: Neurology Service, Hospital Clinic de Barcelona, Barcelona, Spain – sequence: 4 givenname: Anna surname: Antonell fullname: Antonell, Anna organization: Neurology Service, Hospital Clinic de Barcelona, Barcelona, Spain – sequence: 5 givenname: Raquel surname: Sanchez-Valle fullname: Sanchez-Valle, Raquel organization: Neurology Service, Hospital Clinic de Barcelona, Barcelona, Spain – sequence: 6 givenname: Daniel surname: Alcolea fullname: Alcolea, Daniel organization: Centro de Investigacion Biomedica en Red de Enfermedades Neurodegenerativas, CIBERNED, Madrid, Spain – sequence: 7 givenname: Alberto surname: Lleo fullname: Lleo, Alberto organization: Centro de Investigacion Biomedica en Red de Enfermedades Neurodegenerativas, CIBERNED, Madrid, Spain – sequence: 8 givenname: Jose Luis surname: Molinuevo fullname: Molinuevo, Jose Luis organization: Neurology Service, Hospital Clinic de Barcelona, Barcelona, Spain – sequence: 9 givenname: Nuria surname: Serra fullname: Serra, Nuria organization: Neurobiology Unit, Instituto de Investigaciones Biomedicas de Barcelona, Consejo Superior de Investigaciones Cientificas, CSIC, Barcelona, Spain – sequence: 10 givenname: Ramon surname: Trullas fullname: Trullas, Ramon email: ramon.trullas@iibb.csic.es organization: Neurobiology Unit, Instituto de Investigaciones Biomedicas de Barcelona, Consejo Superior de Investigaciones Cientificas, CSIC, Barcelona, Spain |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23794434$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1001/archneur.62.5.758 10.1212/01.wnl.0000219668.47116.e6 10.1212/01.wnl.0000311445.21321.fc 10.1016/j.ymeth.2010.01.033 10.3233/JAD-2010-100351 10.1016/j.jalz.2011.03.003 10.1001/archneur.60.12.1696 10.1002/ana.20730 10.1096/fj.10-157230 10.1515/CCLM.2011.082 10.1126/science.1197623 10.1001/archneurol.2008.596 10.1212/WNL.34.7.939 10.1111/j.1471-4159.2011.07581.x 10.1101/sqb.2011.76.010462 10.3233/JAD-2010-100207 10.1016/j.mito.2009.03.003 10.3233/JAD-2010-100339 10.1016/j.bbagen.2011.08.008 10.1212/WNL.51.6.1546 10.1016/S1474-4422(09)70299-6 10.1373/clinchem.2008.112797 10.2353/ajpath.2009.090219 10.1212/01.WNL.0000046581.81650.D0 |
| ContentType | Journal Article |
| Copyright | 2013 American Neurological Association 2013 American Neurological Association. |
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| References | Hertze J, Minthon L, Zetterberg H, et al. Evaluation of CSF biomarkers as predictors of Alzheimer's disease: a clinical follow-up study of 4.7 years. J Alzheimers Dis 2010;21:1119-1128. Galvin JE, Powlishta KK, Wilkins K, et al. Predictors of preclinical Alzheimer disease and dementia: a clinicopathologic study. Arch Neurol 2005;62:758-765. Sperling RA, Aisen PS, Beckett LA, et al. Toward defining the preclinical stages of Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement 2011;7:280-292. Bustin SA, Benes V, Garson JA, et al. The MIQE guidelines: minimum information for publication of quantitative real-time PCR experiments. Clin Chem 2009;55:611-622. Jack CR Jr, Knopman DS, Jagust WJ, et al. Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade. Lancet Neurol 2010;9:119-128. Guo W, Jiang L, Bhasin S, et al. DNA extraction procedures meaningfully influence qPCR-based mtDNA copy number determination. Mitochondrion 2009;9:261-265. Wallace DC. Bioenergetic origins of complexity and disease. Cold Spring Harb Symp Quant Biol 2011;76:1-16. Fagan AM, Mintun MA, Mach RH, et al. Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Abeta42 in humans. Ann Neurol 2006;59:512-519. Bian H, Van Swieten JC, Leight S, et al. CSF biomarkers in frontotemporal lobar degeneration with known pathology. Neurology 2008;70:1827-1835. Tapiola T, Alafuzoff I, Herukka SK, et al. Cerebrospinal fluid {beta}-amyloid 42 and tau proteins as biomarkers of Alzheimer-type pathologic changes in the brain. Arch Neurol 2009;66:382-389. Bennett DA, Schneider JA, Arvanitakis Z, et al. Neuropathology of older persons without cognitive impairment from two community-based studies. Neurology 2006;66:1837-1844. Mawuenyega KG, Sigurdson W, Ovod V, et al. Decreased clearance of CNS beta-amyloid in Alzheimer's disease. Science 2010;330:1774. Sheng B, Wang X, Su B, et al. Impaired mitochondrial biogenesis contributes to mitochondrial dysfunction in Alzheimer's disease. J Neurochem 2012;120:419-429. Coskun P, Wyrembak J, Schriner S, et al. A mitochondrial etiology of Alzheimer and Parkinson disease. Biochim Biophys Acta 2012;1820:553-564. Neary D, Snowden JS, Gustafson L, et al. Frontotemporal lobar degeneration: a consensus on clinical diagnostic criteria. Neurology 1998;51:1546-1554. Swerdlow RH, Burns JM, Khan SM. The Alzheimer's disease mitochondrial cascade hypothesis. J Alzheimers Dis 2010;20(suppl 2):S265-S279. Coskun PE, Wyrembak J, Derbereva O, et al. Systemic mitochondrial dysfunction and the etiology of Alzheimer's disease and Down syndrome dementia. J Alzheimers Dis 2010;20(suppl 2):S293-S310. Clark CM, Xie S, Chittams J, et al. Cerebrospinal fluid tau and beta-amyloid: how well do these biomarkers reflect autopsy-confirmed dementia diagnoses? Arch Neurol 2003;60:1696-1702. Strozyk D, Blennow K, White LR, et al. CSF Abeta 42 levels correlate with amyloid-neuropathology in a population-based autopsy study. Neurology 2003;60:652-656. Mattsson N. CSF biomarkers in neurodegenerative diseases. Clin Chem Lab Med 2011;49:345-352. Hunter SE, Jung D, Di Giulio RT, et al. The QPCR assay for analysis of mitochondrial DNA damage, repair, and relative copy number. Methods 2010;51:444-451. Area-Gomez E, de Groof AJ, Boldogh I, et al. Presenilins are enriched in endoplasmic reticulum membranes associated with mitochondria. Am J Pathol 2009;175:1810-1816. Pavlov PF, Wiehager B, Sakai J, et al. Mitochondrial gamma-secretase participates in the metabolism of mitochondria-associated amyloid precursor protein. FASEB J 2011;25:78-88. McKhann G, Drachman D, Folstein M, et al. Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease. Neurology 1984;34:939-944. 2009; 66 2009; 55 2010; 21 2010; 20 2012; 120 2006; 66 1984; 34 2006; 59 2012; 1820 2005; 62 2010; 330 2009; 9 2011; 76 2009; 175 2011; 25 2003; 60 2011; 49 1998; 51 2008; 70 2011; 7 2010; 51 2010; 9 e_1_2_8_17_1 e_1_2_8_18_1 e_1_2_8_19_1 e_1_2_8_13_1 e_1_2_8_24_1 e_1_2_8_14_1 e_1_2_8_25_1 e_1_2_8_15_1 e_1_2_8_16_1 e_1_2_8_3_1 e_1_2_8_2_1 e_1_2_8_5_1 e_1_2_8_4_1 e_1_2_8_7_1 e_1_2_8_6_1 e_1_2_8_9_1 e_1_2_8_8_1 e_1_2_8_20_1 e_1_2_8_10_1 e_1_2_8_21_1 e_1_2_8_11_1 e_1_2_8_22_1 e_1_2_8_12_1 e_1_2_8_23_1 24424574 - Ann Neurol. 2014 Mar;75(3):458-60 24431101 - Ann Neurol. 2014 Mar;75(3):460-1 23835537 - Nat Rev Neurol. 2013 Aug;9(8):420 |
| References_xml | – reference: Bian H, Van Swieten JC, Leight S, et al. CSF biomarkers in frontotemporal lobar degeneration with known pathology. Neurology 2008;70:1827-1835. – reference: Sheng B, Wang X, Su B, et al. Impaired mitochondrial biogenesis contributes to mitochondrial dysfunction in Alzheimer's disease. J Neurochem 2012;120:419-429. – reference: Fagan AM, Mintun MA, Mach RH, et al. Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Abeta42 in humans. Ann Neurol 2006;59:512-519. – reference: Wallace DC. Bioenergetic origins of complexity and disease. Cold Spring Harb Symp Quant Biol 2011;76:1-16. – reference: Jack CR Jr, Knopman DS, Jagust WJ, et al. Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade. Lancet Neurol 2010;9:119-128. – reference: Bennett DA, Schneider JA, Arvanitakis Z, et al. Neuropathology of older persons without cognitive impairment from two community-based studies. Neurology 2006;66:1837-1844. – reference: Coskun P, Wyrembak J, Schriner S, et al. A mitochondrial etiology of Alzheimer and Parkinson disease. Biochim Biophys Acta 2012;1820:553-564. – reference: Tapiola T, Alafuzoff I, Herukka SK, et al. Cerebrospinal fluid {beta}-amyloid 42 and tau proteins as biomarkers of Alzheimer-type pathologic changes in the brain. Arch Neurol 2009;66:382-389. – reference: McKhann G, Drachman D, Folstein M, et al. Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease. Neurology 1984;34:939-944. – reference: Sperling RA, Aisen PS, Beckett LA, et al. Toward defining the preclinical stages of Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement 2011;7:280-292. – reference: Neary D, Snowden JS, Gustafson L, et al. Frontotemporal lobar degeneration: a consensus on clinical diagnostic criteria. Neurology 1998;51:1546-1554. – reference: Guo W, Jiang L, Bhasin S, et al. DNA extraction procedures meaningfully influence qPCR-based mtDNA copy number determination. Mitochondrion 2009;9:261-265. – reference: Mawuenyega KG, Sigurdson W, Ovod V, et al. Decreased clearance of CNS beta-amyloid in Alzheimer's disease. Science 2010;330:1774. – reference: Strozyk D, Blennow K, White LR, et al. CSF Abeta 42 levels correlate with amyloid-neuropathology in a population-based autopsy study. Neurology 2003;60:652-656. – reference: Coskun PE, Wyrembak J, Derbereva O, et al. Systemic mitochondrial dysfunction and the etiology of Alzheimer's disease and Down syndrome dementia. J Alzheimers Dis 2010;20(suppl 2):S293-S310. – reference: Swerdlow RH, Burns JM, Khan SM. The Alzheimer's disease mitochondrial cascade hypothesis. J Alzheimers Dis 2010;20(suppl 2):S265-S279. – reference: Bustin SA, Benes V, Garson JA, et al. The MIQE guidelines: minimum information for publication of quantitative real-time PCR experiments. Clin Chem 2009;55:611-622. – reference: Hunter SE, Jung D, Di Giulio RT, et al. The QPCR assay for analysis of mitochondrial DNA damage, repair, and relative copy number. Methods 2010;51:444-451. – reference: Mattsson N. CSF biomarkers in neurodegenerative diseases. Clin Chem Lab Med 2011;49:345-352. – reference: Galvin JE, Powlishta KK, Wilkins K, et al. Predictors of preclinical Alzheimer disease and dementia: a clinicopathologic study. Arch Neurol 2005;62:758-765. – reference: Hertze J, Minthon L, Zetterberg H, et al. Evaluation of CSF biomarkers as predictors of Alzheimer's disease: a clinical follow-up study of 4.7 years. J Alzheimers Dis 2010;21:1119-1128. – reference: Pavlov PF, Wiehager B, Sakai J, et al. Mitochondrial gamma-secretase participates in the metabolism of mitochondria-associated amyloid precursor protein. FASEB J 2011;25:78-88. – reference: Clark CM, Xie S, Chittams J, et al. Cerebrospinal fluid tau and beta-amyloid: how well do these biomarkers reflect autopsy-confirmed dementia diagnoses? Arch Neurol 2003;60:1696-1702. – reference: Area-Gomez E, de Groof AJ, Boldogh I, et al. Presenilins are enriched in endoplasmic reticulum membranes associated with mitochondria. Am J Pathol 2009;175:1810-1816. – volume: 66 start-page: 1837 year: 2006 end-page: 1844 article-title: Neuropathology of older persons without cognitive impairment from two community‐based studies publication-title: Neurology – volume: 7 start-page: 280 year: 2011 end-page: 