Cited by 1,268Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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

Näslund, Jan·2000·JAMA

DOI 10.1001/jama.283.12.1571

Open this paper in CoChat — free account

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.

Integrity signals

Registry

Crossref · 10.1001/jama.283.12.1571

Cites

28 of 28 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

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?

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
The Consortium to Establish a Registry for Alzheimer's Disease (CERAD): Part II. Standardization of the neuropathologic assessment of Alzheimer's disease
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
Seeding “one-dimensional crystallization” of amyloid: A pathogenic mechanism in Alzheimer's disease and scrapie?
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
Neurochemical Correlates of Dementia Severity in Alzheimer's Disease: Relative Importance of the Cholinergic Deficits
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

Show all 28 references

Sorted by citations

Items 101–200 of 1,000

Amyloid imaging in mild cognitive impairment subtypes
Wolk, D. A., Price, J. C., Saxton, J. A., Snitz, B. E., James, J. A., López, O. L., Aizenstein, H. J., Cohen, A. D., Weissfeld, L. A., Mathis, C. A., et al. (2009) · Annals of Neurology · doi:10.1002/ana.21598 · Cited by 349
Cholesterol: its regulation and role in central nervous system disorders
Orth, M., & Bellosta, S. (2012) · Cholesterol · doi:10.1155/2012/292598 · Cited by 339
Intraneuronal Aβ accumulation and origin of plaques in Alzheimer's disease
Gouras, G. K., Almeida, C. G., & Takahashi, R. H. (2005) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2005.05.022 · Cited by 338
Soluble protein oligomers as emerging toxins in Alzheimer’s and other amyloid diseases
Ferreira, S. T., Vieira, M. N. N., & De Felice, F. G. (2007) · IUBMB Life · doi:10.1080/15216540701283882 · Cited by 335
Melatonin increases survival and inhibits oxidative and amyloid pathology in a transgenic model of Alzheimer's disease
Matsubara, E., Bryant‐Thomas, T., Pacheco Quinto, J., Henry, T. L., Poeggeler, B., Herbert, D., Cruz‐Sanchez, F., Chyan, Y., Smith, M. A., Perry, G., et al. (2003) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2003.01654.x · Cited by 332
Copper-Dependent Inhibition of Human Cytochrome c Oxidase by a Dimeric Conformer of Amyloid-β1-42
Crouch, P. J., Blake, R., Duce, J. A., Ciccotosto, G. D., Li, Q.-X., Barnham, K. J., Curtain, C. C., Cherny, R. A., Cappai, R., Dyrks, T., et al. (2005) · The Journal of Neuroscience · doi:10.1523/jneurosci.4276-04.2005 · Cited by 327
Dietary Docosahexaenoic Acid and Docosapentaenoic Acid Ameliorate Amyloid-β and Tau Pathology via a Mechanism Involving Presenilin 1 Levels
Green, K. N., Martínez‐Coria, H., Khashwji, H., Hall, E. B., Yurko‐Mauro, K., Ellis, L., & LaFerla, F. M. (2007) · Journal of Neuroscience · doi:10.1523/jneurosci.0055-07.2007 · Cited by 336
Adult Hippocampal Neurogenesis in Aging and Alzheimer's Disease
Babcock, K. R., Page, J. S., Fallon, J. R., & Webb, A. E. (2021) · Stem Cell Reports · doi:10.1016/j.stemcr.2021.01.019 · Cited by 330
Astrogliosis: An integral player in the pathogenesis of Alzheimer's disease
Osborn, L. M., Kamphuis, W., Wadman, W. J., & Hol, E. M. (2016) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2016.01.001 · Cited by 312
Mild hypercholesterolemia is an early risk factor for the development of Alzheimer amyloid pathology
