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Western blotting was performed in acute hippocampal slices from 3 4 month-old Tg2576 mice, an age well before the development of Aβ plaques but at which time early physiological and functional deficits have been described [16], [17].

The combination of ERT and SRT was evaluated in 3-month old Fabry-Rag mice, an age at which significant GL-3 has accumulated; absolute GL-3 levels were comparable between Fabry and Fabry-Rag mice (data not shown).

Treatment began in 6-month-old P301S tau transgenic mice, an age when tau accumulation becomes apparent by histopathology.

We initially analyzed 14-month mdx mice, an age when there is significant muscle degeneration, no change in SC number but a preference to differentiate (Fig. 5A-C).

Brainstem extracts from 6-month-old homozygous P301S tau transgenic mice (prepared and analysed as previously described [ 3]) were injected into the peritoneal cavity of 3-month-old heterozygous mice, an age at which they lack tau deposits.

Immunohistochemical labelling with anti-PTK2B pan-antibodies and selective antibodies against the phosphorylated form of PTK2B was performed in 10-12 mo-old mice, an age very close to the 9 mo-old mice used for the microarray analyses.

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In both humans and mice, an age-related increase in Cochlin deposition was observed, which was consistently absent in normal TM tissues.

The microarray hybridizations were performed using total RNA prepared from the liver samples of three wild-type mice and four Mir122a -/- mice at an age of 2-months.

Not surprisingly, AC3−/− mice at an age of 10 months were less active than AC3+/+ mice (Figure 5A and 5B).

The younger 569 mutant mice with an age up to 6 months have a metabolic fingerprint close to the wild-type mice (Figure 4E), which is consistent with their microarray profiling at 42 days of age (Figure 2A).

Micro-CT scanning also showed a considerable decrease in bone density in TH mice at an age of 8 weeks (Fig. 1C).

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