Skip to main content
Erschienen in: Neuropsychology Review 4/2009

01.12.2009 | Review

Beta-Amyloid Deposition and the Aging Brain

verfasst von: Karen M. Rodrigue, Kristen M. Kennedy, Denise C. Park

Erschienen in: Neuropsychology Review | Ausgabe 4/2009

Einloggen, um Zugang zu erhalten

Abstract

A central issue in cognitive neuroscience of aging research is pinpointing precise neural mechanisms that determine cognitive outcome in late adulthood as well as identifying early markers of less successful cognitive aging. One promising biomarker is beta amyloid (Aβ) deposition. Several new radiotracers have been developed that bind to fibrillar Aβ providing sensitive estimates of amyloid deposition in various brain regions. Aβ imaging has been primarily used to study patients with Alzheimer’s Disease (AD) and individuals with Mild Cognitive Impairment (MCI); however, there is now building data on Aβ deposition in healthy controls that suggest at least 20% and perhaps as much as a third of healthy older adults show significant deposition. Considerable evidence suggests amyloid deposition precedes declines in cognition and may be the initiator in a cascade of events that indirectly leads to age-related cognitive decline. We review studies of Aβ deposition imaging in AD, MCI, and normal adults, its cognitive consequences, and the role of genetic risk and cognitive reserve.
Fußnoten
1
This bimodal distribution may serve to highlight the arbitrary nature of a categorical MCI group and emphasizes the continuum of cognitive performance from normal to AD, with MCI being a mid-point of this continuum.
 