Pappolla, M. A., Bryant-Thomas, T. K., Herbert, D., Pacheco, J., Fabra Garcia, M., Manjon, M., Girones, X., Henry, T. L., Matsubara, E., Zambon, D., et al. (2003) · Neurology · doi:10.1212/01.wnl.0000070182.02537.84 · Cited by 247
BACE1 inhibitors: Current status and future directions in treating Alzheimer's disease
Moussa‐Pacha, N. M., Abdin, S. M., Omar, H. A., Alniss, H., & Al‐Tel, T. H. (2020) · Medicinal Research Reviews · doi:10.1002/med.21622 · Cited by 274
Intracerebral Transplantation of Bone Marrow-Derived Mesenchymal Stem Cells Reduces Amyloid-Beta Deposition and Rescues Memory Deficits in Alzheimer's Disease Mice by Modulation of Immune Responses
Lee, J. K., Jin, H. K., Endo, S., Schuchman, E. H., Carter, J., & Bae, J.-S. (2009) · Stem Cells · doi:10.1002/stem.277 · Cited by 308
Prediction of Amyloid Fibril-forming Proteins
Kallberg, Y., Gustafsson, M., Persson, B., Thyberg, J., & Johansson, J. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m010402200 · Cited by 305
Post-translational Processing of β-Secretase (β-Amyloid-converting Enzyme) and Its Ectodomain Shedding
Benjannet, S., Elagoz, A., Wickham, L., Mamarbachi, M., Munzer, J. S., Basak, A., Lazure, C., Cromlish, J. A., Sisodia, S., Checler, F., et al. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m009899200 · Cited by 301
Glutamate system, amyloid β peptides and tau protein: functional interrelationships and relevance to Alzheimer disease pathology
Revett, T. J., Baker, G. B., Jhamandas, J. H., & Kar, S. (2012) · Journal of Psychiatry and Neuroscience · doi:10.1503/jpn.110190 · Cited by 308
Sensitive ELISA detection of amyloid‐β protofibrils in biological samples
Englund, H., Sehlin, D., Johansson, A., Nilsson, L. N. G., Gellerfors, P., Paulie, S., Lannfelt, L., & Pettersson, F. E. (2007) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2007.04759.x · Cited by 292
Toll-Like Receptor 2 Acts as a Natural Innate Immune Receptor to Clear Amyloid β1–42and Delay the Cognitive Decline in a Mouse Model of Alzheimer's Disease
Richard, K. L., Filali, M., Préfontaine, P., & Rivest, S. (2008) · The Journal of Neuroscience · doi:10.1523/jneurosci.1146-08.2008 · Cited by 298
Aβ deposits in older non-demented individuals with cognitive decline are indicative of preclinical Alzheimer's disease
Villemagne, V. L., Pike, K. E., Darby, D., Maruff, P. T., Savage, G. R., Ng, S., Ackermann, U., Cowie, T., Currie, J. N., Chan, S. G., et al. (2008) · Neuropsychologia · doi:10.1016/j.neuropsychologia.2008.02.008 · Cited by 302
Alzheimer Disease Pathogenesis: Insights From Molecular and Cellular Biology Studies of Oligomeric Aβ and Tau Species
Chen, X., & Mobley, W. C. (2019) · Frontiers in Neuroscience · doi:10.3389/fnins.2019.00659 · Cited by 302
Novel 18F-Labeled Arylquinoline Derivatives for Noninvasive Imaging of Tau Pathology in Alzheimer Disease
Okamura, N., Furumoto, S., Harada, R., Tago, T., Yoshikawa, T., Fodero‐Tavoletti, M. T., Mulligan, R. S., Villemagne, V. L., Akatsu, H., Yamamoto, T., et al. (2013) · Journal of Nuclear Medicine · doi:10.2967/jnumed.112.117341 · Cited by 289
High-fat diet aggravates amyloid-beta and tau pathologies in the 3xTg-AD mouse model
Julien, C., Tremblay, C., Phivilay, A., Berthiaume, L., Émond, V., Julien, P., & Calon, F. (2010) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2008.08.022 · Cited by 288
A model for studying Alzheimer's Aβ42-induced toxicity in Drosophila melanogaster
Finelli, A. L., Kelkar, A., Song, H., Yang, H., & Konsolaki, M. (2004) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2004.03.001 · Cited by 299
