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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
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?
The cited source says what the claim attributes to it.
In the citing paper
“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]
The cited source says what the claim attributes to it.
In the citing paper
“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]
The cited source says what the claim attributes to it.
In the citing paper
“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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Items 201–231 of 231
Zou, C., Montagna, E., Shi, Y., Peters, F., Blázquez‐Llorca, L., Shi, S., Filser, S., Dorostkar, M. M., & Herms, J. W. (2015) · Acta Neuropathologica · doi:10.1007/s00401-015-1421-4 · Cited by 63
Self-citationTakahashi, R. H., Capetillo‐Zarate, E., Lin, M. T. S., Milner, T. A., & Gouras, G. K. (2013) · PLoS ONE · doi:10.1371/journal.pone.0051965 · Cited by 62
Auffret, A., Gautheron, V., Repici, M., Kraftsik, R., Mount, H. T. J., Mariani, J., & Rovira, C. (2009) · Journal of Neuroscience · doi:10.1523/jneurosci.1856-09.2009 · Cited by 62
Moon, M., Hong, H.-S., Nam, D. W., Baik, S. H., Song, H., Kook, S.-Y., Kim, Y. S., Lee, J., & Mook-Jung, I. (2012) · Journal of Alzheimer's Disease · doi:10.3233/jad-2011-111778 · Cited by 60
Modulation of synaptic plasticity and Tau phosphorylation by wild-type and mutant presenilin1
Dewachter, I., Ris, L., Croes, S., Borghgraef, P., Devijver, H., Voets, T., Nilius, B., Godaux, E., & LEUVEN, F. V. (2007) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2006.11.019 · Cited by 56
Wang, Y., Greig, N. H., Yu, Q.-S., & Mattson, M. P. (2008) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2007.10.009 · Cited by 53
RNA‐binding proteins involved in RNA localization and their implications in neuronal diseases
Tolino, M., Köhrmann, M., & Kiebler, M. A. (2012) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2012.08160.x · Cited by 51
Hyperphosphorylated tau is implicated in acquired epilepsy and neuropsychiatric comorbidities.
Zheng, P., Shultz, S. R., Hovens, C. M., Velakoulis, D., Jones, N. C., & O’Brien, T. J. (2014) · Molecular Neurobiology · doi:10.1007/s12035-013-8601-9 · Cited by 48
Blazquez-Llorca, L., Garcia-Marin, V., Merino-Serrais, P., Ávila, J., & DeFelipe, J. (2011) · Journal of Alzheimer’s Disease · doi:10.3233/jad-2011-110659 · Cited by 44
Fibrillar Amyloid Plaque Formation Precedes Microglial Activation
Jung, C. K. E., Keppler, K., Steinbach, S., Blázquez‐Llorca, L., & Herms, J. W. (2015) · PLoS ONE · doi:10.1371/journal.pone.0119768 · Cited by 43
Self-citationThe Inside-Out Amyloid Hypothesis and Synapse Pathology in Alzheimer's Disease
Gouras, G. K., Willén, K. I., & Faideau, M. (2013) · Neurodegenerative Diseases · doi:10.1159/000354776 · Cited by 42
Relationship Between Late-Life Hypertension, Blood Pressure, and Alzheimer’s Disease
Yang, Y., Roe, C. M., & Morris, J. C. (2011) · American Journal of Alzheimer s Disease & Other Dementias® · doi:10.1177/1533317511421779 · Cited by 41
Boehm, J. (2013) · European Journal of Neuroscience · doi:10.1111/ejn.12251 · Cited by 41
Immunotherapy alleviates amyloid-associated synaptic pathology in an Alzheimer’s disease mouse model
Dorostkar, M. M., Burgold, S., Filser, S., Barghorn, S., Schmidt, B., Anumala, U. R., Hillen, H., Klein, C., & Herms, J. W. (2014) · Brain · doi:10.1093/brain/awu280 · Cited by 40
Self-citationSynaptic control of local translation: the plot thickens with new characters
Thomas, M. G., Pascual, M. L., Maschi, D., Luchelli, L., & Boccaccio, G. L. (2013) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-013-1506-y · Cited by 38
Mutant Presenilin 1 Alters Synaptic Transmission in Cultured Hippocampal Neurons
Priller, C., Dewachter, I., Vassallo, N., Paluch, S., Pace, C., Kretzschmar, H. A., LEUVEN, F. V., & Herms, J. W. (2006) · Journal of Biological Chemistry · doi:10.1074/jbc.m605066200 · Cited by 37
Self-citationKirkwood, C. M., Ciuchta, J., Ikonomovic, M. D., Fish, K. N., Abrahamson, E. E., Murray, P. S., Klunk, W. E., & Sweet, R. A. (2013) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0b013e31829ecc89 · Cited by 35