Literatur
Zurück zum Zitat Aizenstein, H. J., Nebes, R. D., Saxton, J. A., Price, J. C., Mathis, C. A., Tsopelas, N. D., et al. (2008). Frequent amyloid deposition without significant cognitive impairment among the elderly. Archives of Neurology, 65, 1509–1517.CrossRefPubMed Aizenstein, H. J., Nebes, R. D., Saxton, J. A., Price, J. C., Mathis, C. A., Tsopelas, N. D., et al. (2008). Frequent amyloid deposition without significant cognitive impairment among the elderly. Archives of Neurology, 65, 1509–1517.CrossRefPubMed
Zurück zum Zitat Andreasen, N., Minthon, L., Vanmechelen, E., Vanderstichele, H., Davidsson, P., Winblad, B., et al. (1999). Cerebrospinal fluid tau and Abeta42 as predictors of development of Alzheimer’s disease in patients with mild cognitive impairment. Neuroscience Letters, 273, 5–8.CrossRefPubMed Andreasen, N., Minthon, L., Vanmechelen, E., Vanderstichele, H., Davidsson, P., Winblad, B., et al. (1999). Cerebrospinal fluid tau and Abeta42 as predictors of development of Alzheimer’s disease in patients with mild cognitive impairment. Neuroscience Letters, 273, 5–8.CrossRefPubMed
Zurück zum Zitat Andrews-Hanna, J. R., Snyder, A. Z., Vincent, J. L., Lustig, C., Head, D., Raichle, M. E., et al. (2007). Disruption of large-scale brain systems in advanced aging. Neuron, 56, 924–935.CrossRefPubMed Andrews-Hanna, J. R., Snyder, A. Z., Vincent, J. L., Lustig, C., Head, D., Raichle, M. E., et al. (2007). Disruption of large-scale brain systems in advanced aging. Neuron, 56, 924–935.CrossRefPubMed
Zurück zum Zitat Bennett, D. A., Schneider, J. A., Arvanitakis, Z., Kelly, J. F., Aggarwal, N. T., Shah, R. C., et al. (2006). Neuropathology of older persons without cognitive impairment from two community-based studies. Neurology, 66, 1837–1844.CrossRefPubMed Bennett, D. A., Schneider, J. A., Arvanitakis, Z., Kelly, J. F., Aggarwal, N. T., Shah, R. C., et al. (2006). Neuropathology of older persons without cognitive impairment from two community-based studies. Neurology, 66, 1837–1844.CrossRefPubMed
Zurück zum Zitat Bourgeat, P., Villemagne, V.L., Fripp, J., Pike, K.E., Raniga, P., Acosta, O., et al. (2009). Relation between amyloid burden, brain atrophy and memory in Alzheimer’s disease. Alzheimer’s Association 2009 International Conference on Alzheimer’s Disease (ICAD 2009), July. Bourgeat, P., Villemagne, V.L., Fripp, J., Pike, K.E., Raniga, P., Acosta, O., et al. (2009). Relation between amyloid burden, brain atrophy and memory in Alzheimer’s disease. Alzheimer’s Association 2009 International Conference on Alzheimer’s Disease (ICAD 2009), July.
Zurück zum Zitat Braak, H., & Braak, E. (1996). Evolution of the neuropathology of Alzheimer’s disease. Acta Neurologica Scandinavica, 165, 3–12. Braak, H., & Braak, E. (1996). Evolution of the neuropathology of Alzheimer’s disease. Acta Neurologica Scandinavica, 165, 3–12.
Zurück zum Zitat Buckner, R. L., Snyder, A. Z., Shannon, B. J., LaRossa, G., Sachs, R., Fotenos, A. F., et al. (2005). Molecular, structural, and functional characterization of Alzheimer’s disease: evidence for a relationship between default activity, amyloid, and memory. Journal of Neuroscience, 25, 7709–7717.CrossRefPubMed Buckner, R. L., Snyder, A. Z., Shannon, B. J., LaRossa, G., Sachs, R., Fotenos, A. F., et al. (2005). Molecular, structural, and functional characterization of Alzheimer’s disease: evidence for a relationship between default activity, amyloid, and memory. Journal of Neuroscience, 25, 7709–7717.CrossRefPubMed
Zurück zum Zitat Buckner, R. L., Andrews-Hanna, J. R., & Schacter, D. L. (2008). The brain’s default network: anatomy, function, and relevance to disease. Annals of the New York Academy of Sciences, 1124, 1–38.CrossRefPubMed Buckner, R. L., Andrews-Hanna, J. R., & Schacter, D. L. (2008). The brain’s default network: anatomy, function, and relevance to disease. Annals of the New York Academy of Sciences, 1124, 1–38.CrossRefPubMed
Zurück zum Zitat Buckner, R. L., Sepulcre, J., Talukdar, T., Krienen, F. M., Liu, H., Hedden, T., et al. (2009). Cortical hubs revealed by intrinsic functional connectivity: mapping, assessment of stability, and relation to Alzheimer’s disease. Journal of Neuroscience, 29, 1860–1873.CrossRefPubMed Buckner, R. L., Sepulcre, J., Talukdar, T., Krienen, F. M., Liu, H., Hedden, T., et al. (2009). Cortical hubs revealed by intrinsic functional connectivity: mapping, assessment of stability, and relation to Alzheimer’s disease. Journal of Neuroscience, 29, 1860–1873.CrossRefPubMed
Zurück zum Zitat Corder, E. H., Saunders, A. M., Strittmatter, W. J., Schmechel, D. E., Gaskell, P. C., Small, G. W., et al. (1993). Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer’s disease in late onset families. Science, 261, 921–923.CrossRefPubMed Corder, E. H., Saunders, A. M., Strittmatter, W. J., Schmechel, D. E., Gaskell, P. C., Small, G. W., et al. (1993). Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer’s disease in late onset families. Science, 261, 921–923.CrossRefPubMed
Zurück zum Zitat Dickerson, B. C., Bakkour, A., Salat, D. H., Feczko, E., Pacheco, J., Greve, D. N., et al. (2009). The cortical signature of Alzheimer’s disease: regionally specific cortical thinning relates to symptom severity in very mild to mild AD dementia and is detectable in asymptomatic amyloid-positive individuals. Cerebral Cortex, 19, 497–510.CrossRefPubMed Dickerson, B. C., Bakkour, A., Salat, D. H., Feczko, E., Pacheco, J., Greve, D. N., et al. (2009). The cortical signature of Alzheimer’s disease: regionally specific cortical thinning relates to symptom severity in very mild to mild AD dementia and is detectable in asymptomatic amyloid-positive individuals. Cerebral Cortex, 19, 497–510.CrossRefPubMed
Zurück zum Zitat Dickson, D. W., Crystal, H. A., Mattiace, L. A., Masur, D. M., Blau, A. D., Davies, P., et al. (1992). Identification of normal and pathological aging in prospectively studied nondemented elderly humans. Neurobiology of Aging, 13, 179–189.CrossRefPubMed Dickson, D. W., Crystal, H. A., Mattiace, L. A., Masur, D. M., Blau, A. D., Davies, P., et al. (1992). Identification of normal and pathological aging in prospectively studied nondemented elderly humans. Neurobiology of Aging, 13, 179–189.CrossRefPubMed
Zurück zum Zitat Diniz, B. S., Pinto, J. A., & Forlenza, O. V. (2008). 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 Journal of Biological Psychiatry, 9, 172–182.CrossRefPubMed Diniz, B. S., Pinto, J. A., & Forlenza, O. V. (2008). 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 Journal of Biological Psychiatry, 9, 172–182.CrossRefPubMed
