Immunotherapy Reduces Vascular Amyloid- in PDAPP Mice
Open accessAbstract
In addition to parenchymal amyloid-beta (Abeta) plaques, Alzheimer's disease (AD) is characterized by Abeta in the cerebral vasculature [cerebral amyloid angiopathy (CAA)] in the majority of patients. Recent studies investigating vascular Abeta (VAbeta) in amyloid precursor protein transgenic mice have suggested that passive immunization with anti-Abeta antibodies may clear parenchymal amyloid but increase VAbeta and the incidence of microhemorrhage. However, the influences of antibody specificity and exposure levels on VAbeta and microhemorrhage rates have not been well established, nor has any clear causal relationship been identified. This report examines the effects of chronic, passive immunization on VAbeta and microhemorrhage in PDAPP mice by comparing antibodies with different Abeta epitopes (3D6, Abeta(1-5); 266, Abeta(16-23)) and performing a 3D6 dose-response study. VAbeta and microhemorrhage were assessed using concomitant Abeta immunohistochemistry and hemosiderin detection. 3D6 prevented or cleared VAbeta in a dose-dependent manner, whereas 266 was without effect. Essentially complete absence of VAbeta was observed at the highest 3D6 dose, whereas altered morphology suggestive of ongoing clearance was seen at lower doses. The incidence of microhemorrhage was increased in the high-dose 3D6 group and limited to focal, perivascular sites. These colocalized with Abeta deposits having altered morphology and apparent clearance in the lower-dose 3D6 group. Our results suggest that passive immunization can reduce VAbeta levels, and modulating antibody dose can significantly mitigate the incidence of microhemorrhage while still preventing or reducing VAbeta. These observations raise the possibility that Abeta immunotherapy can potentially slow or halt the course of CAA development in AD that is implicated in vascular dysfunction.
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mAbs binding deposited Aβ are generally more effective in clearing VAβ.
“However mAbs binding deposited Aβ are generally more effective in clearing VAβ [12].”
From APOE Genotype Differentially Modulates Effects of Anti-Aβ, Passive Immunization in APP Transgenic Mice (2017) · cites this paper as [12]
The Discussion reports that 3D6 cleared or prevented vascular Aβ, whereas 266, which binds deposited Aβ less avidly, did not. It says this difference was likely dependent on binding deposited amyloid, but a comparison of two antibodies does not establish that such antibodies are generally more effective. (LLM, conf=0.84)
Experimental — accuracy not yet measuredAβ immunotherapy can ameliorate VAβ burden and improve compromised vascular reactivity.
“Aβ immunotherapy can ameliorate VAβ burden and improve compromised vascular reactivity [12, 21, 63], but it is well known to escalate incidence of brain microhemorrhages [21, 26].”
From APOE Genotype Differentially Modulates Effects of Anti-Aβ, Passive Immunization in APP Transgenic Mice (2017) · cites this paper as [12]
The Discussion (page unavailable) reports that passive immunization prevented or nearly cleared vascular Aβ in PDAPP mice. It discusses vascular dysfunction as a potential consequence of amyloid deposition, but does not report a measured improvement in vascular reactivity after treatment. (LLM, conf=0.88)
Experimental — accuracy not yet measured
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The early contribution of cerebrovascular factors to the pathogenesis of Alzheimer’s disease
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Imaging of cerebrovascular pathology in animal models of Alzheimer's disease
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“…Dodart et al., 1999; Chen et al., 2000; Fryer et al., 2003; Nilsson et al., 2004; Domnitz et al., 2005; Hartman et al., 2005; Daumas et al., 2008; Schroeter et al., 2008 APPDutch hAPP E693Q mThy1 Dut – 22–25 mo ++ No n.a. Herzig et al., 2004, 2007 APP/London (APP/Lo, APP(V717I), APP-Ld, APP/Ld,…”
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“A different antibody, 266, designed to capture soluble Aß was ineffective at removing plaque and decreased peripheral clearance of Aß (Schroeter et al., 2008; Seubert et al., 2008).”
BackgroundHampel, H. J., Schneider, L. S., Giacobini, E., Kivipelto, M., Sindi, S., Dubois, B., Broich, K., Nisticò, R., Aisen, P. S. S., & Lista, S. (2014) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.2015.995637 · Cited by 82 · see citing works
“N-terminus are able to enter the brain and decrease amyloid deposits in brain tissue and cerebral vasculature [61,62].”
