Endocytic disturbances distinguish among subtypes of alzheimer's disease and related disorders
Abstract
The endocytic pathway is important in amyloid precursor protein (APP) processing and beta-amyloid formation. Our studies have shown that endocytic pathway activation is a prominent and early feature of neurons in vulnerable regions of the brain in sporadic Alzheimer's disease. We report that endocytic pathway abnormalities are present not only in neurons, but in cerebral endothelia in Alzheimer's disease caused by certain APP mutations. The presence or absence of endocytic abnormalities distinguish subtypes of familial Alzheimer's disease linked to APP mutations from presenilin mutations, supporting the notion that different cellular pathways are involved in the altered processing of APP leading to increased beta-amyloid generation in certain of these different Alzheimer's disease subtypes.
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Early endosomal alterations are the earliest known pathology in sporadic AD and DS.
“Early endosomal alterations are the earliest known pathology in sporadic AD (SAD) and Down syndrome (DS), appearing in DS before birth, and in SAD, developing before -amyloid is deposited and as soluble A peptide levels first rise.”
From <i>App</i>Gene Dosage Modulates Endosomal Abnormalities of Alzheimer's Disease in a Segmental Trisomy 16 Mouse Model of Down Syndrome (2003) · cites this paper as Cataldo et al., 2001
Endosomal abnormalities in AD are influenced by ApoE genotype and do not develop in familial AD caused by presenilin mutations.
“Endosomal abnormalities, which are influenced by ApoE genotype (Cataldo et al., 1997), do not develop in familial AD caused by presenilin mutations (Cataldo et al., 2001), underscoring that they are AD subtype-specific and are also not a response to amyloid deposition.”
From <i>App</i>Gene Dosage Modulates Endosomal Abnormalities of Alzheimer's Disease in a Segmental Trisomy 16 Mouse Model of Down Syndrome (2003) · cites this paper as Cataldo et al., 2001
Cites
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Cataldo, A. M., Barnett, J. L., Pieroni, C., & Nixon, R. A. (1997) · The Journal of Neuroscience · doi:10.1523/jneurosci.17-16-06142.1997 · Cited by 393 · see citing works
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Probing sporadic and familial Alzheimer’s disease using induced pluripotent stem cells
Israel, M. A., Yuan, S. H., Bardy, C., Reyna, S. M., Mu, Y., Herrera, C., Hefferan, M. P., Van Gorp, S., Nazor, K. L., Boscolo, F. S., et al. (2012) · Nature · doi:10.1038/nature10821 · Cited by 1,253 · see citing works
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Ye, S., Huang, Y., Müllendorff, K., Dong, L., Giedt, G., Meng, E. C., Cohen, F. E., Kuntz, I. D., Weisgraber, K. H., & Mahley, R. W. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0508693102 · Cited by 275 · see citing works
Cataldo, A. M., Petanceska, S., Peterhoff, C. M., Terio, N. B., Epstein, C. J., Villar, A., Carlson, E. J., Staufenbiel, M., & Nixon, R. A. (2003) · The Journal of Neuroscience · doi:10.1523/jneurosci.23-17-06788.2003 · Cited by 241 · see citing works
Self-citationSubcellular Topography of Neuronal Aβ Peptide in APPxPS1 Transgenic Mice
Langui, D., Girardot, N., El Hachimi, K. H., Allinquant, B., Blanchard, V., Pradier, L., & Duyckaerts, C. (2004) · The American Journal of Pathology · doi:10.1016/s0002-9440(10)63405-0 · Cited by 165 · see citing works
Hung, C. O. Y., & Livesey, F. J. (2018) · Cell Reports · doi:10.1016/j.celrep.2018.11.095 · Cited by 159 · see citing works
Genetic Heterogeneity in Alzheimer Disease and Implications for Treatment Strategies
Dominantly Inherited Alzheimer Network, Ringman, J. M., Goate, A., Masters, C. L., Cairns, N. J., Danek, A., Graff-Radford, N., Ghetti, B., & Morris, J. C. (2014) · Current Neurology and Neuroscience Reports · doi:10.1007/s11910-014-0499-8 · Cited by 96 · see citing works
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- Authors
- Cataldo, A., Rebeck, G. W., Ghetti, B., Hulette, C., Lippa, C., Van Broeckhoven, C., Van Duijn, C., Cras, P., Bogdanovic, N., Bird, T., Peterhoff, C., & Nixon, R.
- Affiliations
- Nathan Kline Institute for Psychiatric Research (US)
- Harvard University (US)
- Indiana University Indianapolis (US)
- Duke University (US)
- Hahnemann University Hospital (US)
- University of Antwerp (BE)
- Veterans Health Administration (US)
- Corresponding author
- Cataldo, Anne
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2001-10-05
- Volume
- 50
- Issue
- 5
- Pages
- 661-665
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- OpenAlex
- W2038924652
- Cited by
- 90
- References
- 2
- Citations by year
- 2026: 4 · 2025: 2 · 2024: 2 · 2022: 6 · 2021: 2 · 2020: 6 · 2019: 7 · 2018: 4 · 2017: 4 · 2016: 7 · 2015: 8 · 2014: 2 · 2013: 4 · 2012: 5
- FWCI
- 1.39
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, endocytic pathway, amyloid precursor protein, APP mutations, presenilin mutations, brain endothelium, sporadic Alzheimer's disease, neuronal vulnerability
- MeSH terms
- Alzheimer Disease, Apolipoproteins E, Endocytosis, Frontal Lobe, Genotype, Humans, Neurons, Endosomes, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Genetic Predisposition to Disease
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