The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.
Correlation Between Elevated Levels of Amyloid β-Peptide in the Brain and Cognitive Decline
Abstract
CONTEXT: Alzheimer disease (AD) is characterized neuropathologically by the presence of amyloid beta-peptide (Abeta)-containing plaques and neurofibrillary tangles composed of abnormal tau protein. Considerable controversy exists as to whether the extent of accumulation of Abeta correlates with dementia and whether Abeta alterations precede or follow changes in tau. OBJECTIVES: To determine whether accumulation of Abeta correlates with the earliest signs of cognitive deterioration and to define the relationship between Abeta accumulation and early tau changes. DESIGN, SETTING, AND PATIENTS: Postmortem cross-sectional study of 79 nursing home residents with Clinical Dementia Rating (CDR) scale scores of 0.0 to 5.0 who died between 1986 and 1997, comparing the levels of Abeta variants in the cortices of the subjects with no (CDR score, 0.0 [n = 16]), questionable (CDR score, 0.5 [n = 11]), mild (CDR score, 1.0 [n = 22]), moderate (CDR score, 2.0 [n = 15]), or severe (CDR score, 4.0 or 5.0 [n = 15]) dementia. MAIN OUTCOME MEASURES: Levels of total Abeta peptides with intact or truncated amino termini and ending in either amino acid 40 (A(beta)x-40) or 42 (A(beta)x-42) in 5 neocortical brain regions as well as levels of tau protein undergoing early conformational changes in frontal cortex, as a function of CDR score. RESULTS: The levels of both A(beta)x-40 and A(beta)x-42 were elevated even in cases classified as having questionable dementia (CDR score = 0.5), and increases of both peptides correlated with progression of dementia. Levels of the more fibril-prone A(beta)x-42 peptide were higher than those of A(beta)x-40 in nondemented cases and remained higher throughout progression of disease in all regions examined. Finally, increases in A(beta)x-40 and A(beta)x-42 precede significant tau pathology at least in the frontal cortex, an area chosen for examination because of the absence of neuritic changes in the absence of disease. CONCLUSIONS: In this study, levels of total A(beta)x-40 and A(beta)x-42 were elevated early in dementia and levels of both peptides were strongly correlated with cognitive decline. Of particular interest, in the frontal cortex, Abeta was elevated before the occurrence of significant tau pathology. These results support an important role for Abeta in mediating initial pathogenic events in AD dementia and suggest that treatment strategies targeting the formation, accumulation, or cytotoxic effects of Abeta should be pursued.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“The accumulation of Aβ has been suggested to prompt neurodegeneration, thereby leading to the clinical dementia often witnessed in AD patients [15].”
From The Multifaceted Role of Neuroprotective Plants in Alzheimer’s Disease Treatment (2022) · cites this paper as [15]
In the citing paper
“biochemical studies on human AD brain indicated that the soluble pool of Aβ42 correlated best with degree of cognitive loss [108, 118, 130].”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [130]
