Skip to main content
Erschienen in: Neuropsychology Review 4/2017

01.12.2017 | Review

Detectable Neuropsychological Differences in Early Preclinical Alzheimer’s Disease: A Meta-Analysis

verfasst von: S. Duke Han, Caroline P. Nguyen, Nikki H. Stricker, Daniel A. Nation

Erschienen in: Neuropsychology Review | Ausgabe 4/2017

Einloggen, um Zugang zu erhalten

Abstract

The development of methods for in vivo detection of cerebral beta amyloid retention and tau accumulation have been increasingly useful in characterizing preclinical Alzheimer’s disease (AD). While the association between these biomarkers and eventual AD has been demonstrated among cognitively intact older adults, the link between biomarkers and neurocognitive ability remains unclear. We conducted a meta-analysis to test the hypothesis that cognitively intact older adults would show statistically discernable differences in neuropsychological performance by amyloid status (amyloid negative = A-, amyloid positive = A+). We secondarily hypothesized a third group characterized by either CSF tau pathology or neurodegeneration, in addition to amyloidosis (A+/N+ or Stage 2), would show lower neuropsychology scores than the amyloid positive group (A+/N- or Stage 1) when compared to the amyloid negative group. Pubmed, PsychINFO, and other sources were searched for relevant articles, yielding 775 total sources. After review for inclusion/exclusion criteria, duplicates, and risk of bias, 61 studies were utilized in the final meta-analysis. Results showed A+ was associated with poorer performance in the domains of global cognitive function, memory, language, visuospatial ability, processing speed, and attention/working memory/executive functions when compared to A-. A+/N+ showed lower performances on memory measures when compared to A+/N- in secondary analyses based on a smaller subset of studies. Results support the notion that neuropsychological measures are sensitive to different stages of preclinical AD among cognitively intact older adults. Further research is needed to determine what constitutes meaningful differences in neuropsychological performance among cognitively intact older adults.
Literatur
Zurück zum Zitat Aizenstein, H. J., Nebes, R. D., Saxton, J. A., et al. (2008). Frequent amyloid deposition without significant cognitive impairment among the elderly. Archives of Neurology, 65(11), 1509–1517.CrossRefPubMedPubMedCentral Aizenstein, H. J., Nebes, R. D., Saxton, J. A., et al. (2008). Frequent amyloid deposition without significant cognitive impairment among the elderly. Archives of Neurology, 65(11), 1509–1517.CrossRefPubMedPubMedCentral
Zurück zum Zitat Alcolea, D., Martínez-Lage, P., Sánchez-Juan, P., et al. (2015). Amyloid precursor protein metabolism and inflammation markers in preclinical Alzheimer disease. Neurology, 85(7), 626–633.CrossRefPubMed Alcolea, D., Martínez-Lage, P., Sánchez-Juan, P., et al. (2015). Amyloid precursor protein metabolism and inflammation markers in preclinical Alzheimer disease. Neurology, 85(7), 626–633.CrossRefPubMed
Zurück zum Zitat Amariglio, R. E., Becker, J. A., Carmasin, J., et al. (2012). Subjective cognitive complaints and amyloid burden in cognitively normal older individuals. Neuropsychologia, 50, 2880–2886.CrossRefPubMedPubMedCentral Amariglio, R. E., Becker, J. A., Carmasin, J., et al. (2012). Subjective cognitive complaints and amyloid burden in cognitively normal older individuals. Neuropsychologia, 50, 2880–2886.CrossRefPubMedPubMedCentral
Zurück zum Zitat Amariglio, R. E., Mormino, E. C., Pietras, A. C., et al. (2015). Subjective cognitive concerns, amyloid-β, and neurodegeneration in clinically normal elderly. Neurology, 85(1), 56–62.CrossRefPubMedPubMedCentral Amariglio, R. E., Mormino, E. C., Pietras, A. C., et al. (2015). Subjective cognitive concerns, amyloid-β, and neurodegeneration in clinically normal elderly. Neurology, 85(1), 56–62.CrossRefPubMedPubMedCentral
Zurück zum Zitat Andreasen, N., Minthon, L., Davidsson, P., et al. (2001). Evaluation of CSF-tau and CSF-Aβ42 as diagnostic markers for Alzheimer disease in clinical practice. Archives of Neurology, 58, 373–379.CrossRefPubMed Andreasen, N., Minthon, L., Davidsson, P., et al. (2001). Evaluation of CSF-tau and CSF-Aβ42 as diagnostic markers for Alzheimer disease in clinical practice. Archives of Neurology, 58, 373–379.CrossRefPubMed
Zurück zum Zitat Ayutyanont, N., Langbaum, J. B., Hendrix, S. B., et al. (2014). The Alzheimer’s Precention initiative composite cognitive test score: Sample size estimates for the evaluation of preclinical Alzheimer’s disease treatments in presenilin 1 E280A mutation carriers. The Journal of Clinical Psychiatry, 75, 652–660.CrossRefPubMedPubMedCentral Ayutyanont, N., Langbaum, J. B., Hendrix, S. B., et al. (2014). The Alzheimer’s Precention initiative composite cognitive test score: Sample size estimates for the evaluation of preclinical Alzheimer’s disease treatments in presenilin 1 E280A mutation carriers. The Journal of Clinical Psychiatry, 75, 652–660.CrossRefPubMedPubMedCentral
