Dendrite and dendritic spine alterations in alzheimer models

Moolman, Donna L.; Vitolo, Ottavio V.; Vonsattel, Jean-Paul G.; Shelanski, Michael L.

doi:10.1023/b:neur.0000044197.83514.64

Cited by 245Alzheimer's disease research and treatmentsNeuroscience and Neuropharmacology ResearchNeuroinflammation and Neurodegeneration Mechanisms

The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.

Dendrite and dendritic spine alterations in alzheimer models

Moolman, Donna L., Vitolo, Ottavio V., Vonsattel, Jean-Paul G., Shelanski, Michael L.·2004·Journal of Neurocytology

DOI 10.1023/b:neur.0000044197.83514.64

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Abstract

Synaptic damage and loss are factors that affect the degree of dementia experienced in Alzheimer disease (AD) patients. Multicolor DiOlistic labeling of the hippocampus has been undertaken which allows the full dendritic arbor of targeted neurons to be imaged. Using this labeling technique the neuronal morphology of two transgenic mouse lines (J20 and APP/PS1) expressing mutant forms of the Amyloid Precursor Protein (APP), at various ages, have been visualized and compared to Wild Type (WT) littermate controls. Swollen bulbous dystrophic neurites with loss of spines were apparent in the transgenic animals. Upon quantification, statistically significant reductions in the number of spines and total dendrite area was observed in both transgenic mouse lines at 11 months of age. Similar morphological abnormalities were seen in human AD hippocampal tissue both qualitatively and quantitatively. Immunohistochemistry and DiOlistic labeling was combined so that Abeta plaques were imaged in relation to the dendritic trees. No preferential localization of these abnormal dystrophic neurites was seen in regions with plaques. DiI labeled reative astrocytes were often apparent in close proximity to A beta plaques.

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Dendritic spine loss occurs in APP transgenic models.
“Dendritic spine loss occurs in APP transgenic models (Lanz et al., 2003;Moolman et al., 2004;Tsai et al., 2004), an important observation because spines form the postsynaptic element of the vast majority of cortical synapses and are the proposed site of synaptic plasticity underlying learning and memory (Segal, 2002).”
From Dendritic Spine Abnormalities in Amyloid Precursor Protein Transgenic Mice Demonstrated by Gene Transfer and Intravital Multiphoton Microscopy (2005) · cites this paper as Moolman et al., 2004
AD transgenic mice showed physiological and neuritic alterations prior to plaques.
“AD transgenic mice showed physiological [32, 74, 77, 124] and neuritic alterations [22, 125] prior to plaques”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [125]