Zurück zum Zitat Drzezga, A., Grimmer, T., Henriksen, G., Mühlau, M., Perneczky, R., Miederer, I., et al. (2009). Effect of APOE genotype on amyloid plaque load and gray matter volume in Alzheimer disease. Neurology, 72, 1487–1494.CrossRefPubMed Drzezga, A., Grimmer, T., Henriksen, G., Mühlau, M., Perneczky, R., Miederer, I., et al. (2009). Effect of APOE genotype on amyloid plaque load and gray matter volume in Alzheimer disease. Neurology, 72, 1487–1494.CrossRefPubMed
Zurück zum Zitat Edison, P., Archer, H. A., Hinz, R., Hammers, A., Pavese, N., Tai, Y. F., et al. (2007). Amyloid, hypometabolism, and cognition in Alzheimer disease: an [11C]PIB and [18F]FDG PET study. Neurology, 68, 501–508.CrossRefPubMed Edison, P., Archer, H. A., Hinz, R., Hammers, A., Pavese, N., Tai, Y. F., et al. (2007). Amyloid, hypometabolism, and cognition in Alzheimer disease: an [11C]PIB and [18F]FDG PET study. Neurology, 68, 501–508.CrossRefPubMed
Zurück zum Zitat Farlow, M. R., He, Y., Tekin, S., Xu, J., Lane, R., & Charles, H. C. (2004). Impact of APOE in mild cognitive impairment. Neurology, 63, 1898–1901.PubMed Farlow, M. R., He, Y., Tekin, S., Xu, J., Lane, R., & Charles, H. C. (2004). Impact of APOE in mild cognitive impairment. Neurology, 63, 1898–1901.PubMed
Zurück zum Zitat Farrer, L. A., Cupples, L. A., Haines, J. L., Hyman, B., Kukull, W. A., Mayeux, R., et al. (1997). Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. A meta-analysis. APOE and Alzheimer Disease meta analysis consortium. Journal of the American Medical Association, 278, 1349–1356.CrossRefPubMed Farrer, L. A., Cupples, L. A., Haines, J. L., Hyman, B., Kukull, W. A., Mayeux, R., et al. (1997). Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. A meta-analysis. APOE and Alzheimer Disease meta analysis consortium. Journal of the American Medical Association, 278, 1349–1356.CrossRefPubMed
Zurück zum Zitat Forsberg, A., Engler, H., Almkvist, O., Blomquist, G., Hagman, G., Wall, A., et al. (2008). PET imaging of amyloid deposition in patients with mild cognitive impairment. Neurobiology of Aging, 29, 1456–1465.CrossRefPubMed Forsberg, A., Engler, H., Almkvist, O., Blomquist, G., Hagman, G., Wall, A., et al. (2008). PET imaging of amyloid deposition in patients with mild cognitive impairment. Neurobiology of Aging, 29, 1456–1465.CrossRefPubMed
Zurück zum Zitat Fotenos, A. F., Mintun, M. A., Snyder, A. Z., Morris, J. C., & Buckner, R. L. (2008). Brain volume decline in aging: evidence for a relation between socioeconomic status, preclinical Alzheimer disease, and reserve. Archives of Neurology, 65, 113–120.CrossRefPubMed Fotenos, A. F., Mintun, M. A., Snyder, A. Z., Morris, J. C., & Buckner, R. L. (2008). Brain volume decline in aging: evidence for a relation between socioeconomic status, preclinical Alzheimer disease, and reserve. Archives of Neurology, 65, 113–120.CrossRefPubMed
Zurück zum Zitat Fripp, J., Bourgeat, P., Acosta, O., Raniga, P., Modat, M., Pike, K. E., 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, 430–439.CrossRefPubMed Fripp, J., Bourgeat, P., Acosta, O., Raniga, P., Modat, M., Pike, K. E., 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, 430–439.CrossRefPubMed
Zurück zum Zitat Ghisletta, P., & Lindenberger, U. (2003). Age-based structural dynamics between perceptual speed and knowledge in the Berlin aging study: direct evidence for ability dedifferentiation in old age. Psychology and Aging, 18, 696–713.CrossRefPubMed Ghisletta, P., & Lindenberger, U. (2003). Age-based structural dynamics between perceptual speed and knowledge in the Berlin aging study: direct evidence for ability dedifferentiation in old age. Psychology and Aging, 18, 696–713.CrossRefPubMed
Zurück zum Zitat Greicius, M. D., Krasnow, B., Reiss, A. L., & Menon, V. (2003). Functional connectivity in the resting brain: a network analysis of the default mode hypothesis. Proceedings of the National Academy of Sciences of the United States of America, 100, 253–258.CrossRefPubMed Greicius, M. D., Krasnow, B., Reiss, A. L., & Menon, V. (2003). Functional connectivity in the resting brain: a network analysis of the default mode hypothesis. Proceedings of the National Academy of Sciences of the United States of America, 100, 253–258.CrossRefPubMed
Zurück zum Zitat Grimmer, T., Riemenschneider, M., Förstl, H., Henriksen, G., Klunk, W. E., Mathis, C. A., et al. (2009). Beta amyloid in Alzheimer’s disease: increased deposition in brain is reflected in reduced concentration in cerebrospinal fluid. Biological Psychiatry, 65, 927–934.CrossRefPubMed Grimmer, T., Riemenschneider, M., Förstl, H., Henriksen, G., Klunk, W. E., Mathis, C. A., et al. (2009). Beta amyloid in Alzheimer’s disease: increased deposition in brain is reflected in reduced concentration in cerebrospinal fluid. Biological Psychiatry, 65, 927–934.CrossRefPubMed
Zurück zum Zitat Grundman, M., Sencakova, D., Jack, C. R., Jr., Petersen, R. C., Kim, H. T., Schultz, A., et al. (2002). Brain MRI hippocampal volume and prediction of clinical status in a mild cognitive impairment trial. Journal of Molecular Neuroscience, 19, 23–27.CrossRefPubMed Grundman, M., Sencakova, D., Jack, C. R., Jr., Petersen, R. C., Kim, H. T., Schultz, A., et al. (2002). Brain MRI hippocampal volume and prediction of clinical status in a mild cognitive impairment trial. Journal of Molecular Neuroscience, 19, 23–27.CrossRefPubMed
Zurück zum Zitat Gutchess, A. H., Welsh, R. C., Hedden, T., Bangert, A., Minear, M., Liu, L. L., et al. (2005). Aging and the neural correlates of successful picture encoding: frontal activations compensate for decreased medial-temporal activity. Journal of Cognitive Neuroscience, 17, 84–96.CrossRefPubMed Gutchess, A. H., Welsh, R. C., Hedden, T., Bangert, A., Minear, M., Liu, L. L., et al. (2005). Aging and the neural correlates of successful picture encoding: frontal activations compensate for decreased medial-temporal activity. Journal of Cognitive Neuroscience, 17, 84–96.CrossRefPubMed
Zurück zum Zitat Hedden, T., & Gabrieli, J. D. E. (2004). Insights into the ageing mind: a view from cognitive neuroscience. Nature Reviews Neuroscience, 5, 87–97.CrossRefPubMed Hedden, T., & Gabrieli, J. D. E. (2004). Insights into the ageing mind: a view from cognitive neuroscience. Nature Reviews Neuroscience, 5, 87–97.CrossRefPubMed