The Origins of Alzheimer Disease
Selkoe, D. J. (2000) · JAMA · doi:10.1001/jama.283.12.1615 · Cited by 285
Immunotherapeutic Approaches for Alzheimer’s Disease
Wisniewski, T., & Goñi, F. (2015) · Neuron · doi:10.1016/j.neuron.2014.12.064 · Cited by 284
“Supporting a role of Ab in LOAD, the levels of biochemically extracted Ab peptides from the brains of people with sporadic AD correlate well with cognitive deficits (Näslund et al., 2000).”
Alzheimer's disease in Down syndrome: Neurobiology and risk
Zigman, W. B., & Lott, I. T. (2007) · Mental Retardation and Developmental Disabilities Research Reviews · doi:10.1002/mrdd.20163 · Cited by 290
Brain Amyloid Imaging
Rowe, C. C., & Villemagne, V. L. (2011) · Journal of Nuclear Medicine · doi:10.2967/jnumed.110.076315 · Cited by 279
Accumulation of amyloid-β by astrocytes result in enlarged endosomes and microvesicle-induced apoptosis of neurons
Söllvander, S., Nikitidou, E., Brolin, R., Söderberg, L., Sehlin, D., Lannfelt, L., & Erlandsson, A. (2016) · Molecular Neurodegeneration · doi:10.1186/s13024-016-0098-z · Cited by 267
Reviews: Current Concepts in Alzheimer's Disease: A Multidisciplinary Review
Minati, L., Edginton, T. L., Bruzzone, M. G., & Giaccone, G. (2008) · American Journal of Alzheimer s Disease & Other Dementias® · doi:10.1177/1533317508328602 · Cited by 276
The Arctic Alzheimer mutation facilitates early intraneuronal Aβ aggregation and senile plaque formation in transgenic mice
Lord, A., Kalimo, H., Eckman, C., Zhang, X.-Q., Lannfelt, L., & Nilsson, L. N. G. (2006) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2004.12.007 · Cited by 260
Cognitive Dysfunction Syndrome
Landsberg, G. M., Nichol, J., & Araujo, J. A. (2012) · Veterinary Clinics of North America Small Animal Practice · doi:10.1016/j.cvsm.2012.04.003 · Cited by 277
The lesion(s) in traumatic brain injury: implications for clinical neuropsychology
Bigler, E. D. (2001) · Archives of Clinical Neuropsychology · doi:10.1016/s0887-6177(00)00095-0 · Cited by 256
Plaque‐associated disruption of CSF and plasma amyloid‐β (Aβ) equilibrium in a mouse model of Alzheimer's disease
Demattos, R. B., Bales, K. R., Parsadanian, M., O'Dell, M. A., Foss, E. M., Paul, S. M., & Holtzman, D. M. (2002) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2002.00889.x · Cited by 254
Longitudinal CSF and MRI biomarkers improve the diagnosis of mild cognitive impairment
de Leon, M. J., DeSanti, S., Zinkowski, R. P., Mehta, P. D., Praticò, D., Segal, S., Rusinek, H., Li, J., Tsui, W., Louis, L. A. S., et al. (2005) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2005.07.003 · Cited by 255
Intracellular accumulation of amyloid-beta – a predictor for synaptic dysfunction and neuron loss in Alzheimer’s disease
Bayer (2010) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2010.00008 · Cited by 252
Targeting Amyloid-β Peptide (Aβ) Oligomers by Passive Immunization with a Conformation-selective Monoclonal Antibody Improves Learning and Memory in Aβ Precursor Protein (APP) Transgenic Mice
Lee, E. B., Leng, L. Z., Zhang, B., Kwong, L. K., Trojanowski, J. Q., Abel, T. G., & Lee, V. M. ‐. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m511018200 · Cited by 254
The presence of sodium dodecyl sulphate-stable Aβ dimers is strongly associated with Alzheimer-type dementia
Mc Donald, J. M., Savva, G. M., Brayne, C., Welzel, A. T., Forster, G., Shankar, G. M., Selkoe, D. J., Ince, P. G., & Walsh, D. M. (2010) · Brain · doi:10.1093/brain/awq065 · Cited by 234
