Capillary CAA and perivascular Aβ-deposition: Two distinct features of Alzheimer's disease pathology
Abstract
Cerebral amyloid angiopathy (CAA) is frequently seen in Alzheimer's disease (AD) cases and represents one of its histopathological hallmarks. CAA is characterized by amyloid β-protein (Aβ) deposits within vessel walls. In addition to arteries and veins capillaries can also be affected. Aβ deposition into the capillary wall is, thereby, known as capillary CAA (capCAA) and strongly associated with the apolipoprotein E APOEε4 allele as a risk factor. Aβ deposits along the pericapillary glia limitans are described as pericapillary Aβ (pericapAβ: synonymous with pericapillary CAA in other studies). Here, we studied the relationship between pericapAβ and capCAA in 58 human autopsy cases. Although pericapAβ and capCAA were more frequently found in AD cases compared to controls and although they exhibited a correlation to one another, detailed analysis revealed that there is a significant number of cases with pericapAβ lacking capCAA and vice versa. Moreover, single capillaries show either both pathologies or pericapAβ or capCAA only. There was no local association between these pathologies when analyzing multiple capillaries in each given case. Moreover, pericapAβ predominantly exhibited Aβ(42) whereas capCAA contained both Aβ(42) and Aβ(40). These differences as well as differences in the related astroglial reaction indicate that pericapAβ and capCAA are not directly linked. PericapAβ appears to represent initial Aβ accumulation along the glia limitans that is involved in the perivascular drainage of apoE and Aβ regardless of the APOE genotype whereas capCAA could be explained by a limited transendothelial clearance of apoE4-Aβ complexes compared to apoE2/3-Aβ complexes.
Integrity signals
Registry
Cites
Statistics
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?
Type 2 cerebral amyloid angiopathy affects arterioles and small arteries, but not capillaries, and is 2-times more likely to be associated with APOE2.
“Type 2 CAA affects arterioles and small arteries, but not capillaries and is 2-times more likely to associated with APOE2 [47, 48].”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [48]
Type 1 cerebral amyloid angiopathy affects capillaries, arterioles and small arteries and is 4-times more likely to be associated with APOE4.
“Type 1 CAA affects capillaries, arterioles and small arteries and it is 4-times more likely to be associated with APOE4.”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [48]
Cites
Neuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123 · see citing works
Braak, H., Alafuzoff, I., Arzberger, T., Kretzschmar, H., & Del Tredici, K. (2006) · Acta Neuropathologica · doi:10.1007/s00401-006-0127-z · Cited by 3,172 · see citing works
apoE isoform–specific disruption of amyloid β peptide clearance from mouse brain
Deane, R., Sagare, A., Hamm, K., Parisi, M., Lane, S., Finn, M. B., Holtzman, D. M., & Zlokovic, B. V. (2008) · Journal of Clinical Investigation · doi:10.1172/jci36663 · Cited by 771 · see citing works
Thirty years of Alzheimer's disease genetics: the implications of systematic meta-analyses
Bertram, L., & Tanzi, R. E. (2008) · Nature Reviews Neuroscience · doi:10.1038/nrn2494 · Cited by 747 · see citing works
Cerebral amyloid angiopathy without and with cerebral hemorrhages: A comparative histological study
Vonsattel, J. P. G., Myers, R. H., Tessa Hedley‐Whyte, E., Ropper, A. H., Bird, E. D., & Richardson, E. P. (1991) · Annals of Neurology · doi:10.1002/ana.410300503 · Cited by 662 · see citing works
Lemere, C. A., Blusztajn, J. K., Yamaguchi, H., Wisniewski, T., Saido, T. C., & Selkoe, D. J. (1996) · Neurobiology of Disease · doi:10.1006/nbdi.1996.0003 · Cited by 584 · cited 3× · see citing works
“PericapAβ co-localizing apoE often did not exhibit N-terminal Aβ-epitopes indicating that pericapAβ often consists of so-called “N-terminal truncated” Aβ similar as cerebellar Aβ-deposits [38], fleecy amyloid [39], and early Aβ-plaques [40].”