Zurück zum Zitat Ichise, M., Plett, S., Joshi, A., Stern, Y., van Heertum, R., Lowe, V., et al. (2008). Quantitative comparison of three novel 18F-labeled ligands for PET imaging of brain amyloid-β plaques in Alzheimer’s disease. Journal of Nuclear Medicine, 49, 214. Ichise, M., Plett, S., Joshi, A., Stern, Y., van Heertum, R., Lowe, V., et al. (2008). Quantitative comparison of three novel 18F-labeled ligands for PET imaging of brain amyloid-β plaques in Alzheimer’s disease. Journal of Nuclear Medicine, 49, 214.
Zurück zum Zitat Ingelsson, M., Fukumoto, H., Newell, K. L., Growdon, J. H., Hedley-Whyte, E. T., Frosch, M. P., et al. (2004). Early Abeta accumulation and progressive synaptic loss, gliosis, and tangle formation in AD brain. Neurology, 62, 925–931.PubMed Ingelsson, M., Fukumoto, H., Newell, K. L., Growdon, J. H., Hedley-Whyte, E. T., Frosch, M. P., et al. (2004). Early Abeta accumulation and progressive synaptic loss, gliosis, and tangle formation in AD brain. Neurology, 62, 925–931.PubMed
Zurück zum Zitat Jack, C. R., Lowe, V. J., Senjem, M. L., Weigand, S. D., Kemp, B. J., Shiung, M. M., et al. (2008). 11C PiB and structural MRI provide complementary information in imaging of Alzheimer’s disease and amnestic mild cognitive impairment. Brain, 131, 665–680.CrossRefPubMed Jack, C. R., Lowe, V. J., Senjem, M. L., Weigand, S. D., Kemp, B. J., Shiung, M. M., et al. (2008). 11C PiB and structural MRI provide complementary information in imaging of Alzheimer’s disease and amnestic mild cognitive impairment. Brain, 131, 665–680.CrossRefPubMed
Zurück zum Zitat Jack, C. R., Jr., Lowe, V. J., Weigand, S. D., Wiste, H. J., Senjem, M. L., Knopman, D. S., et al. (2009). Serial PIB and MRI in normal, mild cognitive impairment and Alzheimer’s disease: implications for sequence of pathological events in Alzheimer’s disease. Brain, 132, 1355–1365.CrossRefPubMed Jack, C. R., Jr., Lowe, V. J., Weigand, S. D., Wiste, H. J., Senjem, M. L., Knopman, D. S., et al. (2009). Serial PIB and MRI in normal, mild cognitive impairment and Alzheimer’s disease: implications for sequence of pathological events in Alzheimer’s disease. Brain, 132, 1355–1365.CrossRefPubMed
Zurück zum Zitat Jiang, Q., Lee, C. Y., Mandrekar, S., Wilkinson, B., Cramer, P., Zelcer, N., et al. (2008). ApoE promotes the proteolytic degradation of Abeta. Neuron, 58, 681–693.CrossRefPubMed Jiang, Q., Lee, C. Y., Mandrekar, S., Wilkinson, B., Cramer, P., Zelcer, N., et al. (2008). ApoE promotes the proteolytic degradation of Abeta. Neuron, 58, 681–693.CrossRefPubMed
Zurück zum Zitat Josephs, K. A., Whitwell, J. L., Ahmed, Z., Shiung, M. M., Weigand, S. D., Knopman, D. S., et al. (2008). Beta-amyloid burden is not associated with rates of brain atrophy. Annals of Neurology, 63, 204–212.CrossRefPubMed Josephs, K. A., Whitwell, J. L., Ahmed, Z., Shiung, M. M., Weigand, S. D., Knopman, D. S., et al. (2008). Beta-amyloid burden is not associated with rates of brain atrophy. Annals of Neurology, 63, 204–212.CrossRefPubMed
Zurück zum Zitat Kamenetz, F., Tomita, T., Hsieh, H., Seabrook, G., Borchelt, D., Iwatsubo, T., et al. (2003). APP processing and synaptic function. Neuron, 37, 925–937.CrossRefPubMed Kamenetz, F., Tomita, T., Hsieh, H., Seabrook, G., Borchelt, D., Iwatsubo, T., et al. (2003). APP processing and synaptic function. Neuron, 37, 925–937.CrossRefPubMed
Zurück zum Zitat Katzman, R., Terry, R., DeTeresa, R., Brown, T., Davies, P., Fuld, P., et al. (1988). Clinical, pathological, and neurochemical changes in dementia: a subgroup with preserved mental status and numerous neocortical plaques. Annals of Neurology, 23, 138–144.CrossRefPubMed Katzman, R., Terry, R., DeTeresa, R., Brown, T., Davies, P., Fuld, P., et al. (1988). Clinical, pathological, and neurochemical changes in dementia: a subgroup with preserved mental status and numerous neocortical plaques. Annals of Neurology, 23, 138–144.CrossRefPubMed
Zurück zum Zitat Kemppainen, N. M., Aalto, S., Wilson, I. A., Någren, K., Helin, S., Brück, A., et al. (2006). Voxel-based analysis of PET amyloid ligand [11C]PIB uptake in Alzheimer disease. Neurology, 67, 1575–1580.CrossRefPubMed Kemppainen, N. M., Aalto, S., Wilson, I. A., Någren, K., Helin, S., Brück, A., et al. (2006). Voxel-based analysis of PET amyloid ligand [11C]PIB uptake in Alzheimer disease. Neurology, 67, 1575–1580.CrossRefPubMed
Zurück zum Zitat Kemppainen, N. M., Aalto, S., Wilson, I. A., Någren, K., Helin, S., Brück, A., et al. (2007). PET amyloid ligand [11C]PIB uptake is increased in mild cognitive impairment. Neurology, 68, 1603–1606.CrossRefPubMed Kemppainen, N. M., Aalto, S., Wilson, I. A., Någren, K., Helin, S., Brück, A., et al. (2007). PET amyloid ligand [11C]PIB uptake is increased in mild cognitive impairment. Neurology, 68, 1603–1606.CrossRefPubMed
Zurück zum Zitat Kemppainen, N. M., Aalto, S., Karrasch, M., Någren, K., Savisto, N., Oikonen, V., et al. (2008). Cognitive reserve hypothesis: Pittsburgh Compound B and fluorodeoxyglucose positron emission tomography in relation to education in mild Alzheimer’s disease. Annals of Neurology, 63, 112–118.CrossRefPubMed Kemppainen, N. M., Aalto, S., Karrasch, M., Någren, K., Savisto, N., Oikonen, V., et al. (2008). Cognitive reserve hypothesis: Pittsburgh Compound B and fluorodeoxyglucose positron emission tomography in relation to education in mild Alzheimer’s disease. Annals of Neurology, 63, 112–118.CrossRefPubMed
Zurück zum Zitat Klunk, W. E., & Mathis, C. A. (2008). The future of amyloid-beta imaging: a tale of radionuclides and tracer proliferation. Current Opinion in Neurology, 21, 683–687.CrossRefPubMed Klunk, W. E., & Mathis, C. A. (2008). The future of amyloid-beta imaging: a tale of radionuclides and tracer proliferation. Current Opinion in Neurology, 21, 683–687.CrossRefPubMed
Zurück zum Zitat Klunk, W. E., Engler, H., Nordberg, A., Wang, Y., Blomqvist, G., Holt, D. P., et al. (2004). Imaging brain amyloid in Alzheimer’s disease with Pittsburgh Compound-B. Annals of Neurology, 55, 306–319.CrossRefPubMed Klunk, W. E., Engler, H., Nordberg, A., Wang, Y., Blomqvist, G., Holt, D. P., et al. (2004). Imaging brain amyloid in Alzheimer’s disease with Pittsburgh Compound-B. Annals of Neurology, 55, 306–319.CrossRefPubMed
Zurück zum Zitat Li, Y., Rinne, J. O., Mosconi, L., Pirraglia, E., Rusinek, H., DeSanti, S., et al. (2008). Regional analysis of FDG and PIB-PET images in normal aging, mild cognitive impairment, and Alzheimer’s disease. European Journal of Nuclear Medicine and Molecular Imaging, 35, 2169–2181.CrossRefPubMed Li, Y., Rinne, J. O., Mosconi, L., Pirraglia, E., Rusinek, H., DeSanti, S., et al. (2008). Regional analysis of FDG and PIB-PET images in normal aging, mild cognitive impairment, and Alzheimer’s disease. European Journal of Nuclear Medicine and Molecular Imaging, 35, 2169–2181.CrossRefPubMed