Parahippocampal tau pathology in healthy aging, mild cognitive impairment, and early Alzheimer's disease
Mitchell, T. W., Mufson, E. J., Schneider, J. A., Cochran, E. J., Nissanov, J., Han, L., Bienias, J. L., Lee, V. M. ‐., Trojanowski, J. Q., Bennett, D. A., et al. (2002) · Annals of Neurology · doi:10.1002/ana.10086 · Cited by 251
Anti‐amyloidogenic activity of tetracyclines: studies in vitro
Forloni, G., Colombo, L., Girola, L., Tagliavini, F., & Salmona, M. (2001) · FEBS Letters · doi:10.1016/s0014-5793(00)02380-2 · Cited by 242
Gene Expression Alterations in the Sphingolipid Metabolism Pathways during Progression of Dementia and Alzheimer’s Disease: A Shift Toward Ceramide Accumulation at the Earliest Recognizable Stages of Alzheimer’s Disease?
Katsel, P., Li, C., & Haroutunian, V. H. (2007) · Neurochemical Research · doi:10.1007/s11064-007-9297-x · Cited by 244
Mixtures of Wild-type and a Pathogenic (E22G) Form of Aβ40 in Vitro Accumulate Protofibrils, Including Amyloid Pores
Lashuel, H. A., Hartley, D. M., Petre, B. M., Wall, J. S., Simon, M. N., Walz, T., & Lansbury, P. T. (2003) · Journal of Molecular Biology · doi:10.1016/s0022-2836(03)00927-6 · Cited by 240
Neurotoxic effect of oligomeric and fibrillar species of amyloid-beta peptide 1-42: Involvement of endoplasmic reticulum calcium release in oligomer-induced cell death
Resende, R., Ferreiro, E., Pereira, C., & Resende de Oliveira, C. (2008) · Neuroscience · doi:10.1016/j.neuroscience.2008.06.036 · Cited by 235
A Role for Synaptic Zinc in Activity-Dependent Aβ Oligomer Formation and Accumulation at Excitatory Synapses
Deshpande, A., Kawai, H., Metherate, R., Glabe, C. G., & Busciglio, J. (2009) · The Journal of Neuroscience · doi:10.1523/jneurosci.5980-08.2009 · Cited by 232
Inhibition of Glycogen Synthase Kinase-3 Ameliorates β-Amyloid Pathology and Restores Lysosomal Acidification and Mammalian Target of Rapamycin Activity in the Alzheimer Disease Mouse Model
Avrahami, L., Farfara, D., Shaham-Kol, M., Vassar, R. J., Frenkel, D., & Eldar-Finkelman, H. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.m112.409250 · Cited by 235
Pharmacotherapies for Alzheimer's disease: Beyond cholinesterase inhibitors
Tayeb, H. O., Yang, H. D., Price, B. H., & Tarazi, F. I. (2011) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2011.12.002 · Cited by 237
Pro-inflammatory interleukin-18 increases Alzheimer’s disease-associated amyloid-β production in human neuron-like cells
Sutinen, E. M., Pirttilä, T., Anderson, G., Salminen, A., & Ojala, J. O. (2012) · Journal of Neuroinflammation · doi:10.1186/1742-2094-9-199 · Cited by 232
Peripheral Aβ subspecies as risk biomarkers of Alzheimer's disease
Schupf, N., Tang, M. X., Fukuyama, H., Manly, J., Andrews, H., Mehta, P., Ravetch, J., & Mayeux, R. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0805902105 · Cited by 225
Evidence of endothelial dysfunction in the development of Alzheimer's disease: Is Alzheimer's a vascular disorder?
Kelleher, R. J., & Soiza, R. L. (2013) · Europe PMC (PubMed Central) · Cited by 232
Bivalent Brain Shuttle Increases Antibody Uptake by Monovalent Binding to the Transferrin Receptor
Hultqvist, G., Syvänen, S., Fang, X. T., Lannfelt, L., & Sehlin, D. (2017) · Theranostics · doi:10.7150/thno.17155 · Cited by 224
Amyloid precursor protein (APP) and the biology of proteolytic processing: relevance to Alzheimer’s disease
Ling, Y., Morgan, K., & Kalsheker, N. (2003) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/s1357-2725(03)00133-x · Cited by 224
