Brain cytoplasmic (BC) RNA is another lncRNA that causes AD and brain aging. Mouse BC1 RNA and human BC200 RNA are lncRNA transcripts that are transported as ribonucleoprotein particles to the dendritic processes and bind to poly(A)-binding protein (PABP1), a regulator of translation initiation, thus regulating gene expression at the translational level.24 BC200 can interact with some RNA-binding proteins involved in aberrant transport of mRNA, leading to abnormal protein localization. Overexpression of BC200 in AD and the aging brain may cause synaptic/dendritic degeneration. Mus et al.25 found that the level of BC200 in the AD-affected brain region Brodmann area 9 was higher than that in the normal brain, and the relative level of BC200 RNA in the affected region increased in parallel with AD severity. Simultaneously, they found that in the advanced stage of AD, BC200 RNA often assumed a clustered perikaryal localization, indicating that dendritic loss is accompanied by somatic overexpression. Mus et al. concluded that this was a stress compensation mechanism initiated by dendritic sprouting and remodeling in AD degenerative lesions; they also thought that the abnormal localization and distribution of BC200 might be responsible for the cause and course of the disease. Whether BC200 overexpression in brain tissue is the cause of AD or an accompanying compensatory response will require further testing and confirmation.26 Recently, Zhang et al.27 showed that BC1 induces APP mRNA translation via association with a fragile X syndrome protein (FMRP). Inhibition of BC1 or BC1-FMRP association in AD mice blocks the aggregation of Aβ in the brain and improves spatial learning and memory. Expression of exogenous BC1 in mouse excitatory pyramidal neurons shows the opposite result. This study may provide a novel promising target for AD therapy.