Human APOE genotype affects intraneuronal A 1-42 accumulation in a lentiviral gene transfer model
Zhao, W., Dumanis, S. B., Tamboli, I. Y., Rodriguez, G. A., Jo LaDu, M., Moussa, C. E. H., & William Rebeck, G. (2014) · Human Molecular Genetics · doi:10.1093/hmg/ddt525 · Cited by 32
Jiménez, S., Navarro, V., Moyano, J., Sanchez-Mico, M. V., Torres, M., Dávila, J. C., Vizuete, M., Gutiérrez, A., & Vitórica, J. (2014) · PLoS ONE · doi:10.1371/journal.pone.0114041 · Cited by 31
Christensen, D. Z., Hüttenrauch, M., Mitkovski, M., Pradier, L., & Wirths, O. (2014) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2014.00139 · Cited by 29
Involvement of presenilin holoprotein upregulation in calcium dyshomeostasis of Alzheimer's disease
Honarnejad, K., Jung, C. K. E., Lammich, S., Arzberger, T., Kretzschmar, H. A., & Herms, J. W. (2013) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.12008 · Cited by 26
Self-citationMizukami, K., Ishikawa, M., Akatsu, H., Abrahamson, E. E., Ikonomović, M. D., & Asada, T. (2011) · Neuropathology · doi:10.1111/j.1440-1789.2010.01193.x · Cited by 26
Altered Function of Hippocampal CA1 Pyramidal Neurons in the rTg4510 Mouse Model of Tauopathy
Dalby, N. O., Volbracht, C., Helboe, L., Larsen, P. H., Jensen, H. S., Egebjerg, J., & Elvang, A. B. (2014) · Journal of Alzheimer s Disease · doi:10.3233/jad-131358 · Cited by 23
Nizzari, M., Barbieri, F., Gentile, M. T., Passarella, D., Caorsi, C., Diaspro, A., Taglialatela, M., Pagano, A., Colucci-D'Amato, L., Florio, T., et al. (2012) · Journal of Alzheimer's Disease · doi:10.3233/jad-2011-101590 · Cited by 21
Role of presenilin1 in structural plasticity of cortical dendritic spines in vivo
Jung, C. K. E., Fuhrmann, M., Honarnejad, K., LEUVEN, F. V., & Herms, J. W. (2011) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2011.07503.x · Cited by 21
Self-citationNagaishi, M., Arai, M., Osawa, T., Yokoo, H., Hirato, J., Yoshimoto, Y., & Nakazato, Y. (2011) · Neuropathology (Kyoto. 1993) · doi:10.1111/j.1440-1789.2010.01188.x · Cited by 21
Asparagine endopeptidase cleaves tau and promotes neurodegeneration
Rosenmann, H. (2014) · Nature Medicine · doi:10.1038/nm.3749 · Cited by 17
Accumulation of Intraneuronal Amyloid-β is Common in Normal Brain
Blair, J., Siedlak, S. L., Wolfram, J. A., Nunomura, A., Castellani, R. J., Ferreira, S. T., Klein, W. L., Wang, Y., Casadesús, G., Smith, M. A., et al. (2014) · Current Alzheimer Research · doi:10.2174/1567205011666140302200902 · Cited by 17
Molecular Genetics of Familial Alzheimer Disease
Shastry, B. S. (1998) · The American Journal of the Medical Sciences · doi:10.1016/s0002-9629(15)40324-6 · Cited by 16
Upadhaya, A. R., Scheibe, F., Kosterin, I., Abramowski, D., Gerth, J., Kumar, S., Liebau, S., Yamaguchi, H., Walter, J., Staufenbiel, M., et al. (2013) · Acta Neuropathologica Communications · doi:10.1186/2051-5960-1-77 · Cited by 14
The stability provided by the feet during manoeuvres whilst standing.
Rj, W. (1962) · PubMed · Cited by 13
Flagged first, then by citations
1 of the 232 references couldn’t be matched to a known paper.
Cited by
Sorted by citations
Synaptic basis of Alzheimer’s disease: Focus on synaptic amyloid beta, P-tau and mitochondria
John, A., & Reddy, P. H. (2021) · Ageing Research Reviews · doi:10.1016/j.arr.2020.101208 · Cited by 359
Yarjanli, Z., Ghaedi, K., Esmaeili, A., Rahgozar, S., & Zarrabi, A. (2017) · BMC Neuroscience · doi:10.1186/s12868-017-0369-9 · Cited by 303
Neuropathology of amyotrophic lateral sclerosis and its variants
Saberi, S., Stauffer, J. E., Schulte, D. J., & Ravits, J. (2015) · Neurologic Clinics · doi:10.1016/j.ncl.2015.07.012 · Cited by 282
Maestú, F., de Haan, W., Busche, M. A., & DeFelipe, J. (2021) · Ageing Research Reviews · doi:10.1016/j.arr.2021.101372 · Cited by 245
Poor sleep is associated with CSF biomarkers of amyloid pathology in cognitively normal adults
Sprecher, K. E., Koscik, R. L., Carlsson, C. M., Zetterberg, H., Blennow, K., Okonkwo, O. C., Sager, M. A., Asthana, S., Johnson, S. C., Benca, R. M., et al. (2017) · Neurology · doi:10.1212/wnl.0000000000004171 · Cited by 235
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
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
