GPR3, also known as ACCA, is a G-protein coupled receptor that constitutively activates adenylate cyclase and is highly expressed in the central nervous system. Overexpression of GPR3 stimulates the production of amyloid-beta peptide (Abeta), the deposition of which is one of the pathological hallmarks of Alzheimer ’s disease (AD), while the ablation of GPR3 prevented the accumulation of Abeta in vitro and in an AD mouse model. This is of particular interest because of the proximity of a reported candidate Alzheimer ’s disease (AD) locus, suggesting that GPR3 may be a potential therapeutic target for the treatment of AD. GPR3 has also been shown to block the proliferation of cerebellar granule cell precursors (GCP) during postnatal development by inhibiting the Shh-induced proliferation of GCP, indicating that GPR3 activation may represent one of the signals that triggers the postnatal cell cycle exit and terminal differentiation of GPCs.

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