Learning and Memory in Transgenic Mice Modeling Alzheimer's Disease
Ashe, K. H. (2001) · Learning & Memory · doi:10.1101/lm.43701 · Cited by 224
Amyloid β peptide oligomers directly activate NMDA receptors
Texidó, L., Martín-Satué, M., Alberdi, E. M., Solsona, C., & Matute, C. (2011) · Cell Calcium · doi:10.1016/j.ceca.2011.02.001 · Cited by 233
Antibody-based PET imaging of amyloid beta in mouse models of Alzheimer’s disease
Sehlin, D., Fang, X. T., Cato, L., Antoni, G., Lannfelt, L., & Syvänen, S. (2016) · Nature Communications · doi:10.1038/ncomms10759 · Cited by 226
Expanding the association between the APOE gene and the risk of Alzheimer's disease: possible roles for APOE promoter polymorphisms and alterations in APOE transcription
Laws, S. M., Hone, E., Gandy, S., & Martins, R. N. (2003) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2003.01615.x · Cited by 223
Interleukin-1β impairs brain derived neurotrophic factor-induced signal transduction
Tong, L., Balazs, R., Soiampornkul, R., Thangnipon, W., & Cotman, C. W. (2008) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2007.02.027 · Cited by 222
β-Amyloid Peptide at Sublethal Concentrations Downregulates Brain-Derived Neurotrophic Factor Functions in Cultured Cortical Neurons
Tong, L., Balazs, R., Thornton, P. L., & Cotman, C. W. (2004) · The Journal of Neuroscience · doi:10.1523/jneurosci.5463-03.2004 · Cited by 221
MRI and CSF studies in the early diagnosis of Alzheimer's disease
de Leon, M. J., DeSanti, S., Zinkowski, R. P., Mehta, P. D., Praticò, D., Segal, S., Clark, C. M., Kerkman, D. J., DeBernardis, J. F., Li, J., et al. (2004) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.2004.01381.x · Cited by 226
Toxicity of Amyloid β Peptide: Tales of Calcium, Mitochondria, and Oxidative Stress
Canevari, L., Abramov, A. Y., & Duchen, M. R. (2004) · Neurochemical Research · doi:10.1023/b:nere.0000014834.06405.af · Cited by 227
Current drug targets for Alzheimer's disease treatment
Lahiri, D. K., Farlow, M. R., Greig, N. H., & Sambamurti, K. (2002) · Drug Development Research · doi:10.1002/ddr.10081 · Cited by 220
Astrocytic dysfunction: Insights on the role in neurodegeneration
Rossi, D., & Volterra, A. (2009) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2009.07.012 · Cited by 225
Amyloid-Associated Neuron Loss and Gliogenesis in the Neocortex of Amyloid Precursor Protein Transgenic Mice
Bondolfi, L., Calhoun, M., Ermini, F., Kuhn, H. G., Wiederhold, K.-H., Walker, L., Staufenbiel, M., & Jucker, M. (2002) · The Journal of Neuroscience · doi:10.1523/jneurosci.22-02-00515.2002 · Cited by 213
Evidence for the Presence of Three Distinct Binding Sites for the Thioflavin T Class of Alzheimer's Disease PET Imaging Agents on β-Amyloid Peptide Fibrils
Lockhart, A., Ye, L., Judd, D. B., Merritt, A. T., Lowe, P. N., Morgenstern, J. L., Hong, G., Gee, A. D., & Brown, J. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m412056200 · Cited by 213
Ion Channel Formation by Amyloid-β42 Oligomers but Not Amyloid-β40 in Cellular Membranes
Bode, D. C., Baker, M. D., & Viles, J. H. (2016) · Journal of Biological Chemistry · doi:10.1074/jbc.m116.762526 · Cited by 210
CSF Biomarkers in Prediction of Cerebral and Clinical Change in Mild Cognitive Impairment and Alzheimer's Disease
Fjell, A. M., Walhovd, K. B., Fennema‐Notestine, C., McEvoy, L. K., Hagler, D. J., Holland, D., Brewer, J. B., Dale, A. M., & Initiative, A. D. N. (2010) · Journal of Neuroscience · doi:10.1523/jneurosci.3785-09.2010 · Cited by 211