Zurück zum Zitat Besson, F. L., La Joie, R., Doeuvre, L., et al. (2015). Cognitive and brain profiles associated with current neuroimaging biomarkers of preclinical Alzheimer's disease. The Journal of Neuroscience, 35(29), 10402–10411.CrossRefPubMed Besson, F. L., La Joie, R., Doeuvre, L., et al. (2015). Cognitive and brain profiles associated with current neuroimaging biomarkers of preclinical Alzheimer's disease. The Journal of Neuroscience, 35(29), 10402–10411.CrossRefPubMed
Zurück zum Zitat Borenstein, M., Hedges, L. V., Higgins, J. P. T., & Rothstein, H. R. (2009). Introduction to meta-analysis. West Sussex: Wiley.CrossRef Borenstein, M., Hedges, L. V., Higgins, J. P. T., & Rothstein, H. R. (2009). Introduction to meta-analysis. West Sussex: Wiley.CrossRef
Zurück zum Zitat Braak, H., & Del Tredici, K. (2015). The preclinical phase of the pathological process underlying sporadic Alzheimer’s disease. Brain, 138, 2814–2833.CrossRefPubMed Braak, H., & Del Tredici, K. (2015). The preclinical phase of the pathological process underlying sporadic Alzheimer’s disease. Brain, 138, 2814–2833.CrossRefPubMed
Zurück zum Zitat Buckley, R. F., Maruff, P., Ames, D., et al. (2016). Subjective memory decline predicts greater rates of clinical progression in preclinical Alzheimer's disease. Alzheimer’s & Dementia, 12(7), 796–804.CrossRef Buckley, R. F., Maruff, P., Ames, D., et al. (2016). Subjective memory decline predicts greater rates of clinical progression in preclinical Alzheimer's disease. Alzheimer’s & Dementia, 12(7), 796–804.CrossRef
Zurück zum Zitat Chen, K., Roontiva, A., Thiyyagura, P., et al. (2015). Improved power for characterizing longitudinal amyloid-β PET changes and evaluating amyloid-modifying treatments with a cerebral white matter reference region. The Journal of Nuclear Medicine, 56(4), 560–566.CrossRefPubMed Chen, K., Roontiva, A., Thiyyagura, P., et al. (2015). Improved power for characterizing longitudinal amyloid-β PET changes and evaluating amyloid-modifying treatments with a cerebral white matter reference region. The Journal of Nuclear Medicine, 56(4), 560–566.CrossRefPubMed
Zurück zum Zitat Chételat, G., Villemagne, V. L., Pike, K. E., et al. (2010). Larger temporal volume in elderly with high versus low beta-amyloid deposition. Brain, 133(11), 3349–3358.CrossRefPubMed Chételat, G., Villemagne, V. L., Pike, K. E., et al. (2010). Larger temporal volume in elderly with high versus low beta-amyloid deposition. Brain, 133(11), 3349–3358.CrossRefPubMed
Zurück zum Zitat Chételat, G., Villemagne, V. L., Villain, N., et al. (2012). Accelerated cortical atrophy in cognitively normal elderly with high β-amyloid deposition. Neurology, 78(7), 477–484.CrossRefPubMed Chételat, G., Villemagne, V. L., Villain, N., et al. (2012). Accelerated cortical atrophy in cognitively normal elderly with high β-amyloid deposition. Neurology, 78(7), 477–484.CrossRefPubMed
Zurück zum Zitat Cochran, W. G. (1954). The combination of estimates from different experiments. Biometrics, 1, 101–129.CrossRef Cochran, W. G. (1954). The combination of estimates from different experiments. Biometrics, 1, 101–129.CrossRef
Zurück zum Zitat Donohue, M. C., Sperling, R. A., Salmon, D. P., et al. (2014). The preclinical Alzheimer cognitive composite: Measuring amyloid-related decline. JAMA Neurology, 71(8), 961–970.CrossRefPubMedPubMedCentral Donohue, M. C., Sperling, R. A., Salmon, D. P., et al. (2014). The preclinical Alzheimer cognitive composite: Measuring amyloid-related decline. JAMA Neurology, 71(8), 961–970.CrossRefPubMedPubMedCentral
Zurück zum Zitat Doraiswamy, P. M., Sperling, R. A., Coleman, R. E., et al. (2012). Amyloid-β assessed by florbetapir F 18 PET and 18-month cognitive decline: A multicenter study. Neurology, 79(16), 1636–1644.CrossRefPubMed Doraiswamy, P. M., Sperling, R. A., Coleman, R. E., et al. (2012). Amyloid-β assessed by florbetapir F 18 PET and 18-month cognitive decline: A multicenter study. Neurology, 79(16), 1636–1644.CrossRefPubMed
Zurück zum Zitat Doraiswamy, P. M., Sperling, R. A., Johnson, K., et al. (2014). Florbetapir F 18 amyloid PET and 36-month cognitive decline: A prospective multicenter study. Molecular Psychiatry, 19(9), 1044–1051.CrossRefPubMedPubMedCentral Doraiswamy, P. M., Sperling, R. A., Johnson, K., et al. (2014). Florbetapir F 18 amyloid PET and 36-month cognitive decline: A prospective multicenter study. Molecular Psychiatry, 19(9), 1044–1051.CrossRefPubMedPubMedCentral
Zurück zum Zitat Dubois, B., Hampel, H., Feldman, H. H., Scheltens, P., Aisen, P., Andrieu, S., Jack, C. R. (2016). Preclinical Alzheimer’s disease: Definition, natural history, and diagnostic criteria. Alzheimer’s and Dementia, 12, 292–323. Dubois, B., Hampel, H., Feldman, H. H., Scheltens, P., Aisen, P., Andrieu, S., Jack, C. R. (2016). Preclinical Alzheimer’s disease: Definition, natural history, and diagnostic criteria. Alzheimer’s and Dementia, 12, 292–323.
