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Results: 8

1.
Figure 1.

Figure 1. From: Neurodegenerative phenotypes in an A53T ?-synuclein transgenic mouse model are independent of LRRK2.

Breeding strategy to generate double mutant mice. (A) Strategy to generate A53T-α-Syn mice on an LRRK2 null background. F0, F1 and F2 represent each generation of crossbreeding. The expected frequency of each genotype is indicated as a percent. (B) Strategy to generate bigenic mice co-expressing A53T-α-Syn and G2019S-LRRK2.

João Paulo L. Daher, et al. Hum Mol Genet. 2012 June 1;21(11):2420-2431.
2.
Figure 4.

Figure 4. From: Neurodegenerative phenotypes in an A53T ?-synuclein transgenic mouse model are independent of LRRK2.

Progression of the lethal phenotype induced by expression of human A53T-α-Syn is independent of LRRK2. (A) The Kaplan–Meier survival curves of A53T-α-Syn and A53T-α-Syn/G2019S-LRRK2 mice were generated by monitoring cohorts of both genotypes (α-SynA53T, n = 17; α-SynA53T/LRRK2G2019S, n = 13) until mice had to be euthanized due to the onset of terminal disease. (B) Survival curves of A53T-α-Syn (α-SynA53T, n = 11 mice) and A53T-α-Syn/LRRK2-KO (α-SynA53T/LRRK2KO, n = 21 mice) mice are also indicated.

João Paulo L. Daher, et al. Hum Mol Genet. 2012 June 1;21(11):2420-2431.
3.
Figure 2.

Figure 2. From: Neurodegenerative phenotypes in an A53T ?-synuclein transgenic mouse model are independent of LRRK2.

Localization of α-Syn and LRRK2 mRNA in the brain of transgenic mice. (A) In situ hybridization with 33P-labeled antisense oligonucleotide probes specific to total (human + mouse) or mouse α-Syn, mouse LRRK2 or mouse TH. Autoradiographs indicate the localization of human and mouse α-Syn, or endogenous LRRK2 and TH mRNAs in tissue sections containing the striatum/cortex, hippocampus/substantia nigra (SN) and brainstem from 7-month-old human A53T-α-Syn transgenic mice and their non-transgenic (Non-Tg) littermate control mice. (B) Localization of human or mouse LRRK2 mRNA in brain sections from 9- or 12-month-old human G2019S-LRRK2 transgenic and their non-transgenic mice.

João Paulo L. Daher, et al. Hum Mol Genet. 2012 June 1;21(11):2420-2431.
4.
Figure 8.

Figure 8. From: Neurodegenerative phenotypes in an A53T ?-synuclein transgenic mouse model are independent of LRRK2.

A53T-α-Syn and LRRK2 do not interact to influence the number of nigrostriatal dopaminergic neurons in mice. (A and C) Representative images of TH-positive neurons in the SNpc of 13- to 14-month-old end-stage A53T-α-Syn, A53T-α-Syn/G2019S-LRRK2 and A53T-α-Syn/LRRK2-KO mice. (B and D) Stereological assessment of the number of TH-positive and Nissl-positive dopaminergic neurons in the SNpc for each mouse genotype generated by crossbreeding of (B) A53T-α-Syn and LRRK2-G2019S transgenic mice (n = 3–6 mice/genotype) or (D) A53T-α-Syn and LRRK2-KO mice (n = 4 mice/genotype). Data represent the number of TH+ or Nissl+ SNpc neurons expressed as mean ± SEM. There are no statistical differences between mouse genotypes (P> 0.05).

João Paulo L. Daher, et al. Hum Mol Genet. 2012 June 1;21(11):2420-2431.
5.
Figure 7.

Figure 7. From: Neurodegenerative phenotypes in an A53T ?-synuclein transgenic mouse model are independent of LRRK2.

