Pattern of apolipoprotein D immunoreactivity in human brain

Schizophrenia Breakdown in the Well-regulated Lifelong Process of Brain Development and Maturation

“…In normal brain, apolipoprotein D is found primarily in white matter oligodendrocytes (Navarro et al 1998;Ong et al 1999). Finally, in normal younger adults who are continuing to myelinate (Yakovlev and Lecours 1967;Benes et al 1994;Bartzokis et al 2001), brain apolipoprotein D is primarily localized in oligodendrocytes (Schaeren-Wiemers et al 1995;Navarro et al 1998;Kalman et al 2000) as is the case in the rodent CNS where a maturation-associated induction of the gene's expression has been reported (Ong et al 1999).…”

Age-related changes of apolipoprotein D expression in female rat central nervous system with chronic estradiol treatment

“…With aging, a proliferation of reactive glia has been also described (Nichols 1999), which can be responsible for most of the increase in apo D expression. Glial cells are the main cellular type involved in apo D synthesis (Boyles et al 1990b;Del Valle et al 2003;Kalman et al 2002;Navarro et al 2004;Patel et al 1995), but the number of neurons expressing apo D, also increases with aging (Belloir et al 2001;Navarro et al 1998bNavarro et al , 2010Rassart et al 2000). Control animals of 24 months show an overexpression of apo D similar to which is observed in aged humans (Kalman et al 2002;Loerch et al 2008;Navarro et al 1998bNavarro et al , 2010.…”

“…These observations indicate that treatment with estradiol may be able to prevent agerelated effects and neurodegenerative diseases. On the other hand, the expression of apo D increases with normal aging in all species studied (Kalman et al 2002;Loerch et al 2008;Navarro et al 1998bNavarro et al , 2010 as well as with neuropathological diseases, like Alzheimer's dementia (Belloir et al 2001;Ordoñez et al 2011;Terrisse et al 1998) or schizophrenia (Mahadik et al 2002;Thomas et al 2001a, b). Although the specific role of this apolipoprotein is unknown, studies in Drosophila (Muffat et al 2008;Sanchez et al 2006) and mouse (Ganfornina et al 2008) ascribe to apo D a key role in longevity regulation and higher survival rate, taking part in the control of lipoperoxidation.…”

“…Non-specific protein binding to the nitrocellulose membranes was reduced by preincubating the filter in blocking buffer (TNT, 7% BSA), and the membrane was then incubated overnight at 4°C with the primary antibody against apo D (diluted 1:10,000), antibody was a gift from Dr. Carlos López Otín, Departamento de Bioquímica y Biología Molecular, Universidad de Oviedo (see Diez-Itza et al 1994;Lopez-Boado et al 1994;Navarro et al 1998bNavarro et al , 2003Navarro et al , 2008Navarro et al , 2010. After incubation with the primary antibody, the membranes were washed and incubated with an antirabbit antibody coupled to HRP (sc-2004, Santa Cruz Biotechnology; diluted 1:20,000).…”

“…Apo D expression has been identified in humans as well as in other mammalian species (Boyles et al 1990b;Patel et al 1995;Provost et al 1991;Seguin et al 1995;Smith et al 1990). In humans, apo D is expressed in corporal fluids (Balbin et al 1990;Terrisse et al 1998), some systemic tissues (Drayna et al 1986;Rassart et al 2000) as well as in the peripheral nervous system (PNS) and the central nervous system (CNS) (Boyles et al 1990a;De Jonge et al 2003;Ganfornina et al 2010;Navarro et al 1998bNavarro et al , 2010. In the CNS, apo D expression has been described in astrocytes, oligodendrocytes, perivascular cells, and neurons (Boyles et al 1990b;Del Valle et al 2003;Hu et al 2001;Navarro et al 1998bNavarro et al , 2004Navarro et al , 2010Patel et al 1995).…”