American Journal of Pathology
(2015) · American Journal Of Pathology · doi:10.2353/ajpath · Cited by 4,961
Physical basis of cognitive alterations in alzheimer's disease: Synapse loss is the major correlate of cognitive impairment
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
Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
Hsiao, K., Chapman, P., Nilsen, S., Eckman, C., Harigaya, Y., Younkin, S., Yang, F., & Cole, G. (1996) · Science · doi:10.1126/science.274.5284.99 · Cited by 4,210
High-Level Neuronal Expression of Aβ1–42in Wild-Type Human Amyloid Protein Precursor Transgenic Mice: Synaptotoxicity without Plaque Formation
Mucke, L., Masliah, E., Yu, G.-Q., Mallory, M., Rockenstein, E. M., Tatsuno, G., Hu, K., Kholodenko, D., Johnson-Wood, K., & McConlogue, L. (2000) · The Journal of Neuroscience · doi:10.1523/jneurosci.20-11-04050.2000 · Cited by 1,856
Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1
Duff, K., Eckman, C., Zehr, C., Yu, X., Prada, C.-M., Pérez‐Tur, J., Hutton, M., Buée, L., Harigaya, Y., Yager, D., et al. (1996) · Nature · doi:10.1038/383710a0 · Cited by 1,486
Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes
Holcomb, L., Gordon, M. N., McGowan, E., Yu, X., Benkovic, S., Jantzen, P., Wright, K., Saad, I., Mueller, R., Morgan, D., et al. (1998) · Nature Medicine · doi:10.1038/nm0198-097 · Cited by 1,386
Long-term dendritic spine stability in the adult cortex
Grutzendler, J., Kasthuri, N., & Gan, W.-B. (2002) · Nature · doi:10.1038/nature01276 · Cited by 1,198
Plaque-independent disruption of neural circuits in Alzheimer’s disease mouse models
Hsia, A. Y., Masliah, E., McConlogue, L., Yu, G.-Q., Tatsuno, G., Hu, K., Kholodenko, D., Malenka, R. C., Nicoll, R. A., & Mucke, L. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.6.3228 · Cited by 1,123
The Relationship between Aβ and Memory in the Tg2576 Mouse Model of Alzheimer's Disease
Westerman, M. A., Cooper-Blacketer, D., Mariash, A., Kotilinek, L., Kawarabayashi, T., Younkin, L. H., Carlson, G. A., Younkin, S. G., & Ashe, K. H. (2002) · Journal of Neuroscience · doi:10.1523/jneurosci.22-05-01858.2002 · Cited by 731
MUTANT GENES IN FAMILIAL ALZHEIMER'S DISEASE AND TRANSGENIC MODELS
Price, D. L., & Sisodia, S. S. (1998) · Annual Review of Neuroscience · doi:10.1146/annurev.neuro.21.1.479 · Cited by 580
Neuronal depletion of calcium-dependent proteins in the dentate gyrus is tightly linked to Alzheimer's disease-related cognitive deficits
Palop, J. J., Jones, B., Kekonius, L., Chin, J., Yu, G.-Q., Raber, J., Masliah, E., & Mucke, L. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1133381100 · Cited by 402
Comparison of Neurodegenerative Pathology in Transgenic Mice Overexpressing V717F β-Amyloid Precursor Protein and Alzheimer’s Disease
Masliah, E., Sisk, A., Mallory, M. E., Mucke, L., Schenk, D., & Games, D. (1996) · Journal of Neuroscience · doi:10.1523/jneurosci.16-18-05795.1996 · Cited by 389
Behavioral changes in transgenic mice expressing both amyloid precursor protein and presenilin-1 mutations: lack of association with amyloid deposits
Holcomb, L. A., Gordon, M. N., Jantzen, P., Hsiao, K., Duff, K., & Morgan, D. (1999) · Behavior Genetics · doi:10.1023/a:1021691918517 · Cited by 353
Multicolor “DiOlistic” Labeling of the Nervous System Using Lipophilic Dye Combinations
Gan, W., Grutzendler, J., Wong, W. T., Wong, R., & Lichtman, J. W. (2000) · Neuron · doi:10.1016/s0896-6273(00)00031-3 · Cited by 331
Plastic Neuronal Remodeling Is Impaired in Patients with Alzheimer’s Disease Carrying Apolipoprotein ε4 Allele
Arendt, T., Schindler, C., Brückner, M. K., Eschrich, K., Bigl, V., Zedlick, D., & Marcova, L. (1997) · The Journal of Neuroscience · doi:10.1523/jneurosci.17-02-00516.1997 · Cited by 319
THE JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
Weil, A. (1962) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/00005072-196201000-00001 · Cited by 273
Apolipoprotein E and cognitive performance
Raber, J., Wong, D., Yu, G.-Q., Buttini, M., Mahley, R. W., Pitas, R. E., & Mucke, L. (2000) · Nature · doi:10.1038/35006165 · Cited by 237
Diffuse plaques do not accentuate synapse loss in Alzheimer's disease.
(1990) · Europe PMC (PubMed Central) · Cited by 209
Dentate gyrus volume is reduced before onset of plaque formation in PDAPP mice: A magnetic resonance microscopy and stereologic analysis
Redwine, J. M., Kosofsky, B. E., Jacobs, R. E., Games, D., Reilly, J. F., Morrison, J. H., Young, W. G., & Bloom, F. E. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.242746599 · Cited by 204
Neuritic plaques in senile dementia of Alzheimer type: a Golgi analysis in the hippocampal region
Probst, A., Basler, V., Bron, B., & ULRICH, J. (1983) · Brain Research · doi:10.1016/0006-8993(83)90490-0 · Cited by 194
The Contribution of Altered Synapses in the Senile Plaque: An Electron Microscopic Study in Alzheimer's Dementia*†
Gonatas, N. K., Anderson, W., & Evangelista, I. (1967) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/00005072-196701000-00003 · Cited by 186
Three-dimensional analysis of the relationship between synaptic pathology and neuropil threads in Alzheimer disease
Masliah, E., Ellisman, M., Carragher, B., Mallory, M., Young, S., Hansen, L., Deteresa, R., & Terry, R. D. (1992) · Journal of Neuropathology and Experimental Neurology · doi:10.1097/00005072-199207000-00003 · Cited by 183
Modulation of Alzheimer-like synaptic and cholinergic deficits in transgenic mice by human apolipoprotein E depends on isoform, aging, and overexpression of amyloid β peptides but not on plaque formation
Buttini, M., Yu, G.-Q., Shockley, K., Huang, Y., Jones, B., Masliah, E., Mallory, M., Yeo, T., Longo, F. M., & Mucke, L. (2002) · The Journal of Neuroscience · doi:10.1523/jneurosci.22-24-10539.2002 · Cited by 183
Dendritic sprouting in Alzheimer's presenile dementia
Scheibel, A. B., & Tomiyasu, U. (1978) · Experimental Neurology · doi:10.1016/0014-4886(78)90164-4 · Cited by 176
Microtubular reorganization and dendritic growth response in alzheimer's disease
McKee, A. C., Kowall, N. W., & Kosik, K. S. (1989) · Annals of Neurology · doi:10.1002/ana.410260511 · Cited by 159
Development of senile plaques. Relationships of neuronal abnormalities and amyloid deposits.
Cork, L. C., Masters, C. L., Beyreuther, K. T., & Price, D. L. (1990) · Europe PMC (PubMed Central) · Cited by 112
Re-Evaluation of the Structural Organization of Neuritic Plaques in Alzheimerʼs Disease
MASLIAH, E., MALLORY, M., DEERINCK, T., DETERESA, R., LAMONT, S., MILLER, A., TERRY, R. D., CARRAGHER, B., & ELLISMAN, M. (1993) · Journal of Neuropathology and Experimental Neurology · doi:10.1097/00005072-199311000-00009 · Cited by 105
Selective vulnerability of dentate granule cells prior to amyloid deposition in PDAPP mice: Digital morphometric analyses
Wu, C.-C., Chawla, F., Games, D., Rydel, R. E., Freedman, S. B., Schenk, D., Young, W. G., Morrison, J. H., & Bloom, F. E. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0402147101 · Cited by 91
Characterisation of cytoskeletal abnormalities in mice transgenic for wild-type human tau and familial Alzheimer's disease mutants of APP and presenilin-1
Boutajangout, A., Authelet, M., Blanchard, V., Touchet, N., Tremp, G. L., Pradier, L., & Brion, J. (2003) · Neurobiology of Disease · doi:10.1016/j.nbd.2003.09.007 · Cited by 90
Journal of Neuropathology and Experimental Neurology
&NA;, &. (1983) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/00005072-198301000-00016 · Cited by 61
Rapid labeling of neuronal populations by ballistic delivery of fluorescent dyes
Grutzendler, J., Tsai, J., & Gan, W. (2003) · Methods · doi:10.1016/s1046-2023(03)00009-4 · Cited by 54
Dendritic changes in senile and presenile dementias.
Scheibel, A. B. (1979) · PubMed · Cited by 35
Neocortical synapses in a presenile dementia.
Gonatas, N. K. (1967) · PubMed · Cited by 9

