The DOI matches its Crossref record; 225 of the 225 references it cites were found in a registry or an index.
The dendritic hypothesis for Alzheimer's disease pathophysiology
Open accessAbstract
Converging evidence indicates that processes occurring in and around neuronal dendrites are central to the pathogenesis of Alzheimer's disease. These data support the concept of a "dendritic hypothesis" of AD, closely related to the existing synaptic hypothesis. Here we detail dendritic neuropathology in the disease and examine how Aβ, tau, and AD genetic risk factors affect dendritic structure and function. Finally, we consider potential mechanisms by which these key drivers could affect dendritic integrity and disease progression. These dendritic mechanisms serve as a framework for therapeutic target identification and for efforts to develop disease-modifying therapeutics for Alzheimer's disease.
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“Aβ, tau, and AD genetic risk factors affect dendritic integrity and disease progression [14].”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [14]
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Items 201–225 of 225
Hellweg, R., Wirth, Y., Janetzky, W., & Hartmann, S. (2011) · International Journal of Geriatric Psychiatry · doi:10.1002/gps.2766 · Cited by 57
l-type calcium channels in the hippocampus and cerebellum of Alzheimer’s disease brain tissue
Coon, A. L., Wallace, D. R., Mactutus, C. F., & Booze, R. M. (1999) · Neurobiology of Aging · doi:10.1016/s0197-4580(99)00068-8 · Cited by 54
Gertz, H., Cervós‐Navarro, J., & Ewald, V. (1987) · Neuroscience Letters · doi:10.1016/0304-3940(87)90720-8 · Cited by 54
Ho, R., Ortiz, D., & Shea, T. B. (2001) · Journal of Alzheimer s Disease · doi:10.3233/jad-2001-3507 · Cited by 54
Dinamarca, M. C., Weinstein, D. B., Monasterio, O., & Inestrosa, N. C. (2011) · Biochemistry · doi:10.1021/bi201246t · Cited by 53
Tong, M., Arora, K., White, M. M., & Nichols, R. A. (2011) · Journal of Biological Chemistry · doi:10.1074/jbc.m111.241299 · Cited by 48
Polydoro, M., de Calignon, A., Suárez‐Calvet, M., Sanchez, L., Kay, K. R., Nicholls, S. B., Roe, A. D., Pitstick, R., Carlson, G. A., Gómez‐Isla, T., et al. (2013) · Journal of Neuroscience · doi:10.1523/jneurosci.0881-13.2013 · Cited by 47
Clinical findings with nimodipine in dementia: test of the calcium hypothesis.
Fritze, J., & Walden, J. (1995) · PubMed · Cited by 45
αv integrins mediate beta-amyloid induced inhibition of long-term potentiation
Wang, Q., Klyubin, I., Wright, S., Griswold-Prenner, I., Rowan, M. J., & Anwyl, R. (2008) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2007.03.018 · Cited by 42
Signaling of the neurotrophin receptor p75 in relation to Alzheimer’s disease
Diarra, A., Geetha, T., Potter, P., & Babu, J. R. (2009) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2009.09.116 · Cited by 39
Jain, S., Yoon, S. Y., Leung, L., Knöferle, J., & Huang, Y. (2013) · PLoS ONE · doi:10.1371/journal.pone.0059478 · Cited by 39
Yamada, M., Wada, Y., Tsukagoshi, H., et al. (1988) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp.51.8.1088 · Cited by 38
Anderson, K. L., & Ferreira, A. (2004) · Journal of Neuroscience Research · doi:10.1002/jnr.20018 · Cited by 37
Scott, V., Vortherms, T. A., Niforatos, W., Swensen, A. M., Neelands, T. R., Milicic, I., Banfor, P. N., King, A., Zhong, C., Simler, G. H., et al. (2011) · Biochemical Pharmacology · doi:10.1016/j.bcp.2011.10.019 · Cited by 36
Dendritic changes in senile and presenile dementias.
Scheibel, A. B. (1979) · PubMed · Cited by 35
Fyn knock-down increases Aβ, decreases phospho-tau, and worsens spatial learning in 3×Tg-AD mice
Minami, S., Clifford, T. G., Hoe, H., Matsuoka, Y., & Rebeck, G. W. (2011) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2011.05.014 · Cited by 28
Willis, M., Kaufmann, W. A., Wietzorrek, G., Hutter‐Paier, B., Moosmang, S., Humpel, C., Hofmann, F. B., Windisch, M., Knaus, H., & Marksteiner, J. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-091117 · Cited by 26
[Loss of dendritic spines in Alzheimer's disease].
