2009
DOI: 10.1016/j.neurobiolaging.2008.01.009
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Synaptic contact number and size in stratum radiatum CA1 of APP/PS1ΔE9 transgenic mice

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Cited by 49 publications
(43 citation statements)
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“…Our results corroborate these findings by Smith et al (2009) as our 8-month-old APPswe/PS1dE9 mice demonstrate a higher presynaptic density in the total stratum lucidum of the CA3 subregion and in the ventral stratum moleculare of the DG. Increases in postsynaptic density in the stratum radiatum of the CA1 subregion has also been reported by West et al (2009) in 12-month-old APPswe/PS1dE9 mice. In early Braak stage AD patients, an initial rise in cortical synaptic markers has also been observed, followed by significant decreases in later stages (Mukaetova-Ladinska et al, 2000).…”
Section: Tablesupporting
confidence: 59%
“…Our results corroborate these findings by Smith et al (2009) as our 8-month-old APPswe/PS1dE9 mice demonstrate a higher presynaptic density in the total stratum lucidum of the CA3 subregion and in the ventral stratum moleculare of the DG. Increases in postsynaptic density in the stratum radiatum of the CA1 subregion has also been reported by West et al (2009) in 12-month-old APPswe/PS1dE9 mice. In early Braak stage AD patients, an initial rise in cortical synaptic markers has also been observed, followed by significant decreases in later stages (Mukaetova-Ladinska et al, 2000).…”
Section: Tablesupporting
confidence: 59%
“…This concept is supported by our observation of hypertrophy of cortical neurons in the APPsw/PS1 ␦E9 transgenic mouse 27 and the observation of an increased number of synaptic contacts in the same animal model. 28 Another possibility is that the hypertrophic neurons are extending or growing new axonal terminals along with their presynaptic structures. It is plausible that the larger neuronal somata in ASYMAD reflect adaptive changes of neurons and their circuits to compensate for the damage inflicted by neurotoxic effects of A␤ and tau.…”
Section: Resultsmentioning
confidence: 99%
“…Overall, these studies suggest that CTh and gray matter volumes draw an inverted U-shape with disease progression when preclinical phases of the disease are also considered. Evidences obtained from animal models, report volume increases measured with MRI (Maheswaran et al, 2009) or neural hypertrophy in coexistence with higher number of synaptic contacts (Oh et al, 2009;West et al, 2009) because of inflammatory response of the Aß load. In the same direction, recent studies showed that astrocytosis, studied with 11C-Deuterium-L-Deprenyl (11C-DED) precede amyloid deposition both in asymptomatic familiar AD and transgenic mice (Rodriguez-Vieitez et al, 2013Schöll et al, 2013).…”
Section: Discussionmentioning
confidence: 99%