Self-citationApolipoprotein E promotes astrocyte colocalization and degradation of deposited amyloid-β peptides
Koistinaho, M., Lin, S., Wu, X., Esterman, M., Koger, D., Hanson, J., Higgs, R., Liu, F., Malkani, S., Bales, K. R., et al. (2004) · Nature Medicine · doi:10.1038/nm1058 · Cited by 571 · see citing works
What is the blood–brain barrier (not)?
Bechmann, I., Galea, I., & Perry, V. H. (2007) · Trends in Immunology · doi:10.1016/j.it.2006.11.007 · Cited by 520 · see citing works
Lymphatic drainage of the brain and the pathophysiology of neurological disease
Weller, R. O., Djuanda, E., Yow, H.-Y., & Carare, R. O. (2009) · Acta Neuropathologica · doi:10.1007/s00401-008-0457-0 · Cited by 488 · see citing works
Thal, D. R., Schultz, C., Dehghani, F., Yamaguchi, H., Braak, H., & Braak, E. (2000) · Acta Neuropathologica · doi:10.1007/s004010000242 · Cited by 136 · see citing works
Self-citationThal, D. R., Papassotiropoulos, A., Saido, T. C., Griffin, W. S. T., Mrak, R. E., Kölsch, H., Tredici, K. D., Attems, J., & Ghebremedhin, E. (2010) · Acta Neuropathologica · doi:10.1007/s00401-010-0707-9 · Cited by 103 · see citing works
Self-citation
Flagged first, then by citations
Cited by
Sorted by citations
The neuropathological diagnosis of Alzheimer's disease
DeTure, M. A., & Dickson, D. W. (2019) · Molecular Neurodegeneration · doi:10.1186/s13024-019-0333-5 · Cited by 3,329 · see citing works
“Type 2 CAA affects arterioles and small arteries, but not capillaries and is 2-times more likely to associated with APOE2 [47, 48].”
BackgroundThe overlap between vascular disease and Alzheimer’s disease - lessons from pathology
Attems, J., & Jellinger, K. A. (2014) · BMC Medicine · doi:10.1186/s12916-014-0206-2 · Cited by 739 · see citing works
“In addition, pericapillary Aβ refers to Aβ depositions in the glia limitans and adjacent neuropil, whereas in capillary CAA Aβ depositions are present in the capillary wall [88].”
BackgroundSelf-citationAmyloid-Beta: A Crucial Factor in Alzheimer's Disease
Sadigh‐Eteghad, S., Sabermarouf, B., Majdi, A., Talebi, M., Farhoudi, M., & Mahmoudi, J. (2014) · Medical Principles and Practice · doi:10.1159/000369101 · Cited by 542 · see citing works
Review: sporadic cerebral amyloid angiopathy
Attems, J., Jellinger, K., Thal, D. R., & Van Nostrand, W. (2011) · Neuropathology and Applied Neurobiology · doi:10.1111/j.1365-2990.2010.01137.x · Cited by 371 · see citing works
Self-citationDoes vascular pathology contribute to Alzheimer changes?
Kalaria, R. N., Akinyemi, R., & Ihara, M. (2012) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2012.07.032 · Cited by 238 · see citing works
Emerging Concepts in Alzheimer's Disease
Vinters, H. V. (2014) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev-pathol-020712-163927 · Cited by 232 · see citing works
Molecular mechanisms of neuropathological changes in Alzheimer’s disease: a review
Šerý, O., Povová, J., Mı́šek, I., Pešák, L., & Janout, V. (2013) · Folia Neuropathologica · doi:10.5114/fn.2013.34190 · Cited by 193 · see citing works
“Aβ deposition into the capillary wall is strongly associated with the ApoE4 allele as a risk factor [4].”