Hachimi, K. H. E., & Foncin, J. (1990) · PubMed · Cited by 24
Asanuma, M., Ogawa, N., Mizukawa, K., Hara, K., Hirata, H., & Mori, A. (1991) · Neurochemical Research · doi:10.1007/bf00966654 · Cited by 23
Aberrant Dendritic Excitability: A Common Pathophysiology in CNS Disorders Affecting Memory?
Nestor, M. W., & Hoffman, D. A. (2012) · Molecular Neurobiology · doi:10.1007/s12035-012-8265-x · Cited by 20
Han, H.-Y., Zhang, J.-P., Ji, S.-Q., Liang, Q.-M., Kang, H.-C., Tang, R.-H., Zhu, S.-Q., & Xue, Z. (2013) · PLoS ONE · doi:10.1371/journal.pone.0064839 · Cited by 20
Zinc-induced aggregation of Aβ (10–21) potentiates its action on voltage-gated potassium channel
Zhang, C., & Yang, P. (2006) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2006.04.044 · Cited by 19
Liu, Z., Conroy, W. G., Stawicki, T. M., Nai, Q., Neff, R. A., & Berg, D. K. (2008) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2008.02.013 · Cited by 16
Zinc-induced aggregation of Abeta (10-21) potentiates its action on voltage-gated potassium channel.
Zhang, Cf, & Yang, Y. (2006) · 中国生物学文摘 · Cited by 5
Jha, S., & Rasband, M. N. (2011) · The EMBO Journal · doi:10.1038/emboj.2011.409 · Cited by 3
Research works printed but not linked: 7
- Catalá, 1988, Hum. Neurobiol., 6, 255
- el Hachimi, 1990, C. R. Acad. Sci. III, 311, 397
- Fritze, 1995, J. Neural Transm. Suppl., 46, 439
- Holmes, 2013, Proc. Natl. Acad. Sci. U.S.A., 110, E3138
- Holtzman, 2011, Sci. Transl. Med., 3, 77sr71
- Mehraein, 1975, Adv. Neurol., 12, 453
- Scheibel, 1979, Res. Publ. Assoc. Res. Nerv. Ment. Dis., 57, 107
Cited by
Sorted by citations
Roles of tau protein in health and disease
Guo, T., Noble, W., & Hanger, D. P. (2017) · Acta Neuropathologica · doi:10.1007/s00401-017-1707-9 · Cited by 1,003
Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease
Khan, S., Barve, K. H., & Kumar, M. S. (2020) · Current Neuropharmacology · doi:10.2174/1570159x18666200528142429 · Cited by 820
“Aβ, tau, and AD genetic risk factors affect dendritic integrity and disease progression [14].”
BackgroundCurrent Research Therapeutic Strategies for Alzheimer’s Disease Treatment
Folch, J., Petrov, D., Ettcheto, M., Abad, S., Sánchez-López, E., García, M. L., Olloquequi, J., Beas-Zarate, C., Auladell, C., & Camins, A. (2016) · Neural Plasticity · doi:10.1155/2016/8501693 · Cited by 270
Agostinone, J., Alarcon-Martinez, L., Gamlin, C., Yu, W.-Q., Wong, R. O. L., & Di Polo, A. (2018) · Brain · doi:10.1093/brain/awy142 · Cited by 124
Masitinib for the treatment of mild to moderate Alzheimer’s disease
Folch, J., Petrov, D., Ettcheto, M., Pedrós, I., Abad, S., Beas-Zarate, C., Lazarowski, A., Marin, M., Olloquequi, J., Auladell, C., et al. (2015) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.2015.1045419 · Cited by 80
Metadata
- Authors
- Cochran, J. N., Hall, A. M., & Roberson, E. D.
- Affiliations
- University of Alabama at Birmingham (US)
- Corresponding author
- Roberson, Erik D.
- Venue
- Brain Research Bulletin
- Publisher
- Elsevier BV
- Published
- 2014-04
- Volume
- 103
- Pages
- 18-28
- ISSN
- 0361-9230 (ISSN-L)
- PMC
- PMC3989444
- OpenAlex
- W2046296412
- Cited by
- 114
- References
- 225
- Citations by year
- 2026: 5 · 2025: 3 · 2024: 13 · 2023: 10 · 2022: 9 · 2021: 12 · 2020: 13 · 2019: 5 · 2018: 6 · 2017: 13 · 2016: 9 · 2015: 12 · 2014: 4
- FWCI
- 0.92
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Research Bulletin (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of General Medical Sciences (T32GM008111)
- National Institute of Neurological Disorders and Stroke (R01NS075487, T32NS061788)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, dendrites, amyloid-beta, tau protein, genetic risk factors, disease-modifying therapy, therapeutic target
- MeSH terms
- Alzheimer Disease, Animals, Dendrites, Humans, Amyloid beta-Peptides, Neurites, Tauopathies
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