Zurück zum Zitat Duff, K., Norman, N. L., & Hoffman, J. M. (2014). Practice effects and amyloid deposition: Preliminary data on a method for enriching samples in clinical trials. Alzheimer’s Dis Assoc Disord, 28, 247–252.CrossRef Duff, K., Norman, N. L., & Hoffman, J. M. (2014). Practice effects and amyloid deposition: Preliminary data on a method for enriching samples in clinical trials. Alzheimer’s Dis Assoc Disord, 28, 247–252.CrossRef
Zurück zum Zitat Edmonds, E. C., Delano-Wood, L., Galasko, D. R., et al. (2015). Subtle cognitive decline and biomarker staging in preclinical Alzheimer’s disease. Journal of Alzheimer’s Disease, 47, 231–242.CrossRefPubMedPubMedCentral Edmonds, E. C., Delano-Wood, L., Galasko, D. R., et al. (2015). Subtle cognitive decline and biomarker staging in preclinical Alzheimer’s disease. Journal of Alzheimer’s Disease, 47, 231–242.CrossRefPubMedPubMedCentral
Zurück zum Zitat Elman, J. A., Oh, H., Madison, C. M., et al. (2014). Neural compensation in older people with brain amyloid-β deposition. Nature Neuroscience, 17(10), 1316–1318.CrossRefPubMedPubMedCentral Elman, J. A., Oh, H., Madison, C. M., et al. (2014). Neural compensation in older people with brain amyloid-β deposition. Nature Neuroscience, 17(10), 1316–1318.CrossRefPubMedPubMedCentral
Zurück zum Zitat Fortea, J., Sala-Llonch, R., Bartrés-Faz, D., et al. (2011). Cognitively preserved subjects with transitional cerebrospinal fluid ß-amyloid 1-42 values have thicker cortex in Alzheimer's disease vulnerable areas. Biological Psychiatry, 70(2), 183–190.CrossRefPubMed Fortea, J., Sala-Llonch, R., Bartrés-Faz, D., et al. (2011). Cognitively preserved subjects with transitional cerebrospinal fluid ß-amyloid 1-42 values have thicker cortex in Alzheimer's disease vulnerable areas. Biological Psychiatry, 70(2), 183–190.CrossRefPubMed
Zurück zum Zitat Fripp, J., Bourgeat, P., Acosta, O., et al. (2008). Appearance modeling of 11C PiB PET images: Characterizing amyloid deposition in Alzheimer's disease, mild cognitive impairment and healthy aging. NeuroImage, 43(3), 430–439.CrossRefPubMed Fripp, J., Bourgeat, P., Acosta, O., et al. (2008). Appearance modeling of 11C PiB PET images: Characterizing amyloid deposition in Alzheimer's disease, mild cognitive impairment and healthy aging. NeuroImage, 43(3), 430–439.CrossRefPubMed
Zurück zum Zitat Gidicsin, C. M., Maye, J. E., Locascio, J. J., et al. (2015). Cognitive activity relates to cognitive performance but not to Alzheimer disease biomarkers. Neurology, 85(1), 48–55.CrossRefPubMedPubMedCentral Gidicsin, C. M., Maye, J. E., Locascio, J. J., et al. (2015). Cognitive activity relates to cognitive performance but not to Alzheimer disease biomarkers. Neurology, 85(1), 48–55.CrossRefPubMedPubMedCentral
Zurück zum Zitat Gietl, A. F., Warnock, G., Riese, F., et al. (2015). Regional cerebral blood flow estimated by early PiB uptake is reduced in mild cognitive impairment and associated with age in an amyloid-dependent manner. Neurobiology of Aging, 36(4), 1619–1628.CrossRefPubMed Gietl, A. F., Warnock, G., Riese, F., et al. (2015). Regional cerebral blood flow estimated by early PiB uptake is reduced in mild cognitive impairment and associated with age in an amyloid-dependent manner. Neurobiology of Aging, 36(4), 1619–1628.CrossRefPubMed
Zurück zum Zitat Goldman, W. P., Price, J. L., Storandt, M., et al. (2001). Absence of cognitive impairment or decline in preclinical Alzheimer’s disease. Neurology, 56, 361–367.CrossRefPubMed Goldman, W. P., Price, J. L., Storandt, M., et al. (2001). Absence of cognitive impairment or decline in preclinical Alzheimer’s disease. Neurology, 56, 361–367.CrossRefPubMed
Zurück zum Zitat Gu, Y., Razlighi, Q. R., Zahodne, L. B., et al. (2015). Brain amyloid deposition and longitudinal cognitive decline in Nondemented older subjects: Results from a multi-ethnic population. PloS One, 10(7), e0123743.CrossRefPubMedPubMedCentral Gu, Y., Razlighi, Q. R., Zahodne, L. B., et al. (2015). Brain amyloid deposition and longitudinal cognitive decline in Nondemented older subjects: Results from a multi-ethnic population. PloS One, 10(7), e0123743.CrossRefPubMedPubMedCentral
Zurück zum Zitat Hardy, J. A., & Higgins, G. A. (1992). Alzheimer’s disease: The amyloid cascade hypothesis. Science, 256, 184–185.CrossRefPubMed Hardy, J. A., & Higgins, G. A. (1992). Alzheimer’s disease: The amyloid cascade hypothesis. Science, 256, 184–185.CrossRefPubMed
Zurück zum Zitat Hardy, J., & Selkoe, D. J. (2002). The amyloid hypothesis of Alzheimer’s disease: Progress and problems on the road to therapeutics. Science, 297, 353–356.CrossRefPubMed Hardy, J., & Selkoe, D. J. (2002). The amyloid hypothesis of Alzheimer’s disease: Progress and problems on the road to therapeutics. Science, 297, 353–356.CrossRefPubMed
Zurück zum Zitat Harrington, K. D., Gould, E., Lim, Y. Y., et al. (2016). Amyloid burden and incident depressive symptoms in cognitively normal older adults. International Journal of Geriatric Psychiatry. Advance online publication. doi:10.1002/gps.4489. Harrington, K. D., Gould, E., Lim, Y. Y., et al. (2016). Amyloid burden and incident depressive symptoms in cognitively normal older adults. International Journal of Geriatric Psychiatry. Advance online publication. doi:10.​1002/​gps.​4489.
