TABLE 9.

Zebrafish models of huntingtin pathology.

Study	Method	Neuronal loss	Impaired metabolism	Motor deficits	Other phenotype
Diekmann et al., 2009	AMO knockdown	Yes	Reduced BDNF levels.	Not reported	Morphological deformities. Increased mortality.
Henshall et al., 2009	AMO knockdown	Too early	Not reported	Not reported	Impaired brain development. Morphological deformities.
Lo Sardo et al., 2012	AMO knockdown	Not reported	Increased ADAM10 activity. Increased Ncadherin cleavage.	Not reported	Impaired brain development.
Lumsden et al., 2007	AMO knockdown	Not reported	Impaired iron metabolism. Reduced hemoglobin production.	Not reported	Developmental retardation and morphological deformities.
Miller et al., 2005	19Q, 35Q, 56Q, and 80Q polyQ expansion	Yes – Only from 56Q expansion	Not reported – But demonstrated role of CHIP in role of QC	Not reported	Morphological deformities and increased mortality (From 56Q expansion).
Schiffer et al., 2007	4Q, 25Q, and 102Q polyQ expansion	Yes – Only in 102Q	Not reported	Not reported	Morphological deformities and increased mortality (102Q).
Sidik et al., 2020	CRISPR/Cas9 deletion	No	No	Not reported	Reduced fitness and survival in adulthood.
Veldman et al., 2015	Cre-loxP inducible 97Q expansion – in relation to N17 domain	Not reported – But increased mHTT aggregation	Not reported	Yes	Brain atrophy and reduced brain weight (mHTT without N17 domain).