Zurück zum Zitat Linazasoro, G. (2008). Imaging beta-amyloid burden in aging and dementia. Neurology, 70, 1649–1650.CrossRefPubMed Linazasoro, G. (2008). Imaging beta-amyloid burden in aging and dementia. Neurology, 70, 1649–1650.CrossRefPubMed
Zurück zum Zitat Lopresti, B. J., Klunk, W. E., Mathis, C. A., Hoge, J. A., Ziolko, S. K., Lu, X., et al. (2005). Simplified quantification of Pittsburgh Compound B amyloid imaging PET studies: a comparative analysis. Journal of Nuclear Medicine, 46, 1959–1972.PubMed Lopresti, B. J., Klunk, W. E., Mathis, C. A., Hoge, J. A., Ziolko, S. K., Lu, X., et al. (2005). Simplified quantification of Pittsburgh Compound B amyloid imaging PET studies: a comparative analysis. Journal of Nuclear Medicine, 46, 1959–1972.PubMed
Zurück zum Zitat Mintun, M. A., Larossa, G. N., Sheline, Y. I., Dence, C. S., Lee, S. Y., Mach, R. H., et al. (2006). [11C]PIB in a nondemented population: potential antecedent marker of Alzheimer disease. Neurology, 67, 446–452.CrossRefPubMed Mintun, M. A., Larossa, G. N., Sheline, Y. I., Dence, C. S., Lee, S. Y., Mach, R. H., et al. (2006). [11C]PIB in a nondemented population: potential antecedent marker of Alzheimer disease. Neurology, 67, 446–452.CrossRefPubMed
Zurück zum Zitat Mormino, E. C., Kluth, J. T., Madison, C. M., Rabinovici, G. D., Baker, S. L., Miller, B. L., et al. (2009). Episodic memory loss is related to hippocampal-mediated {beta}-amyloid deposition in elderly subjects. Brain, 132, 1310–1323.CrossRefPubMed Mormino, E. C., Kluth, J. T., Madison, C. M., Rabinovici, G. D., Baker, S. L., Miller, B. L., et al. (2009). Episodic memory loss is related to hippocampal-mediated {beta}-amyloid deposition in elderly subjects. Brain, 132, 1310–1323.CrossRefPubMed
Zurück zum Zitat Morris, J. C., Roe, C. M., & Mintun, M. A. (2009). APOE status predicts PiB-positivity in nondemented aging: evidence for Preclinical Alzheimer’s disease. Neurology, 72, A92.CrossRef Morris, J. C., Roe, C. M., & Mintun, M. A. (2009). APOE status predicts PiB-positivity in nondemented aging: evidence for Preclinical Alzheimer’s disease. Neurology, 72, A92.CrossRef
Zurück zum Zitat Nelissen, N., Vandenbulcke, M., Fannes, K., Verbruggen, A., Peeters, R., Dupont, P., et al. (2007). Abeta amyloid deposition in the language system and how the brain responds. Brain, 130, 2055–2069.CrossRefPubMed Nelissen, N., Vandenbulcke, M., Fannes, K., Verbruggen, A., Peeters, R., Dupont, P., et al. (2007). Abeta amyloid deposition in the language system and how the brain responds. Brain, 130, 2055–2069.CrossRefPubMed
Zurück zum Zitat Nitsch, R. M., Farber, S. A., Growdon, J. H., & Wurtman, R. J. (1993). Release of amyloid beta-protein precursor derivatives by electrical depolarization of rat hippocampal slices. Proceedings of the National Academy of Sciences, 90, 5191–5193.CrossRef Nitsch, R. M., Farber, S. A., Growdon, J. H., & Wurtman, R. J. (1993). Release of amyloid beta-protein precursor derivatives by electrical depolarization of rat hippocampal slices. Proceedings of the National Academy of Sciences, 90, 5191–5193.CrossRef
Zurück zum Zitat Nordberg, A. (2008). Amyloid imaging in Alzheimer’s disease. Neuropsychologia, 46, 1636–1641.CrossRefPubMed Nordberg, A. (2008). Amyloid imaging in Alzheimer’s disease. Neuropsychologia, 46, 1636–1641.CrossRefPubMed
Zurück zum Zitat Nordlund, A., Rolstad, S., Klang, O., Lind, K., Pedersen, M., Blennow, K., et al. (2008). Episodic memory and speed/attention deficits are associated with Alzheimer-typical CSF abnormalities in MCI. Journal of the International Neuropsychological Society, 14, 582–590.CrossRefPubMed Nordlund, A., Rolstad, S., Klang, O., Lind, K., Pedersen, M., Blennow, K., et al. (2008). Episodic memory and speed/attention deficits are associated with Alzheimer-typical CSF abnormalities in MCI. Journal of the International Neuropsychological Society, 14, 582–590.CrossRefPubMed
Zurück zum Zitat Park, D. C., & Goh, J. O. (2009). Successful aging. In J. Cacioppo & G. Berntson (Eds.), Handbook of Cognitive Neuroscience for the Behavioral Sciences, Ch. 61 (pp. 1203–1219). Hoboken: Wiley. Park, D. C., & Goh, J. O. (2009). Successful aging. In J. Cacioppo & G. Berntson (Eds.), Handbook of Cognitive Neuroscience for the Behavioral Sciences, Ch. 61 (pp. 1203–1219). Hoboken: Wiley.
Zurück zum Zitat Park, D. C., & Reuter-Lorenz, P. A. (2009). The adaptive brain: aging and neurocognitive scaffolding. Annual Review of Psychology, 60, 173–196.CrossRefPubMed Park, D. C., & Reuter-Lorenz, P. A. (2009). The adaptive brain: aging and neurocognitive scaffolding. Annual Review of Psychology, 60, 173–196.CrossRefPubMed
Zurück zum Zitat Park, D. C., Lautenschlager, G., Hedden, T., Davidson, N. S., Smith, A. D., & Smith, P. K. (2002). Models of visuospatial and verbal memory across the adult life span. Psychology and Aging, 17, 299–320.CrossRefPubMed Park, D. C., Lautenschlager, G., Hedden, T., Davidson, N. S., Smith, A. D., & Smith, P. K. (2002). Models of visuospatial and verbal memory across the adult life span. Psychology and Aging, 17, 299–320.CrossRefPubMed
Zurück zum Zitat Petersen, R. C., Smith, G. E., Waring, S. C., Ivnik, R. J., Tangalos, E. G., & Kokmen, E. (1999). Mild cognitive impairment: clinical characterization and outcome. Archives of Neurology, 56, 303–308.CrossRefPubMed Petersen, R. C., Smith, G. E., Waring, S. C., Ivnik, R. J., Tangalos, E. G., & Kokmen, E. (1999). Mild cognitive impairment: clinical characterization and outcome. Archives of Neurology, 56, 303–308.CrossRefPubMed
Zurück zum Zitat Pike, K. E., Savage, G., Villemagne, V. L., Ng, S., Moss, S. A., Maruff, P., et al. (2007). Beta-amyloid imaging and memory in non-demented individuals: evidence for preclinical Alzheimer’s disease. Brain, 130, 2837–2844.CrossRefPubMed Pike, K. E., Savage, G., Villemagne, V. L., Ng, S., Moss, S. A., Maruff, P., et al. (2007). Beta-amyloid imaging and memory in non-demented individuals: evidence for preclinical Alzheimer’s disease. Brain, 130, 2837–2844.CrossRefPubMed
Zurück zum Zitat Raz, N., & Rodrigue, K. M. (2006). Differential aging of the brain: patterns, cognitive correlates and modifiers. Neuroscience & Biobehavioral Reviews, 30, 730–748.CrossRef Raz, N., & Rodrigue, K. M. (2006). Differential aging of the brain: patterns, cognitive correlates and modifiers. Neuroscience & Biobehavioral Reviews, 30, 730–748.CrossRef