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Animal models of cerebral amyloid angiopathy
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Carbon Quantum Dots for Treatment of Amyloid Disorders
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Amyloid‐related imaging abnormalities from trials of solanezumab for Alzheimer's disease
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“Preclinical animal models suggest that repair and remodeling of cerebral vasculature occurs [15] after ARIA [16] that may prevent further occurrence [17].”
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“decrease during longer treatment periods (Schroeter et al., 2008).”
BackgroundNeutralization of Soluble, Synaptotoxic Amyloid β Species by Antibodies Is Epitope Specific
Zago, W., Buttini, M., Comery, T. A., Nishioka, C., Gardai, S. J., Seubert, P., Games, D., Bard, F., Schenk, D., & Kinney, G. G. (2012) · The Journal of Neuroscience · doi:10.1523/jneurosci.1676-11.2012 · Cited by 62 · see citing works
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“Vascular microhemorrhage has been reported in several preclinical studies using antibodies that are targeted to either N- or C-terminal epitopes, which also mediate clearance of fibrillar Ab [18,21,30].”
BackgroundInfluentialSelf-citationHan, B. W., Zhou, M., Vellimana, A. K., Milner, E., Kim, D. H., Greenberg, J. K., Chu, W., Mach, R. H., & Zipfel, G. J. (2011) · Molecular Neurodegeneration · doi:10.1186/1750-1326-6-86 · Cited by 55 · see citing works
“Excitingly, recent preclinical studies have identified several novel approaches that reduce or even prevent CAA formation [38-41].”
BackgroundBapineuzumab: Anti-β-Amyloid Monoclonal Antibodies for the Treatment of Alzheimer‘s Disease
Panza, F., Frisardi, V., Imbimbo, B. P., D’Onofrio, G., Pietrarossa, G., Seripa, D., Pilotto, A., & Solfrizzi, V. (2010) · Immunotherapy · doi:10.2217/imt.10.80 · Cited by 59 · see citing works
Transferrin receptor-targeted anti-amyloid antibody enhances brain delivery and mitigates ARIA.
Pizzo, M. E., Plowey, E. D., Khoury, N., Kwan, W., Abettan, J., DeVos, S. L., Discenza, C. B., Earr, T., Joy, D., Lye-Barthel, M., et al. (2025) · Science · doi:10.1126/science.ads3204 · Cited by 63 · see citing works
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“Subsequent studies using other anti-AβmAbs andmousemodels also demonstrated significant reductions in amyloid burden (Levites et al., 2006; Schroeter et al., 2008).”
Feinberg, H., Saldanha, J. W., Diep, L., Goel, A. S., Widom, A., Veldman, G. M., Weis, W. I., Schenk, D., & Basi, G. S. (2014) · Alzheimer s Research & Therapy · doi:10.1186/alzrt261 · Cited by 52 · see citing works
“amino-terminal epitopes provided the greatest efficacy across a number of end-points in preclinical studies [5,16,17].”
Self-citationConsidering a new paradigm for Alzheimer's disease research
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Drug pipeline in neurodegeneration based on transgenic mice models of Alzheimer's disease
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Amyloid beta immunization worsens iron deposits in the choroid plexus and cerebral microbleeds
Joseph‐Mathurin, N., Dorieux, O., Trouche, S. G., Boutajangout, A., Kraska, A., Fontès, P., Verdier, J., Sigurdsson, E. M., Mestre‐Francés, N., & Dhénain, M. (2013) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2013.05.013 · Cited by 37 · see citing works
“However, data from a preventative study in mice showed that Ab immunization at an early stage increases microbleeds without increasing CAA (Schroeter et al., 2008).”
BackgroundIs passive immunization for Alzheimer's disease ‘alive and well’ or ‘dead and buried’?
Jicha, G. A. (2009) · Expert Opinion on Biological Therapy · doi:10.1517/14712590902828285 · Cited by 40 · see citing works
“The existing animal data in passive immunization paradigms, demonstrating a largely posterior distribution of these findings that coincide with the distribution of CAA in human AD, instead suggests that interactions between antibody and CAA may be responsible for the presence of edema seen on MRI in these regions [6,2…”
ResultPetrushina, I., Ghochikyan, A., Mkrtichyan, M., Mamikonyan, G., Movsesyan, N., Ajdari, R., Vasilevko, V., Karapetyan, A., Lees, A., Agadjanyan, M. G., et al. (2008) · Journal of Neuroinflammation · doi:10.1186/1742-2094-5-42 · Cited by 37 · see citing works
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“Therapeutic interventions, such as passive immunization, was able to halt CAA progression and even to reduce vascular amyloid in APP transgenic mice, as demonstrated by immunohistochemical analysis (Schroeter et al., 2008; Cattepoel et al., 2011).”