BackgroundFonseca, A. C., Ferreiro, E., Oliveira, C., Cardoso, S., & Pereira, C. (2013) · Biochimica et Biophysica Acta · doi:10.1016/j.bbadis.2013.08.007 · Cited by 122 · see citing works
Endothelial Mitochondrial Dysfunction in Cerebral Amyloid Angiopathy and Alzheimer’s Disease
Parodi‐Rullán, R. M., Sone, J. Y., & Fossati, S. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-190357 · Cited by 108 · see citing works
Walker, L. C. (2020) · Free Neuropathology · doi:10.17879/freeneuropathology-2020-3025 · Cited by 95 · see citing works
“The staining patterns of the two isoforms differ in capillary Aβ-CAA compared to large-vessel Aβ-CAA [24, 25], and in the vessel wall compared to the diffuse Aβ that sometimes extends from the wall into the surrounding parenchyma (dyshoric amyloid angiopathy) [25, 26].”
BackgroundBatarseh, Y. S., Bharate, S. S., Kumar, V., Kumar, A., Vishwakarma, R. A., Bharate, S. B., & Kaddoumi, A. (2017) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.7b00101 · Cited by 99 · see citing works
The effects of cerebral amyloid angiopathy on integrity of the blood-brain barrier
Magaki, S., Tang, Z., Tung, S., Williams, C. K., Lo, D., Yong, W. H., Khanlou, N., & Vinters, H. V. (2018) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2018.06.004 · Cited by 93 · see citing works
“The Aβ deposits of capillary CAA may also occasionally extend into the pericapillary neuropil, termed “dyshoric changes” or “dyshoric plaques” (Attems et al., 2010; Richard et al., 2010).”
BackgroundHecht, M., Krämer, L. M., Arnim, C., Otto, M., & Thal, D. (2018) · Acta Neuropathologica · doi:10.1007/s00401-018-1834-y · Cited by 92 · see citing works
“d High magnification of the perivascular Aβ, which is associated with the glia limitans next to small capillaries, which are free of amyloid deposits representing pericapillary Aβ [5].”
Self-citationZago, W., Schroeter, S., Guido, T., Khan, K., Seubert, P., Yednock, T., Schenk, D., Gregg, K. M., Games, D., Bard, F., et al. (2013) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2012.11.010 · Cited by 75 · see citing works
Kim, S. H., Ahn, J. H., Yang, H. J., Lee, P., Koh, G. Y., & Jeong, Y. (2020) · Acta Neuropathologica Communications · doi:10.1186/s40478-020-01042-0 · Cited by 76 · see citing works
Alzheimer-Related Cerebrovascular Disease in Down Syndrome
Lao, P., Gutierrez, J., Keator, D., Rizvi, B., Banerjee, A., Igwe, K., Laing, K. K., Sathishkumar, M. T., Moni, F., Andrews, H., et al. (2020) · Annals of Neurology · doi:10.1002/ana.25905 · Cited by 65 · see citing works
“There is interest in the role of PVS in the clearance of amyloid and other toxins in the aging brain.(57) The increase of enlarged PVS score with age in the young, CS participants mirrored that in the older, general population (mean age = 68 years(56)).”
ResultBrain arterial aging and its relationship to Alzheimer dementia
Gutierrez, J., Honig, L. S., Elkind, M. S. V., Mohr, J., Goldman, J., Dwork, A., Morgello, S., & Marshall, R. (2016) · Neurology · doi:10.1212/wnl.0000000000002590 · Cited by 65 · see citing works
“association between large artery amyloidosis with age and with AD, it is possible that older individuals with a high BAA score may have some of these genetic variants.(31,32) Among younger individuals with AD, their lifetime risk of intracranial hemorrhage is increased, suggesting perhaps underlying amyloidosis linkin…”
BackgroundIn vivo Detection of Cortical Microinfarcts on Ultrahigh‐Field MRI
Ii, Y., Maeda, M., Kida, H., Matsuo, K., Shindo, A., Taniguchi, A., & Tomimoto, H. (2012) · Journal of Neuroimaging · doi:10.1111/j.1552-6569.2012.00722.x · Cited by 61 · see citing works
Beta amyloid effects on expression of multidrug efflux transporters in brain endothelial cells.