In the citing paper
“Studies have increasingly differentiated between soluble and insoluble pools of Aβ within the brain, where it is the increase in the soluble pool of Aβ42 that tracks best with cognitive decline in AD [108, 118, 130].”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [130]
Citations
Cites
A New Clinical Scale for the Staging of Dementia
Hughes, C. P., Berg, L., Danziger, W., Coben, L. A., & Martin, R. L. (1982) · British Journal of Psychiatry · doi:10.1192/bjp.140.6.566 · Cited by 7,056
Mirra, S. S., Heyman, A., McKeel, D., Sumi, S. M., Crain, B. J., Brownlee, L. M., Vogel, F. S., Hughes, J. P., Belle, G. V., Berg, L., et al. (1991) · Neurology · doi:10.1212/wnl.41.4.479 · Cited by 4,961
Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer's disease
Arriagada, P. V., Growdon, J. H., Hedley-Whyte, E. T., & Hyman, B. T. (1992) · Neurology · doi:10.1212/wnl.42.3.631 · Cited by 2,668
Jarrett, J. T., & Lansbury, P. T. (1993) · Cell · doi:10.1016/0092-8674(93)90635-4 · Cited by 2,178
Amyloid, the presenilins and Alzheimer’s disease
Hardy, J. (1997) · Trends in Neurosciences · doi:10.1016/s0166-2236(96)01030-2 · Cited by 1,370
Mechanisms of Neuronal Degeneration in Alzheimer's Disease
Yankner, B. A. (1996) · Neuron · doi:10.1016/s0896-6273(00)80115-4 · Cited by 953
Alzheimer's Disease--Genotypes, Phenotype, and Treatments
Selkoe, D. J. (1997) · Science · doi:10.1126/science.275.5300.630 · Cited by 879
Cellular processing of β-amyloid precursor protein and the genesis of amyloid β-peptide
Haass, C., & Selkoe, D. J. (1993) · Cell · doi:10.1016/0092-8674(93)90312-e · Cited by 686
Tau protein pathology in neurodegenerative diseases
Spillantini, M. G., & Goedert, M. (1998) · Trends in Neurosciences · doi:10.1016/s0166-2236(98)01337-x · Cited by 683
Bierer, L. M., Haroutunian, V. H., Gabriel, S., Knott, P. J., Carlin, L. S., Purohit, D. P., Perl, D. P., Schmeidler, J., Kanof, P. D., & Davis, K. L. (1995) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.1995.64020749.x · Cited by 580
Cited by
Sorted by citations
Items 601–700 of 1,000
Pistell, P. J., Zhu, M., & Ingram, D. K. (2008) · Neuroscience · doi:10.1016/j.neuroscience.2008.01.025 · Cited by 47
Down‐regulation of glutamatergic terminals (VGLUT1) driven by Aβ in Alzheimer's disease
Rodriguez‐Perdigon, M., Tordera, R. M., Gil-Bea, F. J., Gereñu, G., Ramírez, M. J., & Solas, M. (2016) · Hippocampus · doi:10.1002/hipo.22607 · Cited by 49
Attia, H., Albuhayri, S., Alaraidh, S., Alotaibi, A., Yacoub, H. I., Mohamad, R. A., & Alamin, M. A. (2020) · Journal of Biochemical and Molecular Toxicology · doi:10.1002/jbt.22519 · Cited by 47
Takeuchi, D., Sato, N., Shimamura, M., Kurinami, H., Takeda, S., Shinohara, M., Suzuki, S., Kojima, M., Ogihara, T., & Morishita, R. (2008) · Gene Therapy · doi:10.1038/sj.gt.3303094 · Cited by 47
Magnetic resonance and PET studies in the early diagnosis of Alzheimer’s disease
Mosconi, L., De Santi, S., Rusinek, H., Convit, A., & de Leon, M. J. (2004) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.4.5.831 · Cited by 46