Zurück zum Zitat Raz, N., & Kennedy, K. M. (2009). A systems approach to age-related change: Neuroanatomical changes, their modifiers, and cognitive correlates. In W. Jagust & M. D’Esposito (Eds.), Imaging the aging brain, Ch 4 (pp. 43–70). Oxford UP: NYC. Raz, N., & Kennedy, K. M. (2009). A systems approach to age-related change: Neuroanatomical changes, their modifiers, and cognitive correlates. In W. Jagust & M. D’Esposito (Eds.), Imaging the aging brain, Ch 4 (pp. 43–70). Oxford UP: NYC.
Zurück zum Zitat Reiman, E. M., Chen, K., Liu, X., Bandy, D., Yu, M., Lee, W., et al. (2009). Fibrillar amyloid-beta burden in cognitively normal people at 3 levels of genetic risk for Alzheimer’s disease. Proceedings of the National Academy of Sciences, 106, 6820–6825.CrossRef Reiman, E. M., Chen, K., Liu, X., Bandy, D., Yu, M., Lee, W., et al. (2009). Fibrillar amyloid-beta burden in cognitively normal people at 3 levels of genetic risk for Alzheimer’s disease. Proceedings of the National Academy of Sciences, 106, 6820–6825.CrossRef
Zurück zum Zitat Rodrigue, K. M., & Raz, N. (2004). Shrinkage of the entorhinal cortex over five years predicts memory performance in healthy adults. Journal of Neuroscience, 24, 956–963.CrossRefPubMed Rodrigue, K. M., & Raz, N. (2004). Shrinkage of the entorhinal cortex over five years predicts memory performance in healthy adults. Journal of Neuroscience, 24, 956–963.CrossRefPubMed
Zurück zum Zitat Rolstad, S., Nordlund, A., Eckerström, C., Gustavsson, M. H., Zetterberg, H., & Wallin, A. (2009). Biomarkers in relation to cognitive reserve in patients with mild cognitive impairment—proof of concept. Dementia and Geriatric Cognitive Disorders, 27, 194–200.CrossRefPubMed Rolstad, S., Nordlund, A., Eckerström, C., Gustavsson, M. H., Zetterberg, H., & Wallin, A. (2009). Biomarkers in relation to cognitive reserve in patients with mild cognitive impairment—proof of concept. Dementia and Geriatric Cognitive Disorders, 27, 194–200.CrossRefPubMed
Zurück zum Zitat Rowe, C. C., Ng, S., Ackermann, U., Gong, S. J., Pike, K., Savage, G., et al. (2007). Imaging beta-amyloid burden in aging and dementia. Neurology, 68, 1718–1725.CrossRefPubMed Rowe, C. C., Ng, S., Ackermann, U., Gong, S. J., Pike, K., Savage, G., et al. (2007). Imaging beta-amyloid burden in aging and dementia. Neurology, 68, 1718–1725.CrossRefPubMed
Zurück zum Zitat Rowe, C. C., Ackerman, U., Browne, W., Mulligan, R., Pike, K. L., O’Keefe, G., et al. (2008). Imaging of amyloid beta in Alzheimer’s disease with 18F-BAY94-9172, a novel PET tracer: proof of mechanism. Lancet Neurology, 7, 129–135.CrossRefPubMed Rowe, C. C., Ackerman, U., Browne, W., Mulligan, R., Pike, K. L., O’Keefe, G., et al. (2008). Imaging of amyloid beta in Alzheimer’s disease with 18F-BAY94-9172, a novel PET tracer: proof of mechanism. Lancet Neurology, 7, 129–135.CrossRefPubMed
Zurück zum Zitat Samuels, S. C., Silverman, J. M., Marin, D. B., Peskind, E. R., Younki, S. G., Greenberg, D. A., et al. (1999). CSF beta-amyloid, cognition, and APOE genotype in Alzheimer’s disease. Neurology, 52, 547–551.PubMed Samuels, S. C., Silverman, J. M., Marin, D. B., Peskind, E. R., Younki, S. G., Greenberg, D. A., et al. (1999). CSF beta-amyloid, cognition, and APOE genotype in Alzheimer’s disease. Neurology, 52, 547–551.PubMed
Zurück zum Zitat Scheinin, N.M., Aalto, S., Koikkalainen, J., Lötjönen, J., Karrasch, M., Kemppainen, N., et al. (2009). Follow-up of [11C]PIB uptake and brain volume in patients with Alzheimer disease and controls. Neurology, 73, 1186–1192. Scheinin, N.M., Aalto, S., Koikkalainen, J., Lötjönen, J., Karrasch, M., Kemppainen, N., et al. (2009). Follow-up of [11C]PIB uptake and brain volume in patients with Alzheimer disease and controls. Neurology, 73, 1186–1192.
Zurück zum Zitat Schmidt, M. L., Lee, V. M., & Trojanowski, J. Q. (1990). Relative abundance of tau and neurofilament epitopes in hippocampal neurofibrillary tangles. American Journal of Pathology, 136, 1069–1075. Schmidt, M. L., Lee, V. M., & Trojanowski, J. Q. (1990). Relative abundance of tau and neurofilament epitopes in hippocampal neurofibrillary tangles. American Journal of Pathology, 136, 1069–1075.
Zurück zum Zitat Shoghi-Jadid, K., Small, G. W., Agdeppa, E. D., Kepe, V., Ercoli, L. M., Siddarth, P., et al. (2002). Localization of neurofibrillary tangles and beta-amyloid plaques in the brains of living patients with Alzheimer disease. American Journal of Geriatric Psychiatry, 10, 24–35.PubMed Shoghi-Jadid, K., Small, G. W., Agdeppa, E. D., Kepe, V., Ercoli, L. M., Siddarth, P., et al. (2002). Localization of neurofibrillary tangles and beta-amyloid plaques in the brains of living patients with Alzheimer disease. American Journal of Geriatric Psychiatry, 10, 24–35.PubMed
Zurück zum Zitat Skovronsky, D. (2008). Use of eINDs for evaluation of multiple related PET amyloid plaque imaging agents. Journal of Nuclear Medicine, 49, 47N–48N.PubMed Skovronsky, D. (2008). Use of eINDs for evaluation of multiple related PET amyloid plaque imaging agents. Journal of Nuclear Medicine, 49, 47N–48N.PubMed
Zurück zum Zitat Skovronsky, D., Coleman, R. E., Frey, K., Garg, P., Ichise, M., Lowe, V., et al. (2008). Results of multi-center clinical trials comparing four 18F PET amyloid-imaging agents: preclinical to clinical correlations. Journal of Nuclear Medicine Meeting Abstracts, 49(1), 34P. Skovronsky, D., Coleman, R. E., Frey, K., Garg, P., Ichise, M., Lowe, V., et al. (2008). Results of multi-center clinical trials comparing four 18F PET amyloid-imaging agents: preclinical to clinical correlations. Journal of Nuclear Medicine Meeting Abstracts, 49(1), 34P.
Zurück zum Zitat Small, G. W., Kepe, V., Ercoli, L. M., Siddarth, P., Bookheimer, S. Y., Miller, K. J., et al. (2006). PET of brain amyloid and tau in mild cognitive impairment. New England Journal of Medicine, 355, 2652–2663.CrossRefPubMed Small, G. W., Kepe, V., Ercoli, L. M., Siddarth, P., Bookheimer, S. Y., Miller, K. J., et al. (2006). PET of brain amyloid and tau in mild cognitive impairment. New England Journal of Medicine, 355, 2652–2663.CrossRefPubMed
Zurück zum Zitat Small, G. W., Bookheimer, S. Y., Thompson, P. M., Cole, G. M., Huang, S., Kepe, V., et al. (2008). Current and future uses of neuroimaging for cognitively impaired patients. Lancet Neurology, 7, 161–172.CrossRefPubMed Small, G. W., Bookheimer, S. Y., Thompson, P. M., Cole, G. M., Huang, S., Kepe, V., et al. (2008). Current and future uses of neuroimaging for cognitively impaired patients. Lancet Neurology, 7, 161–172.CrossRefPubMed