Zurück zum Zitat Hassenstab, J., Monsell, S. E., Mock, C., et al. (2015). Neuropsychological markers of cognitive decline in persons with Alzheimer disease neuropathology. J Neuropath Exp Neurol, 74, 1086–1092.CrossRefPubMedPubMedCentral Hassenstab, J., Monsell, S. E., Mock, C., et al. (2015). Neuropsychological markers of cognitive decline in persons with Alzheimer disease neuropathology. J Neuropath Exp Neurol, 74, 1086–1092.CrossRefPubMedPubMedCentral
Zurück zum Zitat Hassenstab, J., Chasse, R., Grabow, P., et al. (2016). Certified normal: Alzheimer’s disease biomarkers and normative estimates of cognitive functioning. Neurobiology of Aging, 43, 23–33.CrossRefPubMedPubMedCentral Hassenstab, J., Chasse, R., Grabow, P., et al. (2016). Certified normal: Alzheimer’s disease biomarkers and normative estimates of cognitive functioning. Neurobiology of Aging, 43, 23–33.CrossRefPubMedPubMedCentral
Zurück zum Zitat Hatashita, S., & Yamasaki, H. (2010). Clinically different stages of Alzheimer's disease associated by amyloid deposition with [11C]-PIB PET imaging. Journal of Alzheimer’s Disease, 21(3), 995–1003.CrossRefPubMed Hatashita, S., & Yamasaki, H. (2010). Clinically different stages of Alzheimer's disease associated by amyloid deposition with [11C]-PIB PET imaging. Journal of Alzheimer’s Disease, 21(3), 995–1003.CrossRefPubMed
Zurück zum Zitat Hedden, T., Oh, H., Younger, A. P., & Patel, T. A. (2013). Meta-analysis of amyloid-cognition relations in cognitively normal older adults. Neurology, 80(14), 1341–1348.CrossRefPubMedPubMedCentral Hedden, T., Oh, H., Younger, A. P., & Patel, T. A. (2013). Meta-analysis of amyloid-cognition relations in cognitively normal older adults. Neurology, 80(14), 1341–1348.CrossRefPubMedPubMedCentral
Zurück zum Zitat Hedges, L. V. (1981). Distribution theory for Glass's estimator of effect size and related estimators. Journal of Educational Statistics, 6(2), 107–128.CrossRef Hedges, L. V. (1981). Distribution theory for Glass's estimator of effect size and related estimators. Journal of Educational Statistics, 6(2), 107–128.CrossRef
Zurück zum Zitat Hedges, L. V., & Vevea, J. L. (1998). Fixed- and random-effects models in meta-analysis. Psychological Methods, 4, 486–504.CrossRef Hedges, L. V., & Vevea, J. L. (1998). Fixed- and random-effects models in meta-analysis. Psychological Methods, 4, 486–504.CrossRef
Zurück zum Zitat Holland, D., McEvoy, L. K., Desikan, R. S., et al. (2012). Enrichment and stratification for Predementia Alzheimer disease clinical trials. PloS One, 7(10), e47739.CrossRefPubMedPubMedCentral Holland, D., McEvoy, L. K., Desikan, R. S., et al. (2012). Enrichment and stratification for Predementia Alzheimer disease clinical trials. PloS One, 7(10), e47739.CrossRefPubMedPubMedCentral
Zurück zum Zitat Hsu, P. J., Shou, H., Benzinger, T., et al. (2014). Amyloid burden in cognitively normal elderly is associated with preferential hippocampal subfield volume loss. Journal of Alzheimer’s Disease, 45(1), 27–33. Hsu, P. J., Shou, H., Benzinger, T., et al. (2014). Amyloid burden in cognitively normal elderly is associated with preferential hippocampal subfield volume loss. Journal of Alzheimer’s Disease, 45(1), 27–33.
Zurück zum Zitat Huijbers, W., Mormino, E. C., Wigman, S. E., et al. (2014). Amyloid deposition is linked to aberrant entorhinal activity among cognitively normal older adults. The Journal of Neuroscience, 34(15), 5200–5210.CrossRefPubMedPubMedCentral Huijbers, W., Mormino, E. C., Wigman, S. E., et al. (2014). Amyloid deposition is linked to aberrant entorhinal activity among cognitively normal older adults. The Journal of Neuroscience, 34(15), 5200–5210.CrossRefPubMedPubMedCentral
Zurück zum Zitat Iturria-Medina, Y., Sotero, R. C., & Toussaint, P. J. (2016). Early role of vascular dysregulation on late-onset Alzheimer’s disease based on multifactorial data-driven analysis. Nature Communications, 7, article number: 11934. Iturria-Medina, Y., Sotero, R. C., & Toussaint, P. J. (2016). Early role of vascular dysregulation on late-onset Alzheimer’s disease based on multifactorial data-driven analysis. Nature Communications, 7, article number: 11934.
Zurück zum Zitat Jack Jr., C. R., Knopman, D. S., Jagust, W. J., et al. (2010). Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade. Lancet Neurology, 9(1), 119–128.CrossRefPubMedPubMedCentral Jack Jr., C. R., Knopman, D. S., Jagust, W. J., et al. (2010). Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade. Lancet Neurology, 9(1), 119–128.CrossRefPubMedPubMedCentral
Zurück zum Zitat Jack Jr., C. R., Knopman, D. S., Weigand, S. D., et al. (2012). An operational approach to National Institute on Aging-Alzheimer's Association criteria for preclinical Alzheimer disease. Annals of Neurology, 71, 765–775.CrossRefPubMedPubMedCentral Jack Jr., C. R., Knopman, D. S., Weigand, S. D., et al. (2012). An operational approach to National Institute on Aging-Alzheimer's Association criteria for preclinical Alzheimer disease. Annals of Neurology, 71, 765–775.CrossRefPubMedPubMedCentral
Zurück zum Zitat Jack Jr., C. R., Knopman, D. S., Jagust, W. J., et al. (2013a). Update on hypothetical model of Alzheimer’s disease biomarkers. Lancet Neurology, 12(2), 207–216.CrossRefPubMedPubMedCentral Jack Jr., C. R., Knopman, D. S., Jagust, W. J., et al. (2013a). Update on hypothetical model of Alzheimer’s disease biomarkers. Lancet Neurology, 12(2), 207–216.CrossRefPubMedPubMedCentral
Zurück zum Zitat Jack Jr., C. R., Wiste, H. J., Weigand, S. D., et al. (2013b). Amyloid-first and neurodegeneration-first profiles characterize incident amyloid PET positivity. Neurology, 81(20), 1732–1740.CrossRefPubMedPubMedCentral Jack Jr., C. R., Wiste, H. J., Weigand, S. D., et al. (2013b). Amyloid-first and neurodegeneration-first profiles characterize incident amyloid PET positivity. Neurology, 81(20), 1732–1740.CrossRefPubMedPubMedCentral