BackgroundAmyloid beta peptide immunotherapy in Alzheimer disease
Delrieu, J., Ousset, P., Voisin, T., & Vellas, B. J. (2014) · Revue Neurologique · doi:10.1016/j.neurol.2014.10.003 · Cited by 35 · see citing works
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“Aβ immunotherapy can ameliorate VAβ burden and improve compromised vascular reactivity [12, 21, 63], but it is well known to escalate incidence of brain microhemorrhages [21, 26].”
BackgroundRETRACTED ARTICLE: Gantenerumab for the treatment of Alzheimer's disease
Delrieu, J., Ousset, P., & Vellas, B. J. (2012) · Expert Opinion on Biological Therapy · doi:10.1517/14712598.2012.688022 · Cited by 32 · see citing works
RetractedFluid Biomarkers in Clinical Trials of Alzheimer’s Disease Therapeutics
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“Infusion of bapineuzumab has also been associated with an increased incidence of microhemorrhage, which is thought to be due to its binding to vascular amyloid (183).”
BackgroundVillarreal, S. A., Zhao, F., Hyde, L. A., Holder, D., Forest, T. W., Sondey, M., Chen, X., Sur, C., Parker, E. M., & Kennedy, M. E. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-170056 · Cited by 29 · see citing works
Prevention of age-associated dementia
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“ing a possible link to the neuroinflammatory complications of the A immunization in the human trial [11,44,109,132].”
BackgroundPrincz-Kranz, F. L., Mueggler, T., Knobloch, M., Nitsch, R. M., & Rudin, M. (2010) · Neurobiology of Disease · doi:10.1016/j.nbd.2010.06.002 · Cited by 28 · see citing works
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Luo, F., Rustay, N. R., Seifert, T. R., Roesner, B., Hradil, V. P., Hillen, H., Ebert, U., Severin, J. M., Cox, B. F., Llano, D. A., et al. (2010) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.110.172932 · Cited by 27 · see citing works
“…M), individual microhemorrhages postmortem in mouse brain is possible by histological examination using Prussian blue (Pfeifer et al., 2002; Racke et al., 2005; Wilcock et al., 2007), it is very time consuming (Pfeifer et al., 2002; Wilcock et al., 2004; Racke et al., 2005; Schroeter et al., 2008).”
BackgroundMethodInfluentialNeuropathology and Amyloid-β Spectrum in a Bapineuzumab Immunotherapy Recipient
Roher, A. E., Maarouf, C. L., Daugs, I. D., Kokjohn, T. A., Hunter, J. M., Sabbagh, M. N., & Beach, T. G. (2011) · Journal of Alzheimer s Disease · doi:10.3233/jad-2011-101809 · Cited by 26 · see citing works
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Therapeutic anti‐amyloid β antibodies cause neuronal disturbances
Adhikari, U. K., Khan, R. H., Mikhael, M., Balez, R., David, M. A., Mahns, D. A., Hardy, J., & Tayebi, M. (2022) · Alzheimer s & Dementia · doi:10.1002/alz.12833 · Cited by 24 · see citing works
Mechanism-based treatments for Alzheimer's disease
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Blockx, I., Einstein, S., Guns, P., Audekerke, J. V., Guglielmetti, C., Zago, W. M., Roose, D., Verhoye, M., der Linden, A. V., & Bard, F. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160023 · Cited by 22 · see citing works
“Previously, it was shown that anti-A antibody treatment in mouse models has been associated with increased incidence of vascular microhemorrhages, detected by hemosiderin staining [6, 17].”
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“Therefore, many researchers are investigating new methods to safely improve the efficiency of mAb delivery to the brain.”