Zurück zum Zitat Small, G. W., Siddarth, P., Burggren, A. C., Kepe, V., Ercoli, L. M., Miller, K. J., et al. (2009). Influence of cognitive status, age, and APOE-4 genetic risk on brain FDDNP positron-emission tomography imaging in persons without dementia. Archives of General Psychiatry, 66, 81–87.CrossRefPubMed Small, G. W., Siddarth, P., Burggren, A. C., Kepe, V., Ercoli, L. M., Miller, K. J., et al. (2009). Influence of cognitive status, age, and APOE-4 genetic risk on brain FDDNP positron-emission tomography imaging in persons without dementia. Archives of General Psychiatry, 66, 81–87.CrossRefPubMed
Zurück zum Zitat Sperling, R. A., Laviolette, P. S., O’Keefe, K., O’Brien, J., Rentz, D. M., Pihlajamaki, M., et al. (2009). Amyloid deposition is associated with impaired default network function in older persons without dementia. Neuron, 63, 178–188.CrossRefPubMed Sperling, R. A., Laviolette, P. S., O’Keefe, K., O’Brien, J., Rentz, D. M., Pihlajamaki, M., et al. (2009). Amyloid deposition is associated with impaired default network function in older persons without dementia. Neuron, 63, 178–188.CrossRefPubMed
Zurück zum Zitat Stern, Y. (2002). What is cognitive reserve? Theory and research application of the reserve concept. Journal of the International Neuropsychological Society, 8, 448–460.CrossRefPubMed Stern, Y. (2002). What is cognitive reserve? Theory and research application of the reserve concept. Journal of the International Neuropsychological Society, 8, 448–460.CrossRefPubMed
Zurück zum Zitat Strozyk, D., Blennow, K., White, L. R., & Launer, L. J. (2003). CSF Abeta 42 levels correlate with amyloid-neuropathology in a population-based autopsy study. Neurology, 60, 652–656.PubMed Strozyk, D., Blennow, K., White, L. R., & Launer, L. J. (2003). CSF Abeta 42 levels correlate with amyloid-neuropathology in a population-based autopsy study. Neurology, 60, 652–656.PubMed
Zurück zum Zitat Tapiola, T., Pirttilä, T., Mikkonen, M., Mehta, P. D., Alafuzoff, I., Koivisto, K., et al. (2000). Three-year follow-up of cerebrospinal fluid tau, beta-amyloid 42 and 40 concentrations in Alzheimer’s disease. Neuroscience Letters, 280, 119–122.CrossRefPubMed Tapiola, T., Pirttilä, T., Mikkonen, M., Mehta, P. D., Alafuzoff, I., Koivisto, K., et al. (2000). Three-year follow-up of cerebrospinal fluid tau, beta-amyloid 42 and 40 concentrations in Alzheimer’s disease. Neuroscience Letters, 280, 119–122.CrossRefPubMed
Zurück zum Zitat Thal, D.R., Capetillo-Zarate, E., Del Tredici, K., & Braak, H. (2006). The development of amyloid beta protein deposits in the aged brain. Science of Aging Knowledge Environment: SAGE KE, 2006(6), re1. Thal, D.R., Capetillo-Zarate, E., Del Tredici, K., & Braak, H. (2006). The development of amyloid beta protein deposits in the aged brain. Science of Aging Knowledge Environment: SAGE KE, 2006(6), re1.
Zurück zum Zitat Tolboom, N., Yaqub, M., van der Flier, W. M., Boellaard, R., Luurtsema, G., Windhorst, A. D., et al. (2009a). Detection of Alzheimer pathology in vivo using both 11C-PIB and 18F-FDDNP PET. Journal of Nuclear Medicine, 50, 191–197.CrossRefPubMed Tolboom, N., Yaqub, M., van der Flier, W. M., Boellaard, R., Luurtsema, G., Windhorst, A. D., et al. (2009a). Detection of Alzheimer pathology in vivo using both 11C-PIB and 18F-FDDNP PET. Journal of Nuclear Medicine, 50, 191–197.CrossRefPubMed
Zurück zum Zitat Tolboom, N., Yaqub, M., Boellaard, R., Luurtsema, G., Windhorst, A.D., Scheltens, P., et al. (2009b). Test-retest variability of quantitative [(11)C]PIB studies in Alzheimer’s disease. European Journal of Nuclear Medicine and Molecular Imaging, 36, 1629–1638. Tolboom, N., Yaqub, M., Boellaard, R., Luurtsema, G., Windhorst, A.D., Scheltens, P., et al. (2009b). Test-retest variability of quantitative [(11)C]PIB studies in Alzheimer’s disease. European Journal of Nuclear Medicine and Molecular Imaging, 36, 1629–1638.
Zurück zum Zitat Villemagne, V. L., Pike, K. E., Darby, D., Maruff, P., Savage, G., Ng, S., et al. (2008). Abeta deposits in older non-demented individuals with cognitive decline are indicative of preclinical Alzheimer’s disease. Neuropsychologia, 46, 1688–1697.CrossRefPubMed Villemagne, V. L., Pike, K. E., Darby, D., Maruff, P., Savage, G., Ng, S., et al. (2008). Abeta deposits in older non-demented individuals with cognitive decline are indicative of preclinical Alzheimer’s disease. Neuropsychologia, 46, 1688–1697.CrossRefPubMed
Zurück zum Zitat Wahlund, L. O., & Blennow, K. (2003). Cerebrospinal fluid biomarkers for disease stage and intensity in cognitively impaired patients. Neuroscience Letters, 339, 99–102.CrossRefPubMed Wahlund, L. O., & Blennow, K. (2003). Cerebrospinal fluid biomarkers for disease stage and intensity in cognitively impaired patients. Neuroscience Letters, 339, 99–102.CrossRefPubMed
Zurück zum Zitat Wishart, H. A., Saykin, A. J., McAllister, T. W., Rabin, L. A., McDonald, B. C., Flashman, L. A., et al. (2006). Regional brain atrophy in cognitively intact adults with a single APOE epsilon4 allele. Neurology, 67, 1221–1224.CrossRefPubMed Wishart, H. A., Saykin, A. J., McAllister, T. W., Rabin, L. A., McDonald, B. C., Flashman, L. A., et al. (2006). Regional brain atrophy in cognitively intact adults with a single APOE epsilon4 allele. Neurology, 67, 1221–1224.CrossRefPubMed
Zurück zum Zitat Wong, D., Rosenberg, P., Zhou, Y., Kumar, A., Ravert, H., Brasic, J., et al. (2008). In vivo imaging of amyloid deposition in Alzheimer’s disease using the novel radioligand [18F] AV-45. Journal of Nuclear Medicine Meeting Abstracts, 49(1), 214P. Wong, D., Rosenberg, P., Zhou, Y., Kumar, A., Ravert, H., Brasic, J., et al. (2008). In vivo imaging of amyloid deposition in Alzheimer’s disease using the novel radioligand [18F] AV-45. Journal of Nuclear Medicine Meeting Abstracts, 49(1), 214P.
Zurück zum Zitat Zhang, W., Kung, M., Oya, S., Hou, C., & Kung, H. F. (2007). 18F-labeled styrylpyridines as PET agents for amyloid plaque imaging. Nuclear Medicine and Biology, 34, 89–97.CrossRefPubMed Zhang, W., Kung, M., Oya, S., Hou, C., & Kung, H. F. (2007). 18F-labeled styrylpyridines as PET agents for amyloid plaque imaging. Nuclear Medicine and Biology, 34, 89–97.CrossRefPubMed
Metadaten
Titel
Beta-Amyloid Deposition and the Aging Brain
verfasst von
Karen M. Rodrigue
Kristen M. Kennedy
Denise C. Park
Publikationsdatum
01.12.2009
Verlag
Springer US
Erschienen in
Neuropsychology Review / Ausgabe 4/2009
Print ISSN: 1040-7308
Elektronische ISSN: 1573-6660
DOI
https://doi.org/10.1007/s11065-009-9118-x