Zurück zum Zitat Jack Jr., C. R., Wiste, H. J., Weigand, S. D., et al. (2014). Age-specific population frequencies of cerebral β-amyloidosis and neurodegeneration among people with normal cognitive function aged 50-89 years: A cross-sectional study. Lancet Neurology, 13(10), 997–1005.CrossRefPubMed Jack Jr., C. R., Wiste, H. J., Weigand, S. D., et al. (2014). Age-specific population frequencies of cerebral β-amyloidosis and neurodegeneration among people with normal cognitive function aged 50-89 years: A cross-sectional study. Lancet Neurology, 13(10), 997–1005.CrossRefPubMed
Zurück zum Zitat Jansen, W. J., Ossenkoppele, R., Knol, D. L., Tijms, B. M., Scheltens, P., Verhey, F. R. J., Visser, P. J., & Amyloid Biomarker Study Group. (2015). Prevalence of cerebral amyloid pathology in persons without dementia: A meta-analysis. JAMA, 313(19), 1924–1938.CrossRefPubMedPubMedCentral Jansen, W. J., Ossenkoppele, R., Knol, D. L., Tijms, B. M., Scheltens, P., Verhey, F. R. J., Visser, P. J., & Amyloid Biomarker Study Group. (2015). Prevalence of cerebral amyloid pathology in persons without dementia: A meta-analysis. JAMA, 313(19), 1924–1938.CrossRefPubMedPubMedCentral
Zurück zum Zitat Jedynak, B. M., Lang, A., Liu, B., et al. (2012). A computational neurodegenerative diease progression score: Method and results with the Alzheimer’s Disease Neuroimaging Initiative cohort. NeuroImage, 63, 1478–1486.CrossRefPubMedPubMedCentral Jedynak, B. M., Lang, A., Liu, B., et al. (2012). A computational neurodegenerative diease progression score: Method and results with the Alzheimer’s Disease Neuroimaging Initiative cohort. NeuroImage, 63, 1478–1486.CrossRefPubMedPubMedCentral
Zurück zum Zitat Jessen, F., Amariglio, R. E., van Boxtel, M., et al. (2014). A conceptual framework for research on subjective cognitive decline in preclinical Alzheimer’s disease. Alzheimer’s & Dementia, 10, 844–852.CrossRef Jessen, F., Amariglio, R. E., van Boxtel, M., et al. (2014). A conceptual framework for research on subjective cognitive decline in preclinical Alzheimer’s disease. Alzheimer’s & Dementia, 10, 844–852.CrossRef
Zurück zum Zitat Knopman, D. S., Jack Jr., C. R., Wiste, H. J., et al. (2012). Short-term clinical outcomes for stages of NIA-AA preclinical Alzheimer disease. Neurology, 78(20), 1576–1582.CrossRefPubMedPubMedCentral Knopman, D. S., Jack Jr., C. R., Wiste, H. J., et al. (2012). Short-term clinical outcomes for stages of NIA-AA preclinical Alzheimer disease. Neurology, 78(20), 1576–1582.CrossRefPubMedPubMedCentral
Zurück zum Zitat Knopman, D. S., Beiser, A., Machulda, M. M., et al. (2015). Spectrum of cognition short of dementia: Framingham heart study and Mayo Clinic study of aging. Neurology, 85, 1712–1721.CrossRefPubMedPubMedCentral Knopman, D. S., Beiser, A., Machulda, M. M., et al. (2015). Spectrum of cognition short of dementia: Framingham heart study and Mayo Clinic study of aging. Neurology, 85, 1712–1721.CrossRefPubMedPubMedCentral
Zurück zum Zitat Lamar, M., Resnick, S. M., & Zonderman, A. B. (2003). Longitudinal changes in verbal memory in older adults. Neurology, 60, 82–86.CrossRefPubMed Lamar, M., Resnick, S. M., & Zonderman, A. B. (2003). Longitudinal changes in verbal memory in older adults. Neurology, 60, 82–86.CrossRefPubMed
Zurück zum Zitat Langbaum, J. B., Hendrix, S. B., Ayutyanont, N., et al. (2014). An empirically derived composite cognitive test score with improved power to track and evaluate treatments for preclinical Alzheimer’s disease. Alzheimer’s & Dementia, 10, 666–674.CrossRef Langbaum, J. B., Hendrix, S. B., Ayutyanont, N., et al. (2014). An empirically derived composite cognitive test score with improved power to track and evaluate treatments for preclinical Alzheimer’s disease. Alzheimer’s & Dementia, 10, 666–674.CrossRef
Zurück zum Zitat Langbaum, J. B., Hendrix, S. B., Ayutyanont, N., et al. (2015). Establishing composite cognitive endpoints for use in preclinical Alzheimer’s disease trials. The Journal of Prevention of Alzheimer’s Disease, 2(1), 2–3.PubMedPubMedCentral Langbaum, J. B., Hendrix, S. B., Ayutyanont, N., et al. (2015). Establishing composite cognitive endpoints for use in preclinical Alzheimer’s disease trials. The Journal of Prevention of Alzheimer’s Disease, 2(1), 2–3.PubMedPubMedCentral
Zurück zum Zitat Liberati, A., Altman, D. G., Tetzlaff, J., Mulrow, C., Gotzsche, P. C., Ioannidis, J. P. A., Moher, D. (2009). The PRISMA statement for reporting systematic reviews and meta-analyses of studies that evaluate health care interventions: explanation and elaboration. PLOS Medicine, 6, e1000100. Liberati, A., Altman, D. G., Tetzlaff, J., Mulrow, C., Gotzsche, P. C., Ioannidis, J. P. A., Moher, D. (2009). The PRISMA statement for reporting systematic reviews and meta-analyses of studies that evaluate health care interventions: explanation and elaboration. PLOS Medicine, 6, e1000100.
Zurück zum Zitat Lim, H. K., Nebes, R., Snitz, B., et al. (2014). Regional amyloid burden and intrinsic connectivity networks in cognitively normal elderly subjects. Brain, 137, 3327–3338.CrossRefPubMedPubMedCentral Lim, H. K., Nebes, R., Snitz, B., et al. (2014). Regional amyloid burden and intrinsic connectivity networks in cognitively normal elderly subjects. Brain, 137, 3327–3338.CrossRefPubMedPubMedCentral
Zurück zum Zitat Lim, Y. Y., Maruff, P., Schindler, R., et al. (2015). Disruption of cholinergic neurotransmission exacerbates Aβ-related cognitive impairment in preclinical Alzheimer’s disease. Neurobiology of Aging, 36, 2709–2715.CrossRefPubMed Lim, Y. Y., Maruff, P., Schindler, R., et al. (2015). Disruption of cholinergic neurotransmission exacerbates Aβ-related cognitive impairment in preclinical Alzheimer’s disease. Neurobiology of Aging, 36, 2709–2715.CrossRefPubMed
Zurück zum Zitat Lim, Y. Y., Snyder, P. J., Pietrzak, R. H., et al. (2016). Sensitivity of composite scores to amyloid burden in preclinical Alzheimer's disease: Introducing the Z-scores of attention, verbal fluency, and episodic memory for Nondemented older adults composite score. Alzheimer’s & Dementia, 2, 19–26. Lim, Y. Y., Snyder, P. J., Pietrzak, R. H., et al. (2016). Sensitivity of composite scores to amyloid burden in preclinical Alzheimer's disease: Introducing the Z-scores of attention, verbal fluency, and episodic memory for Nondemented older adults composite score. Alzheimer’s & Dementia, 2, 19–26.