β-Amyloid-(1–42) Impairs Activity-dependent cAMP-response Element-binding Protein Signaling in Neurons at Concentrations in Which Cell Survival Is Not Compromised
Tong, L., Thornton, P. L., Balazs, R., & Cotman, C. W. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m010450200 · Cited by 206
Co-Localization of Amyloid Beta and Tau Pathology in Alzheimer's Disease Synaptosomes
Fein, J. A., Sokolow, S., Miller, C. A., Vinters, H. V., Yang, F., Cole, G. M., & Gylys, K. H. (2008) · American Journal Of Pathology · doi:10.2353/ajpath.2008.070829 · Cited by 218
Silibinin prevents amyloid β peptide‐induced memory impairment and oxidative stress in mice
Lü, P., Mamiya, T., Lu, L., Mouri, A., Zou, L., Nagai, T., Hiramatsu, M., Ikejima, T., & Nabeshima, T. (2009) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.2009.00295.x · Cited by 201
Age and amyloid effects on human central nervous system amyloid‐beta kinetics
Patterson, B. W., Elbert, D. L., Mawuenyega, K. G., Kasten, T., Ovod, V., Ma, S., Xiong, C., Chott, R., Yarasheski, K., Sigurdson, W., et al. (2015) · Annals of Neurology · doi:10.1002/ana.24454 · Cited by 200
Correlation between cognitive deficits and Aβ deposits in transgenic APP+PS1 mice
Gordon, M. N., King, D. L., Diamond, D. M., Jantzen, P. T., Boyett, K. W., Hope, C. E., Hatcher-Martin, J. M., DiCarlo, G., Gottschall, W. P. E., Morgan, D., et al. (2001) · Neurobiology of Aging · doi:10.1016/s0197-4580(00)00249-9 · Cited by 199
β-Amyloid impairs axonal BDNF retrograde trafficking
Poon, W. W., Blurton-Jones, M. M., Tu, C. H., Feinberg, L. M., Chabrier, M. A., Harris, J. W., Jeon, N. L., & Cotman, C. W. (2009) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2009.05.012 · Cited by 203
The β-amyloid protein of Alzheimer's disease increases neuronal CRMP-2 phosphorylation by a Rho-GTP mechanism
Petratos, S., Li, Q.-X., George, A. J., Hou, X., Kerr, M. L., Unabia, S. E., Hatzinisiriou, I., Maksel, D., Aguilar, M.-I., & Small, D. H. (2008) · Brain · doi:10.1093/brain/awm260 · Cited by 197
Regional Multiple Pathology Scores Are Associated with Cognitive Decline in L ewy Body Dementias
Howlett, D. R., Whitfield, D., Johnson, M. A., Attems, J., O'Brien, J. T., Aarsland, D., Lai, M. K. P., Lee, J. H., Chen, C., Ballard, C. G., et al. (2014) · Brain Pathology · doi:10.1111/bpa.12182 · Cited by 199
Radioiodinated Styrylbenzenes and Thioflavins as Probes for Amyloid Aggregates
Zhuang, Z.-P., KUNG, M. ‐., Hou, C., Skovronsky, D., Gur, T., Plößl, K., Trojanowski, J. Q., Lee, V. M.-Y., & Kung, H. F. (2001) · Journal of Medicinal Chemistry · doi:10.1021/jm010045q · Cited by 196
Neuronal Cyclooxygenase 2 Expression in the Hippocampal Formation as a Function of the Clinical Progression of Alzheimer Disease
Ho, L., Purohit, D. P., Haroutunian, V. H., Luterman, J. D., Willis, F., Näslund, J., Buxbaum, J. D., Mohs, R. C., Aisen, P. S. S., & Pasinetti, G. M. (2001) · Archives of Neurology · doi:10.1001/archneur.58.3.487 · Cited by 197
Self-citation
Conformations and Biological Activities of Amyloid Beta Peptide 25-35
Millucci, L., Ghezzi, L., Bernardini, G., & Santucci, A. (2010) · Current Protein and Peptide Science · doi:10.2174/138920310790274626 · Cited by 197
Mitochondrial Dysfunction: The First Domino in Brain Aging and Alzheimer's Disease?
Leuner, K., Hauptmann, S., Abdel-Kader, R. M., Scherping, I., Keil, U., Strosznajder, J. B., Eckert, A., & Müller, W. E. (2007) · Antioxidants and Redox Signaling · doi:10.1089/ars.2007.1763 · Cited by 195
Site-directed antisense oligonucleotide decreases the expression of amyloid precursor protein and reverses deficits in learning and memory in aged SAMP8 mice
