The DOI matches its Crossref record; 231 of the 232 references it cites were found in a registry or an index.
Analyzing dendritic spine pathology in Alzheimer’s disease: problems and opportunities
Open accessAbstract
Synaptic failure is an immediate cause of cognitive decline and memory dysfunction in Alzheimer's disease. Dendritic spines are specialized structures on neuronal processes, on which excitatory synaptic contacts take place and the loss of dendritic spines directly correlates with the loss of synaptic function. Dendritic spines are readily accessible for both in vitro and in vivo experiments and have, therefore, been studied in great detail in Alzheimer's disease mouse models. To date, a large number of different mechanisms have been proposed to cause dendritic spine dysfunction and loss in Alzheimer's disease. For instance, amyloid beta fibrils, diffusible oligomers or the intracellular accumulation of amyloid beta have been found to alter the function and structure of dendritic spines by distinct mechanisms. Furthermore, tau hyperphosphorylation and microglia activation, which are thought to be consequences of amyloidosis in Alzheimer's disease, may also contribute to spine loss. Lastly, genetic and therapeutic interventions employed to model the disease and elucidate its pathogenetic mechanisms in experimental animals may cause alterations of dendritic spines on their own. However, to date none of these mechanisms have been translated into successful therapeutic approaches for the human disease. Here, we critically review the most intensely studied mechanisms of spine loss in Alzheimer's disease as well as the possible pitfalls inherent in the animal models of such a complex neurodegenerative disorder.
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“Dendritic spines serve as docking points for presynaptic axons, and healthy turnover of dendritic spines depends on cytoskeletal proteins [113].”
From Rlip76: An Unexplored Player in Neurodegeneration and Alzheimer’s Disease? (2022) · cites this paper as [113]
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“The loss of dendritic spines is a characteristic of the brains of AD patients, indicative of synaptic failure and a loss of robust neural networking [113].”
From Rlip76: An Unexplored Player in Neurodegeneration and Alzheimer’s Disease? (2022) · cites this paper as [113]
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“Dendritic spines serve as docking points for presynaptic axons, and healthy turnover of dendritic spines depends on cytoskeletal proteins [113].”
From Rlip76: An Unexplored Player in Neurodegeneration and Alzheimer’s Disease? (2022) · cites this paper as [113]
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Cites
Neuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123
The Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics
Hardy, J., & Selkoe, D. J. (2002) · Science · doi:10.1126/science.1072994 · Cited by 13,864
Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D. (2013) · Neurodegenerative Diseases · doi:10.1159/000337230 · Cited by 10,359
Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid β-peptide
Haass, C., & Selkoe, D. J. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2101 · Cited by 4,744
Terry, R. D., Masliah, E., Salmon, D. P., Butters, N., DeTeresa, R., Hill, R., Hansen, L. A., & Katzman, R. (1991) · Annals of Neurology · doi:10.1002/ana.410300410 · Cited by 4,397
Synaptic Pruning by Microglia Is Necessary for Normal Brain Development