Zurück zum Zitat Llado-Saz, S., Atienzam, M., & Cantero, J. L. (2015). Increased levels of plasma amyloid-beta are related to cortical thinning and cognitive decline in cognitively normal elderly subjects. Neurobiology of Aging, 36(10), 2791–2797.CrossRefPubMed Llado-Saz, S., Atienzam, M., & Cantero, J. L. (2015). Increased levels of plasma amyloid-beta are related to cortical thinning and cognitive decline in cognitively normal elderly subjects. Neurobiology of Aging, 36(10), 2791–2797.CrossRefPubMed
Zurück zum Zitat Machulda, M. M., Hagen, C. E., Wiste, H. J., et al. (in press). Practice effects and longitudinal cognitive change in clinically normal older adutls differ by Alzheimer imaging biomarker status. The Clinical Neuropsychologist. doi:10.1080/13854046.2016.1241303. Machulda, M. M., Hagen, C. E., Wiste, H. J., et al. (in press). Practice effects and longitudinal cognitive change in clinically normal older adutls differ by Alzheimer imaging biomarker status. The Clinical Neuropsychologist. doi:10.​1080/​13854046.​2016.​1241303.
Zurück zum Zitat Marchant, N. L., Reed, B. R., Sanossian, N., et al. (2013). The aging brain and cognition: Contribution of vascular injury and aβ to mild cognitive dysfunction. JAMA Neurology, 70(4), 488–495.CrossRefPubMedPubMedCentral Marchant, N. L., Reed, B. R., Sanossian, N., et al. (2013). The aging brain and cognition: Contribution of vascular injury and aβ to mild cognitive dysfunction. JAMA Neurology, 70(4), 488–495.CrossRefPubMedPubMedCentral
Zurück zum Zitat Mathis, C. A., Kuller, L. H., Klunk, W. E., et al. (2013). In vivo assessment of amyloid-β deposition in nondemented very elderly subjects. Annals of Neurology, 73, 751–761.CrossRefPubMedPubMedCentral Mathis, C. A., Kuller, L. H., Klunk, W. E., et al. (2013). In vivo assessment of amyloid-β deposition in nondemented very elderly subjects. Annals of Neurology, 73, 751–761.CrossRefPubMedPubMedCentral
Zurück zum Zitat Molinuevo, J. L., Ripolles, P., Simó, M., et al. (2014). White matter changes in preclinical Alzheimer's disease: A magnetic resonance imaging-diffusion tensor imaging study on cognitively normal older people with positive amyloid β protein 42 levels. Neurobiology of Aging, 35(12), 2671–2680.CrossRefPubMed Molinuevo, J. L., Ripolles, P., Simó, M., et al. (2014). White matter changes in preclinical Alzheimer's disease: A magnetic resonance imaging-diffusion tensor imaging study on cognitively normal older people with positive amyloid β protein 42 levels. Neurobiology of Aging, 35(12), 2671–2680.CrossRefPubMed
Zurück zum Zitat Mormino, E. C., Brandel, M. G., Madison, C. M., et al. (2012). Not quite PIB-positive, not quite PIB-negative: Slight PIB elevations in elderly normal control subjects are biologically relevant. NeuroImage, 59, 1152–1160.CrossRefPubMed Mormino, E. C., Brandel, M. G., Madison, C. M., et al. (2012). Not quite PIB-positive, not quite PIB-negative: Slight PIB elevations in elderly normal control subjects are biologically relevant. NeuroImage, 59, 1152–1160.CrossRefPubMed
Zurück zum Zitat Nelson, P. T., Alafuzoff, I., Bigio, E. H., Bouras, C., Braak, H., Cairns, N. J., et al. (2012). Correlation of Alzheimer disease neuropathologic changes with cognitive status: A review of the literature. Journal of Neuropathology & Experimental Neurology, 71, 362–381.CrossRef Nelson, P. T., Alafuzoff, I., Bigio, E. H., Bouras, C., Braak, H., Cairns, N. J., et al. (2012). Correlation of Alzheimer disease neuropathologic changes with cognitive status: A review of the literature. Journal of Neuropathology & Experimental Neurology, 71, 362–381.CrossRef
Zurück zum Zitat Oh, H., Mormino, E. C., Madison, C., et al. (2010). β-amyloid affects frontal and posterior brain networks in normal aging. NeuroImage, 54, 1887–1895.CrossRefPubMedPubMedCentral Oh, H., Mormino, E. C., Madison, C., et al. (2010). β-amyloid affects frontal and posterior brain networks in normal aging. NeuroImage, 54, 1887–1895.CrossRefPubMedPubMedCentral
Zurück zum Zitat Oh, H., Madison, C., Haight, T. J., et al. (2012). Effects of age and β-amyloid on cognitive changes in normal elderly people. Neurobiology of Aging, 33(12), 2746–2755.CrossRefPubMedPubMedCentral Oh, H., Madison, C., Haight, T. J., et al. (2012). Effects of age and β-amyloid on cognitive changes in normal elderly people. Neurobiology of Aging, 33(12), 2746–2755.CrossRefPubMedPubMedCentral
Zurück zum Zitat Oh, H., Steffener, J., Razlighi, Q. R., et al. (2015). Aβ-related hyperactivation in frontoparietal control regions in cognitively normal elderly. Neurobiology of Aging, 36(12), 3247–3254.CrossRefPubMedPubMedCentral Oh, H., Steffener, J., Razlighi, Q. R., et al. (2015). Aβ-related hyperactivation in frontoparietal control regions in cognitively normal elderly. Neurobiology of Aging, 36(12), 3247–3254.CrossRefPubMedPubMedCentral