Kania, K., Wijesuriya, H. C., Hladky, S., & Barrand, M. (2011) · Brain Research · doi:10.1016/j.brainres.2011.08.044 · Cited by 63 · see citing works
Does pathology of small venules contribute to cerebral microinfarcts and dementia?
Hartmann, D. A., Hyacinth, H. I., Liao, F., & Shih, A. Y. (2017) · Journal of Neurochemistry · doi:10.1111/jnc.14228 · Cited by 65 · see citing works
“deposition has also been reported near deformed capillaries in Alzheimer’s disease (Attems et al. 2010).”
BackgroundAmyloid-Beta Disrupts Calcium and Redox Homeostasis in Brain Endothelial Cells
Fonseca, A. C., Moreira, P., Oliveira, C., Cardoso, S., Pinton, P., & Pereira, C. (2014) · Molecular Neurobiology · doi:10.1007/s12035-014-8740-7 · Cited by 56 · see citing works
Hunter, S., Arendt, T., & Brayne, C. (2013) · Molecular Neurobiology · doi:10.1007/s12035-013-8445-3 · Cited by 46 · see citing works
“The different disease pathways involved in CAA may also relate to different pathways of vascular senescence [163].”
BackgroundInfluentialCell type-specific potential pathogenic genes and functional pathways in Alzheimer’s Disease
Wang, X., & Li, L. (2021) · BMC Neurology · doi:10.1186/s12883-021-02407-1 · Cited by 46 · see citing works
Li, W.-J., Antuono, P. G., Xie, C.-M., Chen, G., Jones, J. L., Ward, B. D., Singh, S. P., Franczak, M., Goveas, J., & Li, S.-J. (2014) · Cortex; a journal devoted to the study of the nervous system and behavior · doi:10.1016/j.cortex.2014.04.006 · Cited by 43 · see citing works
White matter myelin loss in the brains of aged dogs.
Chambers, J., Uchida, K., & Nakayama, H. (2012) · Experimental Gerontology · doi:10.1016/j.exger.2011.12.003 · Cited by 43 · see citing works
“In humans, CAA is morphologically categorized into two types according to whether Aβ is deposited in the capillary walls, in addition to larger vessels (Attems et al., 2010; Thal et al., 2002).”
Badea, A., Kane, L., Anderson, R. J., Qi, Y., Foster, M., Cofer, G. P., Medvitz, N., Buckley, A. F., Badea, A. K., Wetsel, W. C., et al. (2016) · NeuroImage · doi:10.1016/j.neuroimage.2016.08.014 · Cited by 39 · see citing works
“…first around blood vessels and an apparent failure to clear Aβ from the brain, which is similar to humans with cerebral amyloid angiopathy (CAA) (Attems et al., 2010); 3) CVN-AD mice show AT8 antibody immunopositive hyperphosphorylated tau (Colton et al., 2014), and the subsequent tau…”
InfluentialGan, S., Wong, L.-Z., Wong, J.-W., & Tan, E. (2019) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2018.10.021 · Cited by 37 · see citing works
Cerebral amyloid β(42) deposits and microvascular pathology in ageing baboons
Ndung’u, M., Härtig, W., Wegner, F., Mwenda, J., Low, R., Akinyemi, R., & Kalaria, R. (2012) · Neuropathology and Applied Neurobiology · doi:10.1111/j.1365-2990.2011.01246.x · Cited by 37 · see citing works
Rolyan, H., Feike, A. C., Upadhaya, A. R., Waha, A., Dooren, T. V., Haass, C., Birkenmeier, G., Pietrzik, C. U., LEUVEN, F. V., & Thal, D. R. (2011) · Journal of Neural Transmission · doi:10.1007/s00702-010-0572-7 · Cited by 36 · see citing works
“Pericapillary Ab deposits, i.e., diffuse Ab in the glia limitans near capillaries, might represent such a protein retention problem (Attems et al. 2010).”