Paolicelli, R. C., Bolasco, G., Pagani, F., Maggi, L., Scianni, M., Panzanelli, P., Giustetto, M., Ferreira, T. A., Guiducci, E., Dumas, L., et al. (2011) · Science · doi:10.1126/science.1202529 · Cited by 4,244
Oakley, H., Cole, S. L., Logan, S., Maus, E., Shao, P., Craft, J., Guillozet-Bongaarts, A., Ohno, M., Disterhoft, J., Van Eldik, L., et al. (2006) · The Journal of Neuroscience · doi:10.1523/jneurosci.1202-06.2006 · Cited by 3,530
Phases of Aβ-deposition in the human brain and its relevance for the development of AD
Thal, D. R., Rüb, U., Orantes, M., & Braak, H. (2002) · Neurology · doi:10.1212/wnl.58.12.1791 · Cited by 3,490
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
Microglia promote learning-dependent synapse formation through brain-derived neurotrophic factor
Parkhurst, C. N., Yang, G., Ninan, I., Savas, J. N., Yates, J. R., Lafaille, J. J., Hempstead, B. L., Littman, D. R., & Gan, W.-B. (2013) · Cell · doi:10.1016/j.cell.2013.11.030 · Cited by 2,599
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Items 201–234 of 234
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Neurohistology with a Touch of History: Technology-Driven Research
Wouterlood, F. G., & Langer, T. P. (2020) · Neuromethods · doi:10.1007/978-1-0716-0428-1_1 · Cited by 1
Nichols, T. W. (2023) · Journal of Multiscale Neuroscience · doi:10.56280/1564010613 · Cited by 2
Lam, S. (2021) · theses.fr (ABES) · doi:10.70675/60b353ffz56fcz41a2z9e53zf0d9ac078167 · Cited by 1
Novel Optogenetic Approach Reveals a Function of cGMP in Synaptic Plasticity and Memory
Borovac, J. (2019) · TSpace (University of Toronto)
Emotional Freedom Techniques for Stroke Rehabilitation: A Single Case Study
Fuller, S. A., & Stapleton, P. (2021) · OBM Integrative and Complementary Medicine · doi:10.21926/obm.icm.2104038
Gene-expression control in early and late-onset dementia
Zhou, J. (2022) · eDiss (Georg-August-Universität Göttingen) · doi:10.53846/goediss-9465
Chemobrain: Mysteries and the importance of their revelation
Tuncer, M. (2022) · Hacettepe University Journal of the Faculty of Pharmacy · doi:10.52794/hujpharm.1100269
Maitra, A., Kumar, P., & Jha, M. (2023) · Lecture notes in networks and systems · doi:10.1007/978-981-99-2100-3_34
Screening of Akt and Wnt Pathways for the Early Diagnosis and Treatment of Alzheimer's DiseasePreprint
Wang, Y., Li, H., Zhang, K.-X., Wu, H., Cui, W., Xu, X., Zhi, H., & Zhang, J.-W. (2023) · Research Square · doi:10.21203/rs.3.rs-3450819/v1
Uchihara, T. (2024) · Oxford University Press eBooks · doi:10.1093/med/9780197676592.003.0005
Effect and mechanism of Donepezil hydrochloride on Alzheimer’s disease
Song, W., Xue, J., Wu, X., & He, J.-L. (2024) · Discussion of Clinical Cases · doi:10.5430/dcc.v10n4p21
Ávila-Costa, M. R., Dorado-Martínez, C., Montiel-Flores, E., Ordóñez-Librado, J. L., Gutiérrez-Valdez, A. L., Caballero, C. A. G., Sánchez-Betancourt, J., Erazo, L. R., Tron-Alvarez, R., Rodríguez-Lara, V., et al. (2024) · IntechOpen eBooks · doi:10.5772/intechopen.1007924
Efecto de la sobreexpresión de CCL1 (I-309) en las espinas dendríticas de neuronas del hipocampo
Adames-Torres, L. L., L, A. S. M., A., K. G. M., Flores-Cuadra, J. A., Britton, G. B., Villarreal, A. E., & Carreira, M. B. (2025) · Scientia · doi:10.48204/j.scientia.v35n1.a6658
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Tye, S. J., Yates, C. G., & Postorivo, D. (2022) · Elsevier eBooks · doi:10.1016/b978-0-12-824067-0.00005-0
Hebert, S., Pederson, E. N., & Ouyang, Z. (2025) · Bioinformatics and Biology Insights · doi:10.1177/11779322251358309
Shontell, R. M., Araki, D., Ormsbee, K. M., Delgado, D. D., & Nichols, R. A. (2025) · eNeuro · doi:10.1523/eneuro.0044-25.2025
