ArticleThe Journal of comparative neurology2013
Tau-amyloid interactions in the rTgTauEC model of early Alzheimer's disease suggest amyloid-induced disruption of axonal projections and exacerbated axonal pathology.
Article in The Journal of comparative neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Understanding the complex interplay between tau, amyloid and the network in the spatiotemporal progression of Alzheimer's disease.Progress in neurobiology · 2025Article
- Machine Learning-assisted Quantitative Mapping of Intracortical Axonal Plasticity Following a Focal Cortical Stroke in Rodents.Experimental neurobiology · 2023Article
- Connectome-based biophysics models of Alzheimer's disease diagnosis and prognosis.Translational research : the journal of laboratory and clinical medicine · 2023Review
- Pharmacological Modulators of Tau Aggregation and Spreading.Brain sciences · 2020Review
- Chemogenetic attenuation of neuronal activity in the entorhinal cortex reduces Aβ and tau pathology in the hippocampus.PLoS biology · 2020Article
- Microglia Express Insulin-Like Growth Factor-1 in the Hippocampus of Aged APPFrontiers in cellular neuroscience · 2019Article
- Divergent topological networks in Alzheimer's disease: a diffusion kurtosis imaging analysis.Translational neurodegeneration · 2018Article
- Spread of tau down neural circuits precedes synapse and neuronal loss in the rTgTauEC mouse model of early Alzheimer's disease.Synapse (New York, N.Y.) · 2017Article
- Synaptic Amyloid-β Oligomers Precede p-Tau and Differentiate High Pathology Control Cases.The American journal of pathology · 2016Article
- APOEε2 is associated with milder clinical and pathological Alzheimer disease.Annals of neurology · 2015Article
- Array tomography for the detection of non-dilated, injured axons in traumatic brain injury.Journal of neuroscience methods · 2015Article
- Amyloid accelerates tau propagation and toxicity in a model of early Alzheimer's disease.Acta neuropathologica communications · 2015Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Early observations of the patterns of neurofibrillary tangles and amyloid plaques in Alzheimer's disease suggested a hierarchical vulnerability of neurons for tangles, and a widespread nonspecific pattern of plaques that nonetheless seemed to correlate with the terminal zone of tangle-bearing neurons in some instances. The first neurofibrillary cortical lesions in Alzheimer's disease occur in the entorhinal cortex, thereby disrupting the origin of the perforant pathway projection to the hippocampus, and amyloid deposits are often found in the molecular layer of the dentate gyrus, which is the terminal zone of the entorhinal cortex. We modeled these anatomical changes in a transgenic mouse model that overexpresses both P301L tau (uniquely in the medial entorhinal cortex) and mutant APP/PS1 (in a widespread distribution) to examine the anatomical consequences of early tangles, plaques, or the combination. We find that tau uniformly occupies the terminal zone of the perforant pathway in tau-expressing mice. By contrast, the addition of amyloid deposits in this area leads to disruption of the perforant pathway terminal zone and apparent aberrant distribution of tau-containing axons. Moreover, human P301L tau-containing axons appear to increase the extent of dystrophic axons around plaques. Thus, the presence of amyloid deposits in the axonal terminal zone of pathological tau-containing neurons profoundly impacts their normal connectivity.
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