292 article-title: Toward defining the preclinical stages of Alzheimer's disease: recommendations from the National Institute on Aging‐Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease publication-title: Alzheimers Dement – volume: 9 start-page: 119 year: 2010 end-page: 128 article-title: Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade publication-title: Lancet Neurol – volume: 59 start-page: 512 year: 2006 end-page: 519 article-title: Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Abeta42 in humans publication-title: Ann Neurol – volume: 55 start-page: 611 year: 2009 end-page: 622 article-title: The MIQE guidelines: minimum information for publication of quantitative real‐time PCR experiments publication-title: Clin Chem – volume: 20 start-page: S265 issue: suppl 2 year: 2010 end-page: S279 article-title: The Alzheimer's disease mitochondrial cascade hypothesis publication-title: J Alzheimers Dis – volume: 34 start-page: 939 year: 1984 end-page: 944 article-title: Clinical diagnosis of Alzheimer's disease: report of the NINCDS‐ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease publication-title: Neurology – volume: 20 start-page: S293 issue: suppl 2 year: 2010 end-page: S310 article-title: Systemic mitochondrial dysfunction and the etiology of Alzheimer's disease and Down syndrome dementia publication-title: J Alzheimers Dis – volume: 76 start-page: 1 year: 2011 end-page: 16 article-title: Bioenergetic origins of complexity and disease publication-title: Cold Spring Harb Symp Quant Biol – volume: 60 start-page: 1696 year: 2003 end-page: 1702 article-title: Cerebrospinal fluid tau and beta‐amyloid: how well do these biomarkers reflect autopsy‐confirmed dementia diagnoses? publication-title: Arch Neurol – volume: 330 start-page: 1774 year: 2010 article-title: Decreased clearance of CNS beta‐amyloid in Alzheimer's disease publication-title: Science – volume: 120 start-page: 419 year: 2012 end-page: 429 article-title: Impaired mitochondrial biogenesis contributes to mitochondrial dysfunction in Alzheimer's disease publication-title: J Neurochem – volume: 51 start-page: 444 year: 2010 end-page: 451 article-title: The QPCR assay for analysis of mitochondrial DNA damage, repair, and relative copy number publication-title: Methods – volume: 21 start-page: 1119 year: 2010 end-page: 1128 article-title: Evaluation of CSF biomarkers as predictors of Alzheimer's disease: a clinical follow‐up study of 4.7 years publication-title: J Alzheimers Dis – volume: 9 start-page: 261 year: 2009 end-page: 265 article-title: DNA extraction procedures meaningfully influence qPCR‐based mtDNA copy number determination publication-title: Mitochondrion – volume: 66 start-page: 382 year: 2009 end-page: 389 article-title: Cerebrospinal fluid {beta}‐amyloid 42 and tau proteins as biomarkers of Alzheimer‐type pathologic changes in the brain publication-title: Arch Neurol – volume: 25 start-page: 78 year: 2011 end-page: 88 article-title: Mitochondrial gamma‐secretase participates in the metabolism of mitochondria‐associated amyloid precursor protein publication-title: FASEB J – volume: 70 start-page: 1827 year: 2008 end-page: 1835 article-title: CSF biomarkers in frontotemporal lobar degeneration with known pathology publication-title: Neurology – volume: 1820 start-page: 553 year: 2012 end-page: 564 article-title: A mitochondrial etiology of Alzheimer and Parkinson disease publication-title: Biochim Biophys Acta – volume: 51 start-page: 1546 year: 1998 end-page: 1554 article-title: Frontotemporal lobar degeneration: a consensus on clinical diagnostic criteria publication-title: Neurology – volume: 175 start-page: 1810 year: 2009 end-page: 1816 article-title: Presenilins are enriched in endoplasmic reticulum membranes associated with mitochondria publication-title: Am J Pathol – volume: 62 start-page: 758 year: 2005 end-page: 765 article-title: Predictors of preclinical Alzheimer disease and dementia: a clinicopathologic study publication-title: Arch Neurol – volume: 49 start-page: 345 year: 2011 end-page: 352 article-title: CSF biomarkers in neurodegenerative diseases publication-title: Clin Chem Lab Med – volume: 60 start-page: 652 year: 2003 end-page: 656 article-title: CSF Abeta 42 levels correlate with amyloid‐neuropathology in a population‐based autopsy study publication-title: Neurology – ident: e_1_2_8_9_1 doi: 10.1001/archneur.62.5.758 – ident: e_1_2_8_10_1 doi: 10.1212/01.wnl.0000219668.47116.e6 – ident: e_1_2_8_13_1 doi: 10.1212/01.wnl.0000311445.21321.fc – ident: e_1_2_8_18_1 doi: 10.1016/j.ymeth.2010.01.033 – ident: e_1_2_8_21_1 doi: 10.3233/JAD-2010-100351 – ident: e_1_2_8_3_1 doi: 10.1016/j.jalz.2011.03.003 – ident: e_1_2_8_4_1 doi: 10.1001/archneur.60.12.1696 – ident: e_1_2_8_7_1 doi: 10.1002/ana.20730 – ident: e_1_2_8_24_1 doi: 10.1096/fj.10-157230 – ident: e_1_2_8_11_1 doi: 10.1515/CCLM.2011.082 – ident: e_1_2_8_12_1 doi: 10.1126/science.1197623 – ident: e_1_2_8_8_1 doi: 10.1001/archneurol.2008.596 – ident: e_1_2_8_16_1 doi: 10.1212/WNL.34.7.939 – ident: e_1_2_8_22_1 doi: 10.1111/j.1471-4159.2011.07581.x – ident: e_1_2_8_25_1 doi: 10.1101/sqb.2011.76.010462 – ident: e_1_2_8_5_1 doi: 10.3233/JAD-2010-100207 – ident: e_1_2_8_19_1 doi: 10.1016/j.mito.2009.03.003 – ident: e_1_2_8_14_1 doi: 10.3233/JAD-2010-100339 – ident: e_1_2_8_15_1 doi: 10.1016/j.bbagen.2011.08.008 – ident: e_1_2_8_20_1 doi: 10.1212/WNL.51.6.1546 – ident: e_1_2_8_2_1 doi: 10.1016/S1474-4422(09)70299-6 – ident: e_1_2_8_17_1 doi: 10.1373/clinchem.2008.112797 – ident: e_1_2_8_23_1 doi: 10.2353/ajpath.2009.090219 – ident: e_1_2_8_6_1 doi: 10.1212/01.WNL.0000046581.81650.D0 – reference: 24431101 - Ann Neurol. 2014 Mar;75(3):460-1 – reference: 24424574 - Ann Neurol. 2014 Mar;75(3):458-60 – reference: 23835537 - Nat Rev Neurol. 2013 Aug;9(8):420 |
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| Snippet | Objective
To identify a novel biochemical marker that precedes clinical symptoms in Alzheimer disease (AD).
Methods
Using quantitative polymerase chain... To identify a novel biochemical marker that precedes clinical symptoms in Alzheimer disease (AD). Using quantitative polymerase chain reaction techniques, we... Objective To identify a novel biochemical marker that precedes clinical symptoms in Alzheimer disease (AD). Methods Using quantitative polymerase chain... To identify a novel biochemical marker that precedes clinical symptoms in Alzheimer disease (AD).OBJECTIVETo identify a novel biochemical marker that precedes... |
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| SubjectTerms | Alzheimer Disease - cerebrospinal fluid Alzheimer Disease - genetics Amyloid beta-Protein Precursor - cerebrospinal fluid Animals Biomarkers - cerebrospinal fluid Cognitive Dysfunction - cerebrospinal fluid Cognitive Dysfunction - genetics Deoxyribonucleic acid DNA DNA, Mitochondrial - cerebrospinal fluid Female Humans Male Medical research Mice Mice, Transgenic Mitochondrial DNA Peptide Fragments - cerebrospinal fluid Phosphorylation Presenilin-1 - genetics Prodromal Symptoms tau Proteins - cerebrospinal fluid Transgenic animals |
| Title | Low cerebrospinal fluid concentration of mitochondrial DNA in preclinical Alzheimer disease |
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