a(MESH:Axons)
The axonal density of mitochondria, which is slightly lower in proaggregant compared with antiaggregant Tau transgenic slices, is marginally decreased by 64627 treatment albeit in a genotype-independent manner (Fig. S7) PubMed:27671637
The axonal density of mitochondria, which is slightly lower in proaggregant compared with antiaggregant Tau transgenic slices, is marginally decreased by 64627 treatment albeit in a genotype-independent manner (Fig. S7) PubMed:27671637
The axons of transfected neurons (Fig. 1 G and I) clearly reveal small inclusions of Tau (∼1 μm in size, arrowheads), although presynaptic boutons (e.g., giant mossy fiber boutons) are only marginally stained for Tau (Fig. 1I and Fig. S2 A and B; arrow), indicating that Tau does not accumulate at presynaptic boutons in these slices PubMed:27671637
The axonal density of mitochondria, which is slightly lower in proaggregant compared with antiaggregant Tau transgenic slices, is marginally decreased by 64627 treatment albeit in a genotype-independent manner (Fig. S7) PubMed:27671637
. In ALS, accumulation of NFs is a prominent feature (Rouleau et al., 1996), and it has been demonstrated that NFs contribute heavily to the axonopathy of tau transgenic mice (Ishihara et al., 2001a). PubMed:12428809
Surprisingly, the axonopathy was rescued in the tau x GSK-3β double-transgenic mice, together with a near-total normalization of the functional disabilities. PubMed:12428809
The axons of transfected neurons (Fig. 1 G and I) clearly reveal small inclusions of Tau (∼1 μm in size, arrowheads), although presynaptic boutons (e.g., giant mossy fiber boutons) are only marginally stained for Tau (Fig. 1I and Fig. S2 A and B; arrow), indicating that Tau does not accumulate at presynaptic boutons in these slices PubMed:27671637
. In ALS, accumulation of NFs is a prominent feature (Rouleau et al., 1996), and it has been demonstrated that NFs contribute heavily to the axonopathy of tau transgenic mice (Ishihara et al., 2001a). PubMed:12428809
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