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Authors: Moolman, D. L., Vitolo, O. V., Vonsattel, J.-P. G., & Shelanski, M. L.
Affiliations: Columbia University (US)
Corresponding author: Shelanski, Michael L.
ORCID: Vitolo, Ottavio V.
Shelanski, Michael L.
Venue: Journal of Neurocytology
Publisher: Springer Science and Business Media LLC
Published: 2004-05
Volume: 33
Issue: 3
Pages: 377-387
ISSN: 0300-4864 (ISSN-L)
1573-7381
DOI: 10.1023/b:neur.0000044197.83514.64
OpenAlex: W1967917932
Cited by: 245
References: 33
Citations by year: 2026: 4 · 2025: 5 · 2024: 5 · 2023: 9 · 2022: 13 · 2021: 7 · 2020: 10 · 2019: 7 · 2018: 8 · 2017: 9 · 2016: 14 · 2015: 15 · 2014: 16 · 2013: 23 · 2012: 11
FWCI: 5.97
Type: journal article
Language: en
Open access: closed
Licence: www.springernature.com/gp/researchers/text-and-data-mining (tdm)
www.springernature.com/gp/researchers/text-and-data-mining (vor)
Locations: Journal of Neurocytology (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute on Aging (AG08702, P50AG008702)
National Institute of Neurological Disorders and Stroke (NS15076, R01NS015076)
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: Alzheimer's disease, dendritic spine loss, dendritic morphology, amyloid precursor protein, APP/PS1 mice, dystrophic neurites, amyloid plaques, hippocampus, reactive astrocytes, synaptic damage, DiI labeling
MeSH terms: Aging, Alzheimer Disease, Animals, Astrocytes, Carbocyanines, Dendrites, Disease Models, Animal, Hippocampus, Humans, Immunohistochemistry, Mice, Transgenic, Mutation, Staining and Labeling, Amyloid beta-Protein Precursor, Pyramidal Cells, Biolistics, Dendritic Spines, Mice, Plaque, Amyloid

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Dendrite and dendritic spine alterations in alzheimer models

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