Kumar, V. B., Farr, S. A., Flood, J. F., Kamlesh, V., Franko, M. W., Banks, W. A., & Morley, J. E. (2000) · Peptides · doi:10.1016/s0196-9781(00)00339-9 · Cited by 193
Aβ ion channels. Prospects for treating Alzheimer's disease with Aβ channel blockers
Arispe, N. J., Díaz, J. C., & Šimáková, O. (2007) · Biochimica et Biophysica Acta (BBA) - Biomembranes · doi:10.1016/j.bbamem.2007.03.014 · Cited by 196
Treatment of Alzheimer’s Disease and Blood–Brain Barrier Drug Delivery
Pardridge, W. M. (2020) · Pharmaceuticals · doi:10.3390/ph13110394 · Cited by 198
Alzheimer’s Disease, Oligomers, and Inflammation
Forloni, G., & Balducci, C. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-170819 · Cited by 205
When loss is gain: reduced presenilin proteolytic function leads to increased Aβ42/Aβ40
Wolfe, M. S. (2007) · EMBO Reports · doi:10.1038/sj.embor.7400896 · Cited by 192
The presenilin-1 familial Alzheimer disease mutant P117L impairs neurogenesis in the hippocampus of adult mice
Wen, P. H., Hof, P. R., Chen, X., Gluck, K., Austin, G., Younkin, S. G., Younkin, L. H., DeGasperi, R., Sosa, M. A. G., Robakis, N. K. R. K., et al. (2004) · Experimental Neurology · doi:10.1016/j.expneurol.2004.04.002 · Cited by 193
Genetic and host factors for dementia in Down's syndrome
Schupf, N. (2002) · British Journal of Psychiatry · doi:10.1192/bjp.180.5.405 · Cited by 188
Association between air pollutants and dementia risk in the elderly
Wu, Y., Lin, Y., Yu, H., Chen, J., Chen, T., Sun, Y., Wen, L., Yip, P., Chu, Y., & Chen, Y. (2015) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1016/j.dadm.2014.11.015 · Cited by 187
HIV-1 Tat inhibits neprilysin and elevates amyloid β
Rempel, H. C., & Pulliam, L. (2005) · AIDS · doi:10.1097/00002030-200501280-00004 · Cited by 186
Microglial Scavenger Receptors and Their Roles in the Pathogenesis of Alzheimer's Disease
Wilkinson, K., & Khoury, J. B. E. (2012) · International Journal of Alzheimer s Disease · doi:10.1155/2012/489456 · Cited by 197
Coordinated Expression of β‐Amyloid Precursor Protein and the Putative β‐Secretase BACE and α‐Secretase ADAM10 in Mouse and Human Brain
Marcinkiewicz, M. M., & Seidah, N. G. (2000) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2000.0752133.x · Cited by 190
Modulation of Alzheimer-like synaptic and cholinergic deficits in transgenic mice by human apolipoprotein E depends on isoform, aging, and overexpression of amyloid β peptides but not on plaque formation
Buttini, M., Yu, G.-Q., Shockley, K., Huang, Y., Jones, B., Masliah, E., Mallory, M., Yeo, T., Longo, F. M., & Mucke, L. (2002) · The Journal of Neuroscience · doi:10.1523/jneurosci.22-24-10539.2002 · Cited by 183
“…is responsible for the dysfunction and degeneration of neurons in AD remains a matter of active study and debate (Terry, 1996; Davis and Chisholm, 1997; Hartley et al., 1999; Hsia et al., 1999; Lue et al., 1999; McLean et al., 1999; Mucke et al., 2000; Näslund et al., 2000; Klein et al., 2001).”
Background
Oligomeric Amyloid Decreases Basal Levels of Brain-Derived Neurotrophic factor (BDNF) mRNA via Specific Downregulation of BDNF Transcripts IV and V in Differentiated Human Neuroblastoma Cells
Garzon, D. J., & Fahnestock, M. L. (2007) · Journal of Neuroscience · doi:10.1523/jneurosci.5053-06.2007 · Cited by 182
Excess of nonceruloplasmin serum copper in AD correlates with MMSE, CSF β-amyloid, and h-tau
Squitti, R., Barbati, G., Rossi, L. C., Ventriglia, M., Forno, G. D., Cesaretti, S., Moffa, F., Caridi, I., Cassetta, E., Pasqualetti, P., et al. (2006) · Neurology · doi:10.1212/01.wnl.0000223343.82809.cf · Cited by 180