Sehlin, D., Hedlund, M., Lord, A., Englund, H., Gellerfors, P., Paulie, S., Lannfelt, L., & Pettersson, F. E. (2010) · Neurodegenerative Diseases · doi:10.1159/000316530 · Cited by 47
Belluti, F., Bartolini, M., Bottegoni, G., Bisi, A., Cavalli, A., Andrisano, V., & Rampa, A. (2011) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2011.02.019 · Cited by 46
Luo, W., Su, Y., Chen, H., Tian, R.-G., Su, L.-P., Wang, Y., Yang, L., Yue, J., & Wang, C. (2013) · Bioorganic & Medicinal Chemistry · doi:10.1016/j.bmc.2013.09.061 · Cited by 46
Liu, L., Zhang, L., Niu, L., Xu, M., Mao, X., Yang, Y., & Wang, C. (2011) · ACS Nano · doi:10.1021/nn201773x · Cited by 46
Postmortem Indices Linking Risk Factors to Cognition
Bennett, D. A. (2006) · Alzheimer Disease & Associated Disorders · doi:10.1097/00002093-200607001-00009 · Cited by 46
Adwan, L. I., Subaiea, G. M., & Zawia, N. H. (2014) · Neuropharmacology · doi:10.1016/j.neuropharm.2014.01.009 · Cited by 45
Progressive neuropathology and cognitive decline in a single Arctic APP transgenic mouse model
Rönnbäck, A., Zhu, S., Dillner, K., Aoki, M., Lilius, L., Näslund, J., Winblad, B. G., & Graff, C. (2009) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2009.02.021 · Cited by 47
Self-citationLi, J., Liu, C., Wei, N., Li, X., Liu, Y.-Y., Yang, R., & Jia, Y. (2016) · Brain Research · doi:10.1016/j.brainres.2016.04.011 · Cited by 45
Lebois, E. P., Schroeder, J. P., Esparza, T. J., Bridges, T. M., Lindsley, C. W., Conn, P. J., Brody, D. L., Daniels, J. S., & Levey, A. I. (2017) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.6b00278 · Cited by 45
Genetic Dissection of Alzheimer’s Disease Using Drosophila Models
Jeon, Y., Lee, J., Choi, B., Won, S.-Y., & Cho, K. S. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21030884 · Cited by 46
Memory performance is related to amyloid and tau pathology in the hippocampus
Reitz, C., Honig, L. S., Vonsattel, J. P., Tang, M.-X., & Mayeux, R. P. (2009) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp.2008.154146 · Cited by 49
Amyloid Imaging: From Benchtop to Bedside
Wu, C., Pike, V. W., & Wang, Y. (2005) · Current topics in developmental biology/Current Topics in Developmental Biology · doi:10.1016/s0070-2153(05)70008-9 · Cited by 45
Air Pollution and Traffic Noise Interact to Affect Cognitive Health in Elderly Hispanics
Yu, Y., Su, J. G., Jerrett, M., Paul, K. C., Lee, E. Y., Shih, I., Haan, M. N., & Ritz, B. R. (2022) · Environment International · doi:10.1016/j.envint.2023.107810 · Cited by 44
The Role of β-Amyloid Protein in Synaptic Function: Implications for Alzheimers Disease Therapy
Peña‐Ortega, F., Gutiérrez-Lerma, A. I., Quiroz‐Baez, R., & Arias, C. (2006) · Current Neuropharmacology · doi:10.2174/157015906776359531 · Cited by 45
Lord, A., Philipson, O., Klingstedt, T., Westermark, G. T., Hammarström, P., Nilsson, K. P. R., & Nilsson, L. N. G. (2011) · American Journal Of Pathology · doi:10.1016/j.ajpath.2011.01.052 · Cited by 46
Salivary Biomarkers: Future Approaches for Early Diagnosis of Neurodegenerative Diseases