Zurück zum Zitat Oh, H., Steffener, J., Razlighi, Q. R., et al. (2016). β-amyloid deposition is associated with decreased right prefrontal activation during task switching among cognitively normal elderly. Journal of Neuroscience, 36(6), 1962–1970.CrossRefPubMedPubMedCentral Oh, H., Steffener, J., Razlighi, Q. R., et al. (2016). β-amyloid deposition is associated with decreased right prefrontal activation during task switching among cognitively normal elderly. Journal of Neuroscience, 36(6), 1962–1970.CrossRefPubMedPubMedCentral
Zurück zum Zitat Ossenkoppele, R., Madison, C., Oh, H., et al. (2014). Is verbal episodic memory in elderly with amyloid deposits preserved through altered neuronal function? Cerebral Cortex, 24(8), 2210–2218.CrossRefPubMed Ossenkoppele, R., Madison, C., Oh, H., et al. (2014). Is verbal episodic memory in elderly with amyloid deposits preserved through altered neuronal function? Cerebral Cortex, 24(8), 2210–2218.CrossRefPubMed
Zurück zum Zitat Petersen, R. C., Wiste, H. J., Weigand, S. D., et al. (2016). Association of Elevated Amyloid Levels with Cognition and Biomarkers in cognitively normal people from the community. JAMA Neurology, 73(1), 85–92.CrossRefPubMedPubMedCentral Petersen, R. C., Wiste, H. J., Weigand, S. D., et al. (2016). Association of Elevated Amyloid Levels with Cognition and Biomarkers in cognitively normal people from the community. JAMA Neurology, 73(1), 85–92.CrossRefPubMedPubMedCentral
Zurück zum Zitat Pike, K. E., Ellis, K. A., Villemagne, V. L., et al. (2011). Cognition and beta-amyloid in preclinical Alzheimer's disease: Data from the AIBL study. Neuropsychologia, 49(9), 2384–2390.CrossRefPubMed Pike, K. E., Ellis, K. A., Villemagne, V. L., et al. (2011). Cognition and beta-amyloid in preclinical Alzheimer's disease: Data from the AIBL study. Neuropsychologia, 49(9), 2384–2390.CrossRefPubMed
Zurück zum Zitat Rentz, D. M., Locascio, J. J., Becker, J. A., et al. (2010). Cognition, reserve, and amyloid deposition in normal aging. Annals of Neurology, 67, 353–364.PubMed Rentz, D. M., Locascio, J. J., Becker, J. A., et al. (2010). Cognition, reserve, and amyloid deposition in normal aging. Annals of Neurology, 67, 353–364.PubMed
Zurück zum Zitat Schott, J. M., Bartlett, J. W., Fox, N. C., & Barnes, J. (2010). Increased brain atrophy rates in cognitively normal older adults with low cerebrospinal fluid Aβ1-42. Annals of Neurology, 68(6), 825–834.CrossRefPubMed Schott, J. M., Bartlett, J. W., Fox, N. C., & Barnes, J. (2010). Increased brain atrophy rates in cognitively normal older adults with low cerebrospinal fluid Aβ1-42. Annals of Neurology, 68(6), 825–834.CrossRefPubMed
Zurück zum Zitat Snitz, B. E., Weissfeld, L. A., Lopez, O. L., et al. (2013). Cognitive trajectories associated with β-amyloid deposition in the oldest-old without dementia. Neurology, 80(15), 1378–1384.CrossRefPubMedPubMedCentral Snitz, B. E., Weissfeld, L. A., Lopez, O. L., et al. (2013). Cognitive trajectories associated with β-amyloid deposition in the oldest-old without dementia. Neurology, 80(15), 1378–1384.CrossRefPubMedPubMedCentral
Zurück zum Zitat Soldan, A., Pettigrew, C., Cai, Q., et al. (2016). Hypothetical preclinical Alzheimer disease groups and longitudinal cognitive change. JAMA Neurology, 73(6), 698–705.CrossRefPubMedPubMedCentral Soldan, A., Pettigrew, C., Cai, Q., et al. (2016). Hypothetical preclinical Alzheimer disease groups and longitudinal cognitive change. JAMA Neurology, 73(6), 698–705.CrossRefPubMedPubMedCentral
Zurück zum Zitat Sperling, R. A., Aisen, P. S., Beckett, L. A., et al. (2011). 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. Alzheimer’s & Dementia, 7(3), 280–292.CrossRef Sperling, R. A., Aisen, P. S., Beckett, L. A., et al. (2011). 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. Alzheimer’s & Dementia, 7(3), 280–292.CrossRef
Zurück zum Zitat Sperling, R. A., Johnson, K. A., Doraiswamy, P. M., et al. (2013). Amyloid deposition detected with florbetapir F 18 ((18)F-AV-45) is related to lower episodic memory performance in clinically normal older individuals. Neurobiology of Aging, 34(3), 822–831.CrossRefPubMed Sperling, R. A., Johnson, K. A., Doraiswamy, P. M., et al. (2013). Amyloid deposition detected with florbetapir F 18 ((18)F-AV-45) is related to lower episodic memory performance in clinically normal older individuals. Neurobiology of Aging, 34(3), 822–831.CrossRefPubMed
Zurück zum Zitat Susanto, T. A., Pua, E. P., & Zhou, J. (2015). Cognition, brain atrophy, and cerebrospinal fluid biomarkers changes from preclinical to dementia stage of Alzheimer's disease and the influence of apolipoprotein e. Journal of Alzheimer’s Disease, 45(1), 253–268.PubMed Susanto, T. A., Pua, E. P., & Zhou, J. (2015). Cognition, brain atrophy, and cerebrospinal fluid biomarkers changes from preclinical to dementia stage of Alzheimer's disease and the influence of apolipoprotein e. Journal of Alzheimer’s Disease, 45(1), 253–268.PubMed
Zurück zum Zitat Thai, C., Lim, Y. Y., Villemagne, V. L., et al. (2015). Amyloid-related memory decline in preclinical Alzheimer's disease is dependent on APOE ε4 and is detectable over 18-months. PloS One, 10(10), e0139082.CrossRefPubMedPubMedCentral Thai, C., Lim, Y. Y., Villemagne, V. L., et al. (2015). Amyloid-related memory decline in preclinical Alzheimer's disease is dependent on APOE ε4 and is detectable over 18-months. PloS One, 10(10), e0139082.CrossRefPubMedPubMedCentral
