Changes in extracellular space size and geometry in APP23 transgenic mice: A model of Alzheimer's disease

Syková, Eva; Voříšek, Ivan; Antonova, Tatiana; Mazel, Tomáš; Meyer‐Luehmann, Melanie; Jucker, Mathias; Hájek, Milan; Or, Michael; Bureš, Jan

doi:10.1073/pnas.0408235102

Cited by 104 publications

(88 citation statements)

References 36 publications

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“…One line, denoted Tg(APP23) mice (8), expresses Swedish mutant human APP and first develops disease-associated neuropathological changes by 6-10 mo of age. The onset of amyloid deposition is sex-dependent, with female mice exhibiting earlier Aβ deposition compared with males (23). The other line, Tg(CRND8) mice (9), expresses human APP with Swedish and Indiana mutations and exhibits Aβ deposition beginning at 3-4 mo of age.…”

Section: Resultsmentioning

confidence: 99%

“…Using the Morris water maze, Tg(CRND8) mice showed delayed escape latency at ∼5 mo, but impaired performance in the probe trail was not evident until 9-10 mo of age (31). Delayed escape latency in the Morris water maze was reported in Tg(APP23) mice at 17-25 mo of age (23), whereas elevated BLI signals occurred in Tg(APP23:Gfapluc) mice at ∼14 mo of age. Although some behavioral deficits may precede elevated BLI signals in certain Tg mice, BLI seems to be as sensitive as water-maze tests in monitoring the pathologic effects of Aβ deposition.…”

Section: Comparison Between Bli and Other Techniques Used For Assessingmentioning

confidence: 99%

See 1 more Smart Citation

Bioluminescence imaging of Aβ deposition in bigenic mouse models of Alzheimer's disease

Watts

Giles

Grillo

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

105

109

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The undersigned authors wish to note, "The KefFC system of E. coli is maintained in an inactive state by the binding of glutathione (GSH) and is activated by the formation of GSH adducts (GSX), particularly those with bulky substituents. We described two crystal structures with density present in the ligand-binding domain that we interpreted as GSH and GSX. Recently, an independent, experienced crystallographer, who had viewed the structures from our study in a different context, made representations to us that cast doubt on position of the succinimido ring of GSX. We have further reviewed the density maps with the aid of an experienced crystallographer. As a consequence, we believe it is important to draw this altered interpretation of the crystal structures to the attention of readers. In both structures, the density for the backbone of GSH is clear and allows unequivocal assignment of the position of the tripeptide. In PDB coordinate set 3L9X, the density for the succinimido ring is very weak, making interpretation very speculative and the assignment rests on the identity of the ligand added to the crystallization mixture, for which there are two diastereomers in the solutiona possibility that provides some basis for weakening the density. However, in 3L9W there are two anomalies that affect the interpretation of the bound ligand. First, there is no density for the carbon atom attached to the sulfur of GSH and second, there is extra density adjacent to the position of sulfur that could be modelled as a constrained succinimido ring. However, this density could also be water or any other molecule that is trapped in the structure. Thus, while there is good evidence for the peptide, the evidence that it is in the GSH form is uncertain."There are no new data on either the structures or on the gating mechanism. However, we believe that we should be cautious in interpreting the structural data and that the field in general should be made aware of the alternative views of the electron density data. Note that the mutagenesis and spectroscopic data that were presented in the original manuscript are not affected by this alternative interpretation." Tarmo P. The authors note that the following grant should be added to the Acknowledgments: "NIH Grant AG002132." The authors note "The method used for exogenous expression of Ca V 1.2 channels in ref. 32 was incorrectly described as 'viral transduction' in the text. In fact, Yang et al. created transgenic mice with inducible, cardiomyocyte-specific expression of exogenous Ca V 1.2 channels regulated by a tetracycline-inducible promoter. When crossed with a transgenic mouse line expressing doxycycline-regulated reverse transcriptional activator under control of the α-myosin heavy chain protomer, the resulting double transgenic offspring expressed exogenous Ca V 1.2 channels in their cardiac myocytes after treatment with doxycycline. The authors regret the error in describing these methods."www.pnas.org/cgi

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Section: Resultsmentioning

confidence: 99%

Section: Comparison Between Bli and Other Techniques Used For Assessingmentioning

confidence: 99%

Bioluminescence imaging of Aβ deposition in bigenic mouse models of Alzheimer's disease

Watts

Giles

Grillo

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

105

109

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“…37 Atrophy or reduced GM density has been shown to be highly correlated with the neuronal counts in these regions. 32 The elevation in diffusivity may also be attributed to a loss of neuronal cell membranes that restrict the random motion of water molecules in the tissue, 38 which may explain the similarities between the pattern of cortical diffusivity and GM density changes in AD. However, our data indicate that hippocampal and parahippocampal gyrus diffusivity provided additional information over the GM density in characterizing the neurodegenerative changes in AD.…”