Schepici, G., Silvestro, S., Trubiani, O., Bramanti, P., & Mazzon, E. (2020) · Brain Sciences · doi:10.3390/brainsci10040245 · Cited by 44
Short-term treatment with tolfenamic acid improves cognitive functions in Alzheimer's disease mice
Subaiea, G. M., Adwan, L. I., Ahmed, A. H., Stevens, K. E., & Zawia, N. H. (2013) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2013.04.002 · Cited by 45
Tremblay, C., François, A., Delay, C., Freland, L., Vandal, M., Bennett, D. A., & Calon, F. (2017) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlw109 · Cited by 49
Schenk, D., Games, D., & Seubert, P. (2001) · Journal of Molecular Neuroscience · doi:10.1385/jmn:17:2:259 · Cited by 44
Rönnbäck, A., Sagelius, H., Bergstedt, K. D., Näslund, J., Westermark, G. T., Winblad, B., & Graff, C. (2012) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2011.07.012 · Cited by 43
Self-citationGlimepiride protects neurons against amyloid-β-induced synapse damage
Osborne, C., West, E., Nolan, W., McHale-Owen, H., Williams, A., & Bate, C. (2015) · Neuropharmacology · doi:10.1016/j.neuropharm.2015.09.030 · Cited by 43
Kawamoto, E. M., Lepsch, L. B., Cury‐Boaventura, M. F., Munhoz, C. D., Lima, L. S., Yshii, L., Avellar, M. C. W., Curi, R., Mattson, M. P., & Scavone, C. (2007) · Journal of Neuroscience Research · doi:10.1002/jnr.21548 · Cited by 43
Abnormal kalirin signaling in neuropsychiatric disorders
Remmers, C. L., Sweet, R. A., & Penzes, P. (2013) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2013.12.006 · Cited by 45
Orejana, L., Barros-Miñones, L., Jordán, J., Cedazo-Mı́nguez, Á., Tordera, R. M., Aguirre, N., & Puerta, E. (2014) · The Journals of Gerontology Series A · doi:10.1093/gerona/glu106 · Cited by 42
Alzheimer’s Disease and the Blood–Brain Barrier: Past, Present and Future
Bowman, G. L., & Quinn, J. F. (2008) · Aging Health · doi:10.2217/1745509x.4.1.47 · Cited by 43
Adult Astrogenesis and the Etiology of Cortical Neurodegeneration
Mohn, T. C., & Koob, A. O. (2015) · Journal of Experimental Neuroscience · doi:10.4137/jen.s25520 · Cited by 44
Dysfunctional γ-Secretase in Familial Alzheimer’s Disease
Wolfe, M. S. (2018) · Neurochemical Research · doi:10.1007/s11064-018-2511-1 · Cited by 47
Summers, K. L., Schilling, K. M., Roseman, G. P., Markham, K. A., Dolgova, N. V., Kröll, T., Sokaras, D., Millhauser, G. L., Pickering, I. J., & George, G. N. (2019) · Inorganic Chemistry · doi:10.1021/acs.inorgchem.9b00507 · Cited by 42
Dufort‐Gervais, J., Provost, C., Charbonneau, L., Norris, C. M., Calon, F., Mongrain, V., & Brouillette, J. (2020) · Scientific Reports · doi:10.1038/s41598-020-63255-6 · Cited by 48
Kung, M., Skovronsky, D., Hou, C., Zhuang, Z., Gur, T., Zhang, B., Trojanowski, J. Q., Lee, V. M. ‐., & Kung, H. F. (2003) · Journal of Molecular Neuroscience · doi:10.1385/jmn:20:1:15 · Cited by 42
Dar‐Nimrod, I., Chapman, B. P., Franks, P. J., Robbins, J. A., Porsteinsson, A. P., Mapstone, M. E., & Duberstein, P. R. (2012) · American Journal of Geriatric Psychiatry · doi:10.1097/jgp.0b013e318267016b · Cited by 41
Intraneuronal Aβ as a trigger for neuron loss: can this be translated into human pathology?