Cerebrospinal fluid β-amyloid1–42 and tau in control subjects at risk for Alzheimer’s disease: The effect of APOE ε4 allele
Sunderland, T., Mirza, N., Putnam, K. T., Linker, G., Bhupali, D., Durham, R., Soares, H., Kimmel, L., Friedman, D., Bergeson, J., et al. (2004) · Biological Psychiatry · doi:10.1016/j.biopsych.2004.07.021 · Cited by 179
Effect of reductions in amyloid levels on cognitive change in randomized trials: instrumental variable meta-analysis
Ackley, S. F., Zimmerman, S. C., Brenowitz, W. D., Tchetgen, E. J. T., Gold, A. L., Manly, J. J., Mayeda, E. R., Filshtein, T. J., Power, M. C., Elahi, F. M., et al. (2021) · BMJ · doi:10.1136/bmj.n156 · Cited by 184
Transgenic mouse models of alzheimer disease: Developing a better model as a tool for therapeutic interventions.
Kitazawa, M., Medeiros, R., & M. LaFerla, F. (2012) · Current Pharmaceutical Design · doi:10.2174/138161212799315786 · Cited by 178
Astrocyte physiopathology: At the crossroads of intercellular networking, inflammation and cell death
Rossi, D. (2015) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2015.04.003 · Cited by 185
Filamentous phage as vector-mediated antibody delivery to the brain
Frenkel, D., & Solomon, B. (2002) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.072027199 · Cited by 178
The role of beta amyloid in Alzheimer?s disease: still a cause of everything or the only one who got caught?
Verdile, G. (2004) · Pharmacological Research · doi:10.1016/j.phrs.2003.12.028 · Cited by 181
Masitinib as an adjunct therapy for mild-to-moderate Alzheimer's disease: a randomised, placebo-controlled phase 2 trial
Piette, F., Belmin, J., Vincent, H., Schmidt, N., Pariel, S., Verny, M., Marquis, C., Mely, J., Hugonot-Diener, L., Kinet, J., et al. (2011) · Alzheimer s Research & Therapy · doi:10.1186/alzrt75 · Cited by 180
Intraneuronal pyroglutamate-Abeta 3–42 triggers neurodegeneration and lethal neurological deficits in a transgenic mouse model
Wirths, O., Breyhan, H., Cynis, H., Schilling, S., Demuth, H.-U., & Bayer, T. A. (2009) · Acta Neuropathologica · doi:10.1007/s00401-009-0557-5 · Cited by 174
Prophylactic treatment with paroxetine ameliorates behavioral deficits and retards the development of amyloid and tau pathologies in 3xTgAD mice
NELSON, R., GUO, Z., HALAGAPPA, V, PEARSON, M., GRAY, A., MATSUOKA, Y., BROWN, M., MARTIN, B., IYUN, T., & MAUDSLEY, S. (2007) · Experimental Neurology · doi:10.1016/j.expneurol.2007.01.037 · Cited by 173
High Striatal Amyloid β-Peptide Deposition Across Different Autosomal Alzheimer Disease Mutation Types
Villemagne, V. L., Ataka, S., Mizuno, T., Brooks, W. S., Wada, Y., Kondo, M., Jones, G. R., Watanabe, Y., Mulligan, R. S., Nakagawa, M., et al. (2009) · Archives of Neurology · doi:10.1001/archneurol.2009.285 · Cited by 176
How Do Membranes Initiate Alzheimer’s Disease? Formation of Toxic Amyloid Fibrils by the Amyloid β-Protein on Ganglioside Clusters
Matsuzaki, K. (2014) · Accounts of Chemical Research · doi:10.1021/ar500127z · Cited by 173

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
DOI: 10.1001/jama.283.12.1571
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

Correlation Between Elevated Levels of Amyloid β-Peptide in the Brain and Cognitive Decline

Abstract

Overview

Integrity signals

Verification

Claims the paper makes

Claims other papers make about this one

Citations

Cites

Cited by

Related

Metadata

Record

About these checks