Microglial pathology in A53T-α-Syn transgenic mice is not affected by modulating LRRK2 expression. (A) Representative images of Iba1 immunoreactivity in the LCN and RF from 13- to 14-month-old end-stage A53T-α-Syn, A53T-α-Syn/G2019S-LRRK2 or A53T-α-Syn/LRRK2-KO mice and their WT littermate controls. A normal pattern of Iba1-positive microglial staining is observed in WT mice, whereas mice expressing human A53T-α-Syn reveal a marked microglial response in the RF but not the LCN. Scale bar: 50 µm. (B) Stereological assessment of Iba1 immunoreactivity in the LCN and RF from each mouse genotype (n = 3 mice/genotype). Data represent the percent area fraction of immunoreactivity expressed as mean ± SEM. There are no statistical differences between mouse genotypes (P> 0.05).

João Paulo L. Daher, et al. Hum Mol Genet. 2012 June 1;21(11):2420-2431.
6.
Figure 5.

Figure 5. From: Neurodegenerative phenotypes in an A53T ?-synuclein transgenic mouse model are independent of LRRK2.

Abnormal accumulation of human α-Syn in the brainstem of A53T-α-Syn transgenic mice is modestly altered by modulating LRRK2 expression. (A) Representative images of phospho-Ser129-α-Syn immunoreactivity in the LVN, LCN, RF, SNpc and cerebral cortex from 13- to 14-month-old end-stage A53T-α-Syn, A53T-α-Syn/G2019S-LRRK2 or A53T-α-Syn/LRRK2-KO mice and their WT littermate controls. Human α-Syn pathology is absent from WT mice, whereas mice expressing A53T-α-Syn exhibit the abnormal accumulation of phospho-Ser129-α-Syn in neuronal cell bodies and processes. Scale bar: 50 µm. (B) Stereological assessment of phospho-Ser129-α-Syn immunoreactivity in distinct brain regions from each mouse genotype (n = 3 mice/genotype). Data represent the percent area fraction of immunoreactivity expressed as mean ± SEM (*P< 0.05, **P< 0.01 or ***P< 0.001).

João Paulo L. Daher, et al. Hum Mol Genet. 2012 June 1;21(11):2420-2431.
7.
Figure 3.

Figure 3. From: Neurodegenerative phenotypes in an A53T ?-synuclein transgenic mouse model are independent of LRRK2.

Behavioral deficits in A53T-α-Syn transgenic mice are not altered by the absence of LRRK2. (A) In the open-field test, A53T-α-Syn mice and A53T-α-Syn/LRRK2-KO mice display a non-significant increase in locomotor activity compared with WT or LRRK2-KO mice at 6 months of age (n = 4–7 mice/genotype). Data indicate the total number of beam breaks during the first 15 min period expressed as mean ± SEM. (B) Analysis of acoustic startle reveals markedly reduced startle in A53T-α-Syn and A53T-α-Syn/LRRK2-KO mice, and a smaller reduction in the startle response in LRRK2-KO mice compared with WT control mice at 6 months of age (n> 8 mice/genotype). Data indicate startle amplitude in millinewtons (mN) expressed as mean ± SEM (**P< 0.001; n.s., non-significant).

João Paulo L. Daher, et al. Hum Mol Genet. 2012 June 1;21(11):2420-2431.
8.
Figure 6.

Figure 6. From: Neurodegenerative phenotypes in an A53T ?-synuclein transgenic mouse model are independent of LRRK2.

Astrocytic pathology in A53T-α-Syn transgenic mice is not affected by modulating LRRK2 expression. (A) Representative images of glial fibrillary acidic protein (GFAP) immunoreactivity in the LVN, LCN, RF and SNpc from 13- to 14-month-old end-stage A53T-α-Syn, A53T-α-Syn/G2019S-LRRK2 or A53T-α-Syn/LRRK2-KO mice and their WT littermate controls. A normal pattern of GFAP-positive astrocytic staining is observed in WT mice, whereas mice expressing human A53T-α-Syn reveal a marked astrocytic response in the RF and SNpc. Scale bar: 50 µm. (B) Stereological assessment of GFAP immunoreactivity in distinct brain regions from each mouse genotype (n = 3 mice/genotype). Data represent the percent area fraction of immunoreactivity expressed as mean ± SEM (*P< 0.05 or **P< 0.01).

João Paulo L. Daher, et al. Hum Mol Genet. 2012 June 1;21(11):2420-2431.

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