Bayer, T. A., & Wirths, O. (2011) · Biochemical Society Transactions · doi:10.1042/bst0390857 · Cited by 41
Nucleobindin 1 binds to multiple types of pre-fibrillar amyloid and inhibits fibrillization
Bonito-Oliva, A., Barbash, S., Sakmar, T. P., & Graham, W. V. (2017) · Scientific Reports · doi:10.1038/srep42880 · Cited by 41
Zhong, Z., Yuan, K., Tong, X., Hu, J., Song, Z., Zhang, G., Fang, X., & Zhang, W. (2018) · Neuroreport · doi:10.1097/wnr.0000000000001118 · Cited by 41
Chen, J., Long, Z., Li, Y., Luo, M., Luo, S., & He, G. (2019) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2019.4198 · Cited by 42
Peterman, J. L., White, J. D., Calcagno, A., Hagen, C. W., Quiring, M. E., Paulhus, K., Gurney, T., Eimerbrink, M. J., Curtis, M., Boehm, G. W., et al. (2019) · Behavioural Brain Research · doi:10.1016/j.bbr.2019.112366 · Cited by 41
Bridging the Gap Between Fluid Biomarkers for Alzheimer’s Disease, Model Systems, and Patients
Bjorkli, C., Sandvig, A., & Sandvig, I. (2020) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2020.00272 · Cited by 41
Sokolow, S., Luu, S. H., Headley, A. J., Hanson, A. Y., Kim, T., Miller, C. A., Vinters, H. V., & Gylys, K. H. (2011) · Cell Calcium · doi:10.1016/j.ceca.2010.12.008 · Cited by 41
Brown, A. M., Sheu, R. K.-F., Mohs, R., Haroutunian, V., & Blass, J. P. (2001) · Journal of Molecular Neuroscience · doi:10.1385/jmn:16:1:41 · Cited by 40
Pro-inflammatory effect of freshly solubilized β-amyloid peptides in the brain
Paris, D., Townsend, K. P., Obregon, D. F., Humphrey, J., & Mullan, M. (2002) · Prostaglandins & Other Lipid Mediators · doi:10.1016/s0090-6980(02)00111-9 · Cited by 40
From Soluble A β to Progressive A β Aggregation: Could Prion‐Like Templated Misfolding Play a Role?
Eisele, Y. S. (2013) · Brain Pathology · doi:10.1111/bpa.12049 · Cited by 43
Xie, K., Qin, Q., Long, Z., Yang, Y., Peng, C., Xi, C., Li, L., Wu, Z., Daria, V., Zhao, Y., et al. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.602887 · Cited by 41
What is the dominant aβ species in human brain tissue? A review
Gregory, G. C., & Halliday, G. M. (2005) · Neurotoxicity Research · doi:10.1007/bf03033774 · Cited by 41
Templating Effect of Lipid Membranes on Alzheimer's Amyloid Beta Peptide
Ege, C., Majewski, J. P., Wu, G., Kjær, K., & Lee, K. Y. C. (2005) · ChemPhysChem · doi:10.1002/cphc.200400468 · Cited by 40
New developments in animal models of Alzheimer’s disease
Janus, C., Phinney, A. L., Chishti, M. A., & Westaway, D. A. (2001) · Current Neurology and Neuroscience Reports · doi:10.1007/s11910-001-0105-8 · Cited by 40
Die Alzheimer‐Demenz: von der Pathologie zu therapeutischen Ansätzen
Jakob‐Roetne, R., & Jacobsen, H. (2009) · Angewandte Chemie · doi:10.1002/ange.200802808 · Cited by 41
Amyloid-β at sublethal level impairs BDNF-induced arc expression in cortical neurons
Wang, D., Chen, S.-S., Lee, Y., & Chen, T. (2006) · Neuroscience Letters · doi:10.1016/j.neulet.2005.12.057 · Cited by 40
Shoghi, K. I., Barrio, J. R., Kepe, V., Wu, H.-M., Small, G. W., Phelps, M. E., & Huang, S. (2005) · Nuclear Medicine and Biology · doi:10.1016/j.nucmedbio.2005.02.003 · Cited by 40
Vercauteren, F., Clerens, S., Roy, L., Hamel, N., Arckens, L., Vandesande, F., Alhonen, L. I., Jänne, J., Szyf, M., & Cuello, A. C. (2004) · Molecular Brain Research · doi:10.1016/j.molbrainres.2004.10.012 · Cited by 40
Campbell, S. N., Zhang, C., Roe, A. D., Lee, N., Lao, K., Monte, L., Donohue, M., & Rissman, R. A. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-142844 · Cited by 39
