As part of its education program, the club recently began offering a four-month workshop on Saturday mornings at the Cradle of Aviation Museum in Garden City, teaching 10- to 16-year-olds to build and fly models.
We next performed morphological analysis of these fly models.
Our fly models may recapitulate neuronal dysfunction and degeneration induced by such abnormal intracellular metabolisms of Aβ42.
Similarly, in the SCA8 fly models mentioned above, no muscular disorder was induced by the CUG expansion [42].
We have identified and thoroughly validated 21 candidate genes in our study using in vivo fly models of HD.
Whether altered propensity to maintain wakefulness is a necessary condition of altered neural inertia remains unknown, but eminently testable in both mouse and fly models.
In conclusion, our novel fly models have extended the non-cell autonomous pathology hypothesis as well as the developmental effect hypothesis to multiple polyQ diseases.
In addition, the fly models would be available for analyzing molecular pathologies and developing novel therapeutics against the non-cell autonomous polyQ pathology.
Our results, therefore, rule out the possibility that a specific length of RNA repeats is the primary determinant in the gain-of-function toxicity in fly models.
On the other hand, as our fly models are expressing the partial molecule, loss of physiological function of hHtt [18] is not highly plausible in our case.
In fact in fly models of AD, APP and APPL overexpression have been associated to transport defects [53], and were proposed to correlate to impaired synaptic plasticity [42].
