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Studies on vascular endothelial growth factor B (VEGF-B) during the past decade or so have shown that VEGF-B appears to be a mysterious molecule with obscure, if not controversial, functions. When VEGF-B was initially discovered (Grimmond et al., 1996; Olofsson et al., 1996a), it was naturally believed to be an angiogenic factor, due to its high sequence homology and similar receptor binding pattern to VEGF, the prototypic angiogenic molecule. Much of our research effort was focused on this speculated angiogenic activity of VEGF-B for a long time. However, studies into this aspect, most of the time, turned out to be disappointing because of the negative findings. Unlike VEGF-A, VEGF-B did not seem to play a significant role in inducing blood vessel growth or vascular permeability, etc (Li et al., 2009). In addition, VEGF-B deficiency in mice did not seem to matter greatly, since VEGF-Bnull mice appeared largely healthy (Aase et al., 2001; Bellomo et al., 2000; Louzier et al., 2003; Reichelt et al., 2003), in contrast to the early embryonic lethality of VEGF-A null mice (Carmeliet et al., 1996; Ferrara et al., 1996). Based on the negative findings, we had once suspected that VEGF-B might be a redundant molecule. In recent years, VEGF-B has been shown to be a potent neuroprotective factor and an apoptosis inhibitor (Li et al., 2009; Li et al., 2008b; Poesen et al., 2008; Sun et al., 2004; Sun et al., 2006), opening up a new research avenue in VEGF-B biology. Thus far, there are five members within the VEGF family, VEGF-A, VEGF-B, PlGF, VEGF-C and VEGF-D (Li and Eriksson, 2001; Lohela et al., 2009). As a prototypic angiogenic factor, VEGF-A has a potent and “universal” angiogenic effect under most physiological and pathological conditions (Carmeliet & Jain, 2000; Ferrara & Kerbel, 2005; Folkman, 2007). The placenta growth factor (PlGF) is required for pathological angiogenesis (Luttun et al., 2002). However, when PlGF-1 is produced in the same population of cells with VEGF-A, it can also act as a natural antagonist of VEGF-A (Cao, 2009; Eriksson et al., 2002). VEGF-C and VEGFD are important players in lymphangiogenesis (Alitalo et al., 2005; Lohela et al., 2009). Remarkably, the biological function of VEGF-B has remained less studied. VEGF-B displays a high degree of sequence homology to VEGF-A and PlGF, and also binds to the tyrosine kinase VEGF receptor-1 (VEGFR-1) and neuropilin-1 (NP-1), like VEGF-A and PlGF (Olofsson et al., 1998; Olofsson et al., 1996a). VEGF-B is abundantly expressed in most tissues and organs (Aase et al., 1999; Li et al., 2001; Olofsson et al., 1996a). However, VEGF-B under most conditions appeared to be “redundant” or “inert” with no obvious function. The

Can VEGF-B Be Used to Treat Neurodegenerative Diseases?