BackgroundSelf-citationCapillary Amyloid-β Protein Deposition in a Population-Based Study (Vantaa 85+)
Mäkelä, M., Paetau, A., Polvikoski, T., Myllykangas, L., & Tanskanen, M. (2015) · Journal of Alzheimer's Disease · doi:10.3233/jad-150241 · Cited by 31 · see citing works
mNos2Deletion and HumanNOS2Replacement in Alzheimer Disease Models
Colton, C. A., Wilson, J. G., Everhart, A. L., Wilcock, D. M., Puoliväli, J. T., Heikkinen, T., Oksman, J., Jääskeläinen, O., Lehtimäki, K. K., Laitinen, T., et al. (2014) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0000000000000094 · Cited by 37 · see citing works
“A-Amyloid deposits in CVN-AD mice initially appeared as ‘‘caplike’’ structures reminiscent of CAA found in humans with AD (11, 31) (Fig.”
BackgroundZito, G., Polimanti, R. A., Panetta, V., Ventriglia, M., Salustri, C., Siotto, M., Moffa, F., Altamura, C., Vernieri, F., Lupoi, D., et al. (2012) · Rejuvenation Research · doi:10.1089/rej.2012.1383 · Cited by 22 · see citing works
“Indeed, some studies hypothesized that the APOE genotype has a complex role in the vascular damage of AD patients.(50,51) The outcome of the present study seems to confirm the correlation of the APOE e4 allele with the severity of cerebral amyloid angiopathy (CAA), commonly encountered in the walls of small and medium…”
Cerebral Superficial Siderosis
Weidauer, S., Neuhaus, E., & Hattingen, E. (2022) · Clinical Neuroradiology · doi:10.1007/s00062-022-01231-5 · Cited by 34 · see citing works
Agyare, E. K., Leonard, S. R., Curran, G. L., Yu, C. C., Lowe, V. J., Paravastu, A. K., Poduslo, J. F., & Kandimalla, K. K. (2012) · Molecular Pharmaceutics · doi:10.1021/mp300352c · Cited by 27 · see citing works
Wang, X.-F., Liu, D.-X., Liang, Y., Xing, L.-L., Zhao, W.-H., Qin, X.-X., Shang, D.-S., Li, B., Fang, W.-G., Cao, L., et al. (2016) · PLoS ONE · doi:10.1371/journal.pone.0161093 · Cited by 24 · see citing works
“In more than 80% of AD individuals, Aβ is deposited within cerebral vessel wall, termed as cerebral amyloid angiopathy (CAA) [2,3].”
BackgroundInfluentialTsay, H.-J., Liu, H., Kuo, Y., Chiu, C.-S., Liang, C.-C., Chung, C.-W., Chen, C., Chen, Y.-P., & Shiao, Y. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms221910413 · Cited by 19 · see citing works
Timosaponin-BII inhibits the up-regulation of BACE1 induced by Ferric Chloride in rat retina
Huang, J.-F., Shang, L., Liu, P., Zhang, M.-Q., Chen, S., Chen, D., Fan, C.-L., Wang, H., & Xiong, K. (2012) · BMC Complementary and Alternative Medicine · doi:10.1186/1472-6882-12-189 · Cited by 21 · see citing works
“Senile plaques, neurofibrillary tangles, capillary cerebral amyloid angiopathy and the abnormal loss of synapses are proposed to be the principal pathological changes in AD [1,2].”
BackgroundGut instincts: Unveiling the connection between gut microbiota and Alzheimer's disease.