Zurück zum Zitat Vemuri, P., Lesnick, T. G., Przybelski, S. A., et al. (2015). Vascular and amyloid pathologies are independent predictors of cognitive decline in normal elderly. Brain, 138, 761–771.CrossRefPubMedPubMedCentral Vemuri, P., Lesnick, T. G., Przybelski, S. A., et al. (2015). Vascular and amyloid pathologies are independent predictors of cognitive decline in normal elderly. Brain, 138, 761–771.CrossRefPubMedPubMedCentral
Zurück zum Zitat Villemagne, V. L., Burnham, S., Bourgeat, P., et al. (2013). Amyloid β deposition, neurodegeneration, and cognitive decline in sporadic Alzheimer's disease: A prospective cohort study. Lancet Neurology, 12(4), 357–367.CrossRefPubMed Villemagne, V. L., Burnham, S., Bourgeat, P., et al. (2013). Amyloid β deposition, neurodegeneration, and cognitive decline in sporadic Alzheimer's disease: A prospective cohort study. Lancet Neurology, 12(4), 357–367.CrossRefPubMed
Zurück zum Zitat Villeneuve, S., Reed, B. R., Wirth, M., et al. (2014). Cortical thickness mediates the effect of β-amyloid on episodic memory. Neurology, 82(9), 761–767.CrossRefPubMedPubMedCentral Villeneuve, S., Reed, B. R., Wirth, M., et al. (2014). Cortical thickness mediates the effect of β-amyloid on episodic memory. Neurology, 82(9), 761–767.CrossRefPubMedPubMedCentral
Zurück zum Zitat Viola, K. L., & Klein, W. L. (2015). Amyloid B oligomers in Alzheimer’s disease pathogenesis, treatment, and diagnosis. Acta Neuropathologica, 129, 183–206.CrossRefPubMedPubMedCentral Viola, K. L., & Klein, W. L. (2015). Amyloid B oligomers in Alzheimer’s disease pathogenesis, treatment, and diagnosis. Acta Neuropathologica, 129, 183–206.CrossRefPubMedPubMedCentral
Zurück zum Zitat Vlassenko, A. G., McCue, L., Jasielec, M. S., et al. (2016). Imaging and cerebrospinal fluid biomarkers in early preclinical alzheimer disease. Annals of Neurology, 80(3), 379–387.CrossRefPubMedPubMedCentral Vlassenko, A. G., McCue, L., Jasielec, M. S., et al. (2016). Imaging and cerebrospinal fluid biomarkers in early preclinical alzheimer disease. Annals of Neurology, 80(3), 379–387.CrossRefPubMedPubMedCentral
Zurück zum Zitat Voevodskaya, O., Sundgren, P. C., Strandberg, O., et al. (2016). Myo-inositol changes precede amyloid pathology and relate to APOE genotype in Alzheimer disease. Neurology, 86(19), 1754–1761.CrossRefPubMedPubMedCentral Voevodskaya, O., Sundgren, P. C., Strandberg, O., et al. (2016). Myo-inositol changes precede amyloid pathology and relate to APOE genotype in Alzheimer disease. Neurology, 86(19), 1754–1761.CrossRefPubMedPubMedCentral
Zurück zum Zitat Vos, S. J., Xiong, C., Visser, P. J., et al. (2013). Preclinical Alzheimer's disease and its outcome: A longitudinal cohort study. Lancet Neurology, 12(10), 957–965.CrossRefPubMedPubMedCentral Vos, S. J., Xiong, C., Visser, P. J., et al. (2013). Preclinical Alzheimer's disease and its outcome: A longitudinal cohort study. Lancet Neurology, 12(10), 957–965.CrossRefPubMedPubMedCentral
Zurück zum Zitat Vos, S. J., Gordon, B. A., Su, Y., et al. (2016). NIA-AA staging of preclinical Alzheimer disease: Discordance and concordance of CSF and imaging biomarkers. Neurobiology of Aging, 44, 1–8.CrossRefPubMedPubMedCentral Vos, S. J., Gordon, B. A., Su, Y., et al. (2016). NIA-AA staging of preclinical Alzheimer disease: Discordance and concordance of CSF and imaging biomarkers. Neurobiology of Aging, 44, 1–8.CrossRefPubMedPubMedCentral
Zurück zum Zitat Wirth, M., Madison, C. M., Rabinovici, G. D., et al. (2013a). Alzheimer’s disease neurodegenerative biomarkers are associated with decreased cognitive function but not β-amyloid in cognitively normal older individuals. Neurobiology of Disease, 33(13), 5553–5563. Wirth, M., Madison, C. M., Rabinovici, G. D., et al. (2013a). Alzheimer’s disease neurodegenerative biomarkers are associated with decreased cognitive function but not β-amyloid in cognitively normal older individuals. Neurobiology of Disease, 33(13), 5553–5563.
Zurück zum Zitat Wirth, M., Oh, H., Mormino, E. C., et al. (2013b). The effect of amyloid β on cognitive decline is modulated by neural integrity in cognitively normal elderly. Alzheimer’s & Dementia, 9(6), 687–698.CrossRef Wirth, M., Oh, H., Mormino, E. C., et al. (2013b). The effect of amyloid β on cognitive decline is modulated by neural integrity in cognitively normal elderly. Alzheimer’s & Dementia, 9(6), 687–698.CrossRef
Metadaten
Titel
Detectable Neuropsychological Differences in Early Preclinical Alzheimer’s Disease: A Meta-Analysis
verfasst von
S. Duke Han
Caroline P. Nguyen
Nikki H. Stricker
Daniel A. Nation
Publikationsdatum
01.12.2017
Verlag
Springer US
Erschienen in
Neuropsychology Review / Ausgabe 4/2017
Print ISSN: 1040-7308
Elektronische ISSN: 1573-6660
DOI
https://doi.org/10.1007/s11065-017-9345-5

Weitere Artikel der Ausgabe 4/2017

Neuropsychology Review 4/2017 Zur Ausgabe

Leitlinien kompakt für die Neurologie

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Update Neurologie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.