Naert, G., & Rivest, S. (2012) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2012.00051 · Cited by 42
MRI Evidence of Neuropathic Changes in Former College Football Players
Adler, C. M., DelBello, M. P., Weber, W., Williams, M., Durán, L. R. P., Fleck, D. E., Boespflug, E. L., Eliassen, J. C., Strakowski, S. M., & Divine, J. G. (2016) · Clinical Journal of Sport Medicine · doi:10.1097/jsm.0000000000000391 · Cited by 39
Immunotherapeutic approaches for Alzheimer’s disease in transgenic mouse models
Wısnıewskı, T., & Boutajangout, A. (2009) · Brain Structure and Function · doi:10.1007/s00429-009-0236-2 · Cited by 39
Leverone, J. F. (2003) · Vaccine · doi:10.1016/s0264-410x(02)00754-5 · Cited by 39
Alzheimer’s Disease: Genes, Pathogenesis and Risk Prediction
Sleegers, K., & van Duijn, C. M. (2001) · Public Health Genomics · doi:10.1159/000064193 · Cited by 39
Rhodin, J. A. G., Thomas, T. N., Clark, L. C., Garces, A. H., & Bryant, M. (2003) · Journal of Alzheimer s Disease · doi:10.3233/jad-2003-5403 · Cited by 40
Terahertz Spectroscopic Differentiation of Microstructures in Protein Gels
Png, G. M., Falconer, R. J., Fischer, B. M., Zakaria, H. A., Mickan, S. P., Middelberg, A. P. J., & Abbott, D. (2009) · Optics Express · doi:10.1364/oe.17.013102 · Cited by 38
Heme and hemoglobin suppress amyloid β–mediated inflammatory activation of mouse astrocytes
Sankar, S. B., Donegan, R. K., Shah, K. J., Reddi, A. R., & Wood, L. B. (2018) · Journal of Biological Chemistry · doi:10.1074/jbc.ra117.001050 · Cited by 41
The Effects of Soluble A.β Oligomers on Neurodegeneration in Alzheimer's Disease
Brouillette, J. (2014) · Current Pharmaceutical Design · doi:10.2174/13816128113199990498 · Cited by 39
Müller, M., Jacobi, E., Sakimura, K., Malinow, R., & von Engelhardt, J. (2018) · Acta Neuropathologica Communications · doi:10.1186/s40478-018-0611-4 · Cited by 40
“What Doesn’t Kill You Makes You Stronger”: Future Applications of Amyloid Aggregates in Biomedicine
Abdelrahman, S., Alghrably, M., Lachowicz, J. I., Emwas, A.-H. M., Hauser, C. A. E., & Jaremko, M. (2020) · Molecules · doi:10.3390/molecules25225245 · Cited by 38
Advances on the Understanding of the Origins of Synaptic Pathology in AD
Lacor, P. N. (2007) · Current Genomics · doi:10.2174/138920207783769530 · Cited by 40
Moinuddin, A., Morley, J. E., & Banks, W. A. (2000) · NeuroImmunoModulation · doi:10.1159/000054814 · Cited by 38
Jacobsen, L. K., Picciotto, M. R., Heath, C. J., Mencl, W. E., & Gelernter, J. E. (2008) · Biological Psychiatry · doi:10.1016/j.biopsych.2008.10.024 · Cited by 38
Rai, D. K., Sharma, V. K., Anunciado, D. B., O’Neill, H., Mamontov, E., Urban, V. S., Heller, W. T., & Qian, S. (2016) · Scientific Reports · doi:10.1038/srep30983 · Cited by 38
Spotlight on BACE: The secretases as targets for treatment in Alzheimer disease
Dingwall, C. (2001) · Journal of Clinical Investigation · doi:10.1172/jci14402 · Cited by 38
Hanna, A., Iremonger, K., Das, P., Dickson, D., Golde, T., & Janus, C. (2012) · Alzheimer's Research & Therapy · doi:10.1186/alzrt124 · Cited by 38
Parikh, V., Bernard, C. S., Naughton, S. X., & Yegla, B. (2014) · Behavioural Brain Research · doi:10.1016/j.bbr.2014.07.046 · Cited by 37
Adav, S. S., Gallart‐Palau, X., Tan, K. H., Lim, S. K., Tam, J. P., & Sze, S. K. (2016) · Molecular Brain · doi:10.1186/s13041-016-0200-z · Cited by 38