Antibodies bound to Aβ oligomers potentiate the neurotoxicity of Aβ by activating microglia
Morkūnienė, R., Žvirblienė, A., Dalgėdienė, I., Čižas, P., Jankevičiūtė, S., Baliūtytė, G., Jokubka, R., Jankunec, M., Valinčius, G., & Borutaitė, V. (2013) · Journal of Neurochemistry · doi:10.1111/jnc.12332 · Cited by 21 · see citing works
“We used primary rat and mouse cultures and found cytotoxic effects of different mouse IgG subtype complexes, IgG2b (anti-Ab, clone #11E12, anti-MTP-N, clone #4A2 and antiMeN, #10F7), IgG2a (anti-VP1,clone #6D11), and IgG1 (anti-Ab42, clone #G2-13) indicating that neurotoxic effect was not animal species dependent as m…”
BackgroundInfluentialA Comparative Evaluation of a Novel Vaccine in APP/PS1 Mouse Models of Alzheimer’s Disease
Carrera, I., Etcheverrı́a, I., Fernández‐Novoa, L., Lombardi, V., Lakshmana, M. K., Cacabelos, R., & Vigo, C. (2015) · BioMed Research International · doi:10.1155/2015/807146 · Cited by 20 · see citing works
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Update on Disease-Modifying/Preventive Therapies in Alzheimer’s Disease
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Generation and Characterization of Anti-AA Amyloid-Specific Monoclonal Antibodies
Wall, J. S., Kennel, S. J., Richey, T., Allen, A. L., Stuckey, A. C., Weiss, D. T., Macy, S. D., Barbour, R., Seubert, P. A., Solomon, A., et al. (2011) · Frontiers in Immunology · doi:10.3389/fimmu.2011.00032 · Cited by 18 · see citing works
“Additionally,given that other fibril-specific mAbs have been shown to opsonize and effect removal of pathologic light chain or Aβ amyloid (Bard et al., 2000, 2003; Hrncic et al., 2000; Schroeter et al., 2008), our anti-AA reagents also may have therapeutic potential.”
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“Although Aβ immunotherapy was effective in animal models [13], some adverse effects appeared during clinical trials.”
BackgroundA review of therapeutic failures in late-stage clinical trials
Jain, R., Subramanian, J., & Rathore, A. S. (2022) · Expert Opinion on Pharmacotherapy · doi:10.1080/14656566.2022.2161366 · Cited by 18 · see citing works
Mass spectrometric studies of the variety of beta‐amyloid proteoforms in Alzheimer's disease
Zakharova, N. V., Kononikhin, A. S., Indeykina, M. I., Bugrova, A. E., Strelnikova, P. A., Игоревич, П. С., Kozin, S. A., Popov, I. A., Mitkevich, V. A., Makarov, A. А., et al. (2022) · Mass Spectrometry Reviews · doi:10.1002/mas.21775 · Cited by 16 · see citing works
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“Some Aβ antibodies can bind to and effectively reduce either soluble and fibrillar forms of Aβ, thereby preventing synaptic degeneration and cognitive deficits in animal models of AD (Bard et al., 2000; Schroeter et al., 2008; Pul et al., 2011; Zago et al., 2012).”
BackgroundChronological Age Impacts Immunotherapy and Monocyte Uptake Independent of Amyloid Load
Li, Q., Lebson, L. A., Lee, D. C., Nash, K. R., Grimm, J., Rosenthal, A., Selenica, M. B., Morgan, D., & Gordon, M. N. (2011) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-011-9329-9 · Cited by 14 · see citing works
“Other groups have also found hemorrhages in mice that were older than those typically evaluated (Racke et al. 2005; Schroeter et al. 2008).”
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Amyloid beta 42 alters cardiac metabolism and impairs cardiac function in male mice with obesity
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Anti-Amyloid-β Immunotherapy for Alzheimer’s Disease
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- Authors
- Schroeter, S., Khan, K., Barbour, R., Doan, M., Chen, M., Guido, T., Gill, D., Basi, G., Schenk, D., Seubert, P., & Games, D.
- Affiliations
- Wyeth (US)
- Elan Pharmaceuticals, Inc. (Ireland) (IE)
- Corresponding author
- Games, D.
- ORCID
- Schroeter, S.
- Venue
- Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2008-07-02
- Volume
- 28
- Issue
- 27
- Pages
- 6787-6793
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6670967
- OpenAlex
- W2069315029
- Cited by
- 133
- References
- 32
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 15 · 2023: 2 · 2022: 6 · 2021: 3 · 2020: 3 · 2019: 1 · 2017: 5 · 2016: 5 · 2015: 6 · 2014: 12 · 2013: 6 · 2012: 19
- FWCI
- 9.96
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Intracerebral and Subarachnoid Hemorrhage Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- cerebral amyloid angiopathy, Alzheimer's disease, passive immunization, anti-amyloid beta antibodies, antibody epitope specificity, microhemorrhages, amyloid-beta clearance, PDAPP mice, hemosiderin, vascular dysfunction
- MeSH terms
- Animals, Antibodies, Epitopes, Cerebral Arteries, Cerebral Hemorrhage, Disease Models, Animal, Dose-Response Relationship, Drug, Female, Immunization, Passive, Metabolic Clearance Rate, Mice, Transgenic, Down-Regulation, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Cerebral Amyloid Angiopathy, Treatment Outcome, Mice
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