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Fig. 1 | Molecular Neurodegeneration

Fig. 1

From: Tau accumulation in the retina promotes early neuronal dysfunction and precedes brain pathology in a mouse model of Alzheimer’s disease

Fig. 1

Tau protein accrues in the retina and precedes accumulation in the brain. a Representative western blots of soluble retinal extracts from 3-month-old 3xTg mice and wild-type (WT) age-matched controls probed with an antibody against total tau (K9JA) revealed the presence of four tau isoforms: 37-kDa, 50-kDa, 55-kDa and 100-kDa. All retinal tau isoforms were detected in both wild-type and 3xTg retinas. No signal was detected in tau knockout mice validating the specificity of the K9JA antibody. b Western blot analysis of brain homogenates from 3-month-old 3xTg mice and age-matched controls revealed four isoforms of 37-kDa, 50-kDa, 55-kDa and 65-kDa, while no signal was detected in brains from tau knockout mice. c Densitometry analysis showed a 1.8-, 1.6-, 2- and 2-fold increase in the 37-kDa, 50-kDa, 55-kDa, and 100-kDa tau variants, respectively, in retinal samples from 3xTg mice (n = 10) compared to WT controls (n = 8) (Student’s t-test, * = p < 0.05). d Quantitative analysis revealed no changes in brain tau levels between 3xTg mice (n = 10) and WT controls (n = 10) (Student’s t-test, n.s.: not significant, p > 0.05). e, f Western blots using retinal (e) or brain (f) samples from 6-month-old 3xTg mice demonstrated that only the 55-kDa tau form increased relative to age-matched WT controls. g, h Densitometry analysis indicated a ~ 1.4-fold increase in the 55-kDa tau isoform in the retina (g) and brain (h) of 3xTg mice compared to controls (3xTg: n = 5, WT: n = 4, Student’s t-test, * = p < 0.05). Vertical lines represent non-consecutive samples from the same gel

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