Philipson, O., Lord, A., Lalowski, M. M., Soliymani, R., Baumann, M., Thyberg, J., Bogdanović, N., Olofsson, T., Tjernberg, L. O., Ingelsson, M., et al. (2011) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2011.10.022 · Cited by 40
Yang, T.-T., Hsu, C.-T., & Kuo, Y. (2009) · Journal of Neural Transmission · doi:10.1007/s00702-009-0311-0 · Cited by 38
Kiefer, C., Brockhaus, L., Cattapan-Ludewig, K., Ballinari, P., Burren, Y., Schroth, G., & Wiest, R. (2009) · NeuroImage · doi:10.1016/j.neuroimage.2009.07.005 · Cited by 39
LPYFDa Neutralizes Amyloid-β-Induced Memory Impairment and Toxicity
Granic, I., Masman, M. F., Mulder, C. K., Nijholt, I. M., Naudé, P., de Haan, A., Borbély, E., Penke, B., Luiten, P. G. M., & Eisel, U. L. M. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-1297 · Cited by 37
Botanical Sources for Alzheimer’s: A Review on Reports From Traditional Persian Medicine
Hosseinkhani, A., Sahragard, A., Namdari, A., & Zarshenas, M. M. (2017) · American Journal of Alzheimer s Disease & Other Dementias® · doi:10.1177/1533317517717013 · Cited by 37
βAPP and Furin mRNA Concentrates in Immature Senile Plaques in the Brain of Alzheimer Patients
Marcinkiewicz, M. M. (2002) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/61.9.915 · Cited by 37
Ghosh, U., Yau, W., Collinge, J., & Tycko, R. (2021) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2111863118 · Cited by 38
Schupf, N., Lee, A., Park, N., Dang, L. T., Pang, D. I., Yale, A., Oh, D. K. T., Krinsky‐McHale, S. J., Jenkins, E. C., Luchsinger, J. A., et al. (2015) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2015.06.020 · Cited by 36
Cationization increases brain distribution of an amyloid-beta protofibril selective F(ab’)2 fragment
Syvänen, S., Edén, D., & Sehlin, D. (2017) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2017.09.065 · Cited by 36
Maharjan, A., Wang, E., Peng, M., & Çakmak, Y. Ö. (2018) · Frontiers in Neuroscience · doi:10.3389/fnins.2018.00225 · Cited by 39
Komatsu, H., Liu, L., Murray, I. V. J., & Axelsen, P. H. (2007) · Biochimica et Biophysica Acta (BBA) - Biomembranes · doi:10.1016/j.bbamem.2007.05.026 · Cited by 36
Soluble Aβ homeostasis in AD and DS: impairment of anti-amyloidogenic protection by lipoproteins
Matsubara, E., Sekijima, Y., Tokuda, T., Urakami, K., Amari, M., Shizuka‐Ikeda, M., Tomidokoro, Y., Ikeda, M., Kawarabayashi, T., Harigaya, Y., et al. (2004) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2003.10.004 · Cited by 36
COURT, J. A., Johnson, M., Religa, D., Keverne, J., Kalaria, R. N., Jaros, E., McKeith, I. G., Perry, R., Näslund, J., & Perry, E. K. (2005) · Neuropathology and Applied Neurobiology · doi:10.1111/j.1365-2990.2005.00674.x · Cited by 36
Self-citationSöderberg, L., Kakuyama, H., Möller, A., Itô, A., Winblad, B. G., Tjernberg, L. O., & Näslund, J. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m403628200 · Cited by 36
Self-citationMartins, R. N., Taddei, K., Kendall, C. L., Evin, G. M., Bates, K. A., & Harvey, A. R. (2001) · Neuroscience · doi:10.1016/s0306-4522(01)00289-5 · Cited by 36
Changing the Course of Alzheimer's Disease
Christensen, D. D. (2007) · The Primary Care Companion to The Journal of Clinical Psychiatry · doi:10.4088/pcc.v09n0106 · Cited by 37
Morris, J. C. (2003) · Alzheimer Disease & Associated Disorders · doi:10.1097/00002093-200310000-00010 · Cited by 36
Burns, L. H., Pei, Z., & Wang, H. (2023) · Drug Development Research · doi:10.1002/ddr.22085 · Cited by 35
Aducanumab and Its Effects on Tau Pathology: Is This the Turning Point of Amyloid Hypothesis?