Weitere Artikel der Ausgabe 4/2009

Neuropsychology Review 4/2009 Zur Ausgabe

Leitlinien kompakt für die Neurologie

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Akuter Schwindel: Wann lohnt sich eine MRT?

28.04.2024 Schwindel Nachrichten

Akuter Schwindel stellt oft eine diagnostische Herausforderung dar. Wie nützlich dabei eine MRT ist, hat eine Studie aus Finnland untersucht. Immerhin einer von sechs Patienten wurde mit akutem ischämischem Schlaganfall diagnostiziert.

Niedriger diastolischer Blutdruck erhöht Risiko für schwere kardiovaskuläre Komplikationen

25.04.2024 Hypotonie Nachrichten

Wenn unter einer medikamentösen Hochdrucktherapie der diastolische Blutdruck in den Keller geht, steigt das Risiko für schwere kardiovaskuläre Ereignisse: Darauf deutet eine Sekundäranalyse der SPRINT-Studie hin.

Frühe Alzheimertherapie lohnt sich

25.04.2024 AAN-Jahrestagung 2024 Nachrichten

Ist die Tau-Last noch gering, scheint der Vorteil von Lecanemab besonders groß zu sein. Und beginnen Erkrankte verzögert mit der Behandlung, erreichen sie nicht mehr die kognitive Leistung wie bei einem früheren Start. Darauf deuten neue Analysen der Phase-3-Studie Clarity AD.

Viel Bewegung in der Parkinsonforschung

25.04.2024 Parkinson-Krankheit Nachrichten

Neue arznei- und zellbasierte Ansätze, Frühdiagnose mit Bewegungssensoren, Rückenmarkstimulation gegen Gehblockaden – in der Parkinsonforschung tut sich einiges. Auf dem Deutschen Parkinsonkongress ging es auch viel um technische Innovationen.

Update Neurologie

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