Peddinti, V., Avaghade, M. M., Suthar, S., Rout, B., Gomte, S. S., Agnihotri, T., & Jain, A. (2024) · Clinical Nutrition ESPEN · doi:10.1016/j.clnesp.2024.02.019 · Cited by 20 · see citing works
Prospects of Saffron and its Derivatives in Alzheimer's Disease.
Zandi, N., Pazoki, B., Roudsari, N. M., Lashgari, N.-A., Jamshidi, V., Momtaz, S., Abdolghaffari, A., & Akhondzadeh, S. (2021) · Archives of Iranian medicine · doi:10.34172/aim.2021.35 · Cited by 19 · see citing works
Fu, H., Li, J., Du, P., Jin, W., Gao, G., & Cui, D. (2022) · FEBS Letters · doi:10.1002/1873-3468.14549 · Cited by 20 · see citing works
Structural polymorphism and cytotoxicity of brain‐derived β‐amyloid extracts
Adem, K. A., & Lee, S.-M. (2023) · Protein Science · doi:10.1002/pro.4639 · Cited by 14 · see citing works
“In addition to brain parenchyma deposition, Aβ aggregates are observed to accumulate in the cortical blood vessels with an estimated 85%–95% of AD cases having cerebral amyloid deposition (Attems et al., 2010; DeTure & Dickson, 2019).”
BackgroundFrequent Alzheimer’s disease neuropathological change in patients with glioblastoma
Greutter, L., Miller-Michlits, Y., Klotz, S., Reimann, R., Nenning, K., Platzek, S., Krause, E., Kiesel, B., Widhalm, G., Langs, G., et al. (2024) · Neuro-Oncology Advances · doi:10.1093/noajnl/vdae118 · Cited by 9 · see citing works
“53,54 Third, our custom digital image analysis pipeline was based on multiple serial sections per tissue block.”
MethodDeregulation of the Glymphatic System in Alzheimer’s Disease: Genetic and Non-Genetic Factors
Hu, Y., Su, T., Wu, L., Wu, J., Liu, D., Zhu, L., & Yuan, M. (2024) · Aging and Disease · doi:10.14336/ad.2023.1229 · Cited by 14 · see citing works
Lou, T.-W., Tao, B., & Chen, M. (2023) · Neuroscience · doi:10.1016/j.neuroscience.2023.01.032 · Cited by 16 · see citing works
Ong, J. J. H., Leow, Y. J., Qiu, B., Tanoto, P., Zailan, F. Z., Sandhu, G., & Kandiah, N. (2025) · Neurology · doi:10.1212/wnl.0000000000213836 · Cited by 11 · see citing works
“These fi ndings also align with autopsy studies, 12,13 which similarly demonstrated strong associations between EPVS enlargement, A β deposition, Braak NFT staging, and other CSVD and white matter histopathologic changes.”
Aurelian, S., Ciobanu, A., Carare, R. O., Stoica, S., Anghelescu, A., Ciobanu, V., Onose, G., Munteanu, C., Popescu, C., Andone, I., et al. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms242216533 · Cited by 10 · see citing works
“The amyloid in neuritic plaques consists of 42–43 amino acids at its C-terminal [55].”
InfluentialCerebral venous impairment and cerebral venous sinus thrombosis
Wang, J.-Q., Manaenko, A., Hu, Q., & Zhang, X.-H. (2024) · Brain Hemorrhages · doi:10.1016/j.hest.2024.03.002 · Cited by 9 · see citing works
Blood-Brain Barrier Damage in the Context of HIV Infection and Drug Abuse
Vinters, H., & Tung, S. (2015) · doi:10.1201/b19299-17 · Cited by 9
Ortner, M., Hauser, C., Schmaderer, C., Muggenthaler, C., Hapfelmeier, A., Sorg, C., Diehl‐Schmid, J., Kurz, A., Förstl, H., Ikenberg, B. D., et al. (2019) · Neuropsychiatric Disease and Treatment · doi:10.2147/ndt.s225754 · Cited by 7 · see citing works
Chukwu, L. C., Ekenjoku, J. A., Ohadoma, S. C., Olisa, C. L., Okam, P. C., Okany, C. C., Ramalam, M. A., & Innocent, O. C. (2023) · World Journal of Advanced Research and Reviews · doi:10.30574/wjarr.2023.17.2.20200335 · Cited by 10 · see citing works
“Several vascular risk factors e.g. diabetes mellitus, hypertension, atherosclerosis, hypercholesterolemia, metabolic syndrome and obesity, have been found to be associated with Alzheimer’s disease (Pluta, et (Attems, et al 2010).”