Silvestro, S., Valeri, A., & Mazzon, E. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23042011 · Cited by 37
Brain cholinesterases: III. Future perspectives of AD research and clinical practice
Shen, Z. X. (2004) · Medical Hypotheses · doi:10.1016/j.mehy.2004.03.001 · Cited by 35
Uncoupling of M1 muscarinic receptor/G-protein interaction by amyloid β1–42
Janíčková, H., Rudajev, V., Zimčík, P., Jakubík, J., Tanila, H., El‐Fakahany, E. E., & Doležal, V. (2012) · Neuropharmacology · doi:10.1016/j.neuropharm.2012.11.014 · Cited by 37
Nocera, S., Bonato, D., & Telser, H. (2002) · International Journal of Health Care Finance and Economics · doi:10.1023/a:1020441726964 · Cited by 35
Cerebral amyloidosis associated with cognitive decline in autosomal dominant Alzheimer disease
Wang, F., Gordon, B. A., Ryman, D. C., Ma, S., Xiong, C., Hassenstab, J. J., Goate, A., Fagan, A. M., Cairns, N. J., Marcus, D. S., et al. (2015) · Neurology · doi:10.1212/wnl.0000000000001903 · Cited by 34
Lin, C., Chang, L., Tseng, G. C., Kirkwood, C. M., Sibille, E. L., & Sweet, R. A. (2015) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2015.00030 · Cited by 35
Wu, K., Gao, X., Shi, B., Chen, S., Zhou, X., Li, Z., Gan, Y., Cui, L., Kang, J. X., Li, W., et al. (2016) · Neuroscience · doi:10.1016/j.neuroscience.2016.07.038 · Cited by 34
New Th2 adjuvants for preventive and active immunotherapy of neurodegenerative proteinopathies
Marciani, D. J. (2014) · Drug Discovery Today · doi:10.1016/j.drudis.2014.02.015 · Cited by 34
Metadata
- Authors
- Näslund, J.
- Affiliations
- Rockefeller University (US)
- Corresponding author
- Näslund, Jan
- Venue
- JAMA
- Publisher
- American Medical Association (AMA)
- Published
- 2000-03-22
- Volume
- 283
- Issue
- 12
- Pages
- 1571
- ISSN
- 0002-9955 (ISSN-L)
- 0098-7484
- OpenAlex
- W2000706612
- Cited by
- 1,268
- References
- 28
- Citations by year
- 2026: 9 · 2025: 14 · 2024: 32 · 2023: 23 · 2022: 28 · 2021: 32 · 2020: 31 · 2019: 29 · 2018: 34 · 2017: 29 · 2016: 57 · 2015: 56 · 2014: 60 · 2013: 59 · 2012: 65
- FWCI
- 40.95
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- JAMA (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (AG-02219, AG 05138, P50AG005138, AG 14996, P01AG002219)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- amyloid-beta, Alzheimer's disease, cognitive decline, dementia progression, tau protein, amyloid-beta 42, Aβ40, frontal cortex, Clinical Dementia Rating, postmortem brain, neocortex, nursing home residents, amyloid plaques, neurofibrillary tangles
- MeSH terms
- Aged, Aged, 80 and over, Brain, Cognition Disorders, Cross-Sectional Studies, Dementia, Enzyme-Linked Immunosorbent Assay, Female, Frontal Lobe, Humans, Immunoenzyme Techniques, Male, Immunoblotting, Amyloid beta-Peptides, tau Proteins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review