López-Barrios, J. D., Ontiveros‐Torres, M. Á., & Cantoral-Ceballos, J. A. (2025) · IEEE/CVF Conference on Computer Vision and Pattern Recognition Workshops (CVPRW) · doi:10.1109/cvprw67362.2025.00462
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Liu, H., Li, J., Wang, X., Luo, S., Luo, D., Ge, W., & Ma, C. (2024) · Figshare · doi:10.6084/m9.figshare.26703235
van Nifterick, A. M., Gouw, A. A., van Kesteren, R. E., Scheltens, P., Stam, C. J., & de Haan, W. (2022) · Figshare · doi:10.6084/m9.figshare.20374707
Liu, H., Li, J., Wang, X., Luo, S., Luo, D., Ge, W., & Ma, C. (2024) · Figshare · doi:10.6084/m9.figshare.26703238
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Yu, T., Li, Y., Li, S., Nie, S., Feng, H., Zhang, Z., & Meng, L. (2025) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-025-05978-1
Luo, Y., Liu, Y., Long, H., Pei, C., Mao, L., Rose, G. M., & Zhang, H. (2026) · Journal of Integrative Neuroscience · doi:10.31083/jin46077
Pathophysiological role of Pyk2 in the nervous system
de Pins, B. (2019) · theses.fr (ABES) · doi:10.70675/e9fd4e35z9e7ez42d4za65cz5d999e5b2d5e
Valverde, A. (2020) · theses.fr (ABES) · doi:10.70675/f1b70734zf4e3z4870z8fbdz950d831642a7
Woo, H., Kim, S. W., Kim, S., Chae, S., & Kim, J. (2026) · Archives of Pharmacal Research · doi:10.1007/s12272-026-01608-x
Kuhn, F. R., Klaassen, R. V., Koopmans, F., Koolman, T. S. Z., SMIT, A. B., & Spijker, S. (2026) · Cells · doi:10.3390/cells15080736
Li, C., Cui, S., Yang, Y., Lei, J., Li, Y. W., Guo, R., Yang, Y., Tian, Y., Han, J., Tai, F., et al. (2026) · Current Zoology · doi:10.1093/cz/zoag029
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Ruiz-Serrano, M., Martín-Cámara, O., Barbero-Moreno, A., Cores, Á., & Menéndez, J. C. (2026) · Elsevier eBooks · doi:10.1016/b978-0-443-44173-8.00003-6
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Farzeen, I., Nazir, M. M., Jaan, Z., Ghaffar, W., Masood, A., YASMEEN, M., Ashraf, A., & Różański, H. (2026) · Journal of Alzheimer s Disease · doi:10.1177/13872877261469864
Yang, T., Tran, K. C., Leng, A., Langness, V. F., Massa, S. M., & Longo, F. M. (2026) · Cells · doi:10.3390/cells15191822
Wu, Y., Maurya, N. S., Yang, Y., Chen, W., Wang, G., Liu, Z., Hu, X., Zheng, W. J., & Xu, Z. (2026) · Briefings in Bioinformatics · doi:10.1093/bib/bbag601
Metadata
- Authors
- Dorostkar, M. M., Zou, C., Blazquez-Llorca, L., & Herms, J.
- Affiliations
- Institut für Neuropathologie (DE)
- German Center for Neurodegenerative Diseases (DE)
- Corresponding author
- Herms, Jochen
- Venue
- Acta Neuropathologica
- Published
- 2015-06-11
- Volume
- 130
- Issue
- 1
- Pages
- 1-19
- ISSN
- 0001-6322 (ISSN-L)
- 1432-0533
- PMC
- PMC4469300
- OpenAlex
- W622376569
- Cited by
- 235
- References
- 232
- Citations by year
- 2026: 15 · 2025: 30 · 2024: 34 · 2023: 20 · 2022: 25 · 2021: 29 · 2020: 23 · 2019: 19 · 2018: 13 · 2017: 13 · 2016: 12 · 2015: 2
- FWCI
- 1.59
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Acta Neuropathologica (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DZNE Pub (submittedVersion, cc-by)
- 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
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- dendritic spine loss, Alzheimer's disease, synaptic dysfunction, amyloid-beta, amyloid oligomers, tau hyperphosphorylation, microglial activation, animal models of Alzheimer's disease, cognitive decline, memory impairment
- MeSH terms
- Alzheimer Disease, Amyloid, Animals, Brain, Humans, Dendritic Spines
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