Section: Resultsmentioning

confidence: 99%

Dementia with Lewy bodies and Alzheimer disease

et al. 2010

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Objective: To identify the patterns of diffusivity changes in patients with dementia with Lewy bodies (DLB) and Alzheimer disease (AD) and to determine whether diffusion tensor MRI (DTI) is complementary to structural MRI in depicting the tissue abnormalities characteristic of DLB and AD. Methods:We studied clinically diagnosed age-, gender-, and education-matched subjects with DLB (n ϭ 30), subjects with AD (n ϭ 30), and cognitively normal (CN) subjects (n ϭ 60) in a case-control study. DTI was performed at 3T with a fluid-attenuated inversion recovery-based DTI sequence that enabled cortical diffusion measurements. Mean diffusivity (MD) and gray matter (GM) density were measured from segmented cortical regions. Tract-based diffusivity was measured using color-coded fractional anisotropy (FA) maps. Results:Patients with DLB were characterized by elevated MD in the amygdala and decreased FA in the inferior longitudinal fasciculus (ILF). ILF diffusivity was associated with the presence of visual hallucinations (p ϭ 0.007), and amygdala diffusivity was associated with Unified Parkinson's Disease Rating Scale (r ϭ 0.50; p ϭ 0.005) in DLB. In contrast, patients with AD were characterized by elevated MD in the medial temporal, temporal, and parietal lobe association cortices and decreased FA in the fornix, cingulum, and ILF. Amygdala diffusivity was complementary to GM density in discriminating DLB from CN; hippocampal and parahippocampal diffusivity was complementary to GM density in discriminating AD from CN. Conclusion:Increased amygdalar diffusivity in the absence of tissue loss in dementia with Lewy bodies (DLB) may be related to microvacuolation, a common pathology associated with Lewy body disease in the amygdala. Diffusivity measurements were complementary to structural MRI, demonstrating that measures of diffusivity on diffusion tensor MRI are valuable tools for characterizing the tissue abnormalities characteristic of Alzheimer disease and DLB. Neurology ® 2010;74:1814 -1821 GLOSSARY AD ϭ Alzheimer disease; CN ϭ cognitively normal; DLB ϭ dementia with Lewy bodies; DTI ϭ diffusion tensor MRI; FA ϭ fractional anisotropy; FDR ϭ false discovery rate; FLAIR ϭ fluid-attenuated inversion recovery; GM ϭ gray matter; ILF ϭ inferior longitudinal fasciculus; LB ϭ Lewy body; MD ϭ mean diffusivity; RBD ϭ REM sleep behavior disorder; ROI ϭ region of interest; SLF ϭ superior longitudinal fasciculus; TE ϭ echo time; TI ϭ inversion time; TR ϭ repetition time; UPDRS ϭ Unified Parkinson's Disease Rating Scale; WM ϭ white matter.Dementia with Lewy bodies (DLB) is the second most common cause of neurodegenerative dementia after Alzheimer disease (AD).1 Although patients with Lewy body (LB) pathology typically have some AD pathology, 2 noninvasive imaging markers that can distinguish the contribution of these different pathologies to the dementia syndrome may be useful for the differential diagnosis and may provide insight into the pathologic mechanisms underlying these disorders.Diffusion tensor MRI (DTI) provides infor...

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“…Values of ␣ (0.18 -0.19) and (1.61) found in wildtype mice in the present study can be compared with other in vivo studies on wild-type mouse cortex. For ages 3-6 months, Anděrová et al (2001) found ␣ ϭ 0.23, ϭ 1.67; for ages 6 -8 months, Syková et al (2005a) reported ␣ ϭ 0.20, ϭ 1.47-1.50; for ages 5-9 months, Syková et al (2005b) reported ␣ ϭ 0.17, ϭ 1.57. Variations among mouse strains probably account for the small differences in values.…”

Section: Comparison With Other Wild-type Mouse Studiesmentioning

confidence: 96%

Aquaporin-4-Deficient Mice Have Increased Extracellular Space without Tortuosity Change

Yao¹,

Hrabětová²,

Nicholson³

et al. 2008

J. Neurosci.

136

113

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Aquaporin-4 (AQP4) isϪ/Ϫ mice, and no differences in and k between the two genotypes. This is the first direct comparison of ECS properties in adult mice lacking AQP4 water channels with wild-type animals and demonstrates a significant enlargement of the volume fraction but no difference in hindrance to TMA ϩ diffusion, expressed as tortuosity. These findings provide direct evidence for involvement of AQP4 in modulation of the ECS volume fraction and provide a basis for future modeling of water and ion transport in the CNS.

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Changes in extracellular space size and geometry in APP23 transgenic mice: A model of Alzheimer's disease

Cited by 104 publications

References 36 publications

Bioluminescence imaging of Aβ deposition in bigenic mouse models of Alzheimer's disease

Bioluminescence imaging of Aβ deposition in bigenic mouse models of Alzheimer's disease

Dementia with Lewy bodies and Alzheimer disease

Aquaporin-4-Deficient Mice Have Increased Extracellular Space without Tortuosity Change

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