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PS1-M146V transgenic AD mice, and that this upre-(Delay et al., 2012). miRNA precursors are first processed into 0 and PS1-M146V mouse hippocampal neurons, miR-342-5p, a miRNA that targets AnkG mRNA 30 UTR, is highly upregulatedence of senile plaques and neurofibrillary tangles (Price et al., 1995), together with axonal pathology involving dystrophic neurites decorating amyloid plaques, axonal swellings, and embryonic day 14 (E14). Our data showed that, with the criterion of a 2-fold cutoff, seven miRNAs were upregulated (Figure 1A, red dots) and seven miRNAs were downregulated (green dots)abnormal accumulation of axonal proteins (Bayer et al., 2001). Axonopathy and axonal transport deficits have been found in in APP/PS1 hippocampal tissues as compared with WT hippo-campal tissues. Among these altered miRNAs, miR-342-5pa single-stranded miRNA that interacts with the 3 UTR of the complementary mRNA sequences (Peters and Meister, 2007), resulting in translation repression or target degradation (Eulalio et al., 2009; Meister, 2007). A single miRNA can have up to several hundred target genes and thus may regulate multiple pathways at the same time (Baek et al., 2008; Selbach et al., 2008). Many miRNAs have demonstrated implications in neuro-degenerative diseases, such as Alzheimer’s disease (AD) (Chan and Kocerha, 2012; Delay and Hébert, 2011; Delay et al., 2012), which is the most common cause of dementia in people over 65 years of age and is associated with impairments in memory, language, behavior, and cognition (Price et al., 1995). The brains of patients with AD are characterized by the pres-compared with wild-type (WT) mouse neurons. Furthermore, we show that downregulation of AnkG by miR-342-5p is medi-ated through translation repression. Our results point to miRNA regulation as a critical determinant of axonal and neuronal pathology in AD mouse models