Bali, P., Bammidi, S., Banik, A., Nehru, B., & Anand, A. (2018) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2018.00222 · Cited by 7 · see citing works
Cerebral Amyloid Angiopathy: Clinical Presentation, Sequelae and Neuroimaging Features—An Update
Weidauer, S., & Hattingen, E. (2025) · Biomedicines · doi:10.3390/biomedicines13030603 · Cited by 10 · see citing works
“In contrast to CAA type 1, which is characterized by capillary deposits, CAA type 2 is not associated with such deposits [3,19,24].”
Targeting cerebrovascular impairments in Huntington's disease: a novel treatment perspective.
St-Amour, I., Aubé, B., Rieux, M., & Cicchetti, F. (2015) · Neurodegenerative Disease Management · doi:10.2217/nmt.15.41 · Cited by 5 · see citing works
Weidauer, S., Tafreshi, M., Förch, C., Hattingen, E., Arendt, C. T., & Friedauer, L. (2024) · European Journal of Neurology · doi:10.1111/ene.16425 · Cited by 4 · see citing works
Pathologically Confirmed Alzheimer’s Disease in APOE ε2 Homozygotes is Rare but Does Occur
Stipho, F., Jackson, R., & Sabbagh, M. (2018) · Journal of Alzheimer's Disease · doi:10.3233/jad-171060 · Cited by 3 · see citing works
The role of proteotoxic stress in vascular dysfunction in the pathogenesis of Alzheimer’s disease
Fonseca, A. C. R. G., Resende, R., Cardoso, S. M., & Pereira, C. (2015) · Endoplasmic Reticulum Stress in Diseases · doi:10.1515/ersc-2015-0005 · Cited by 3 · see citing works
- Authors
- Attems, J., Yamaguchi, H., Saido, T. C., & Thal, D. R.
- Affiliations
- Newcastle University (GB)
- Gunma University (JP)
- RIKEN (JP)
- Universität Ulm (DE)
- Corresponding author
- Thal, Dietmar Rudolf
- Venue
- Journal of the Neurological Sciences
- Publisher
- Elsevier BV
- Published
- 2010-12
- Volume
- 299
- Issue
- 1-2
- Pages
- 155-162
- ISSN
- 0022-510X (ISSN-L)
- OpenAlex
- W2111046068
- Cited by
- 63
- References
- 71
- Citations by year
- 2025: 2 · 2024: 5 · 2023: 4 · 2022: 1 · 2021: 4 · 2020: 9 · 2019: 3 · 2018: 5 · 2017: 2 · 2016: 3 · 2015: 2 · 2014: 9 · 2013: 4 · 2012: 5
- FWCI
- 3.03
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of the Neurological Sciences (publishedVersion)
- PubMed (publishedVersion)
- Funders
- NIHR Newcastle Biomedical Research Centre
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Intracerebral and Subarachnoid Hemorrhage Research
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease pathology, amyloid-beta, apolipoprotein E, APOE ε4, glia limitans, astroglial reaction, amyloid-beta 42, Aβ40
- MeSH terms
- Aged, Aged, 80 and over, Alleles, Alzheimer Disease, Brain, Capillaries, Female, Genotype, Humans, Immunohistochemistry, Male, Middle Aged, Amyloid beta-Peptides, Cerebral Amyloid Angiopathy, Statistics, Nonparametric, Apolipoprotein E4
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
