Affiliations: [a] Dpt. Morfología y Biología Celular, Facultad de Biología y Medicina, Universidad de Oviedo, Oviedo, Spain | [b] CIMA, Área de Neurociencias, Avda. Pío XII, Pamplona, Spain
Correspondence:
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Correspondence to: Jorge Tolivia, Department Morfología y Biología Celular, Facultad de Biología y Medicina, Universidad de Oviedo, Julián Clavería s/n, Oviedo 33006, Spain. Tel.: +34 985 103061; Fax: +34 985 103618; E-mail: jtolivia@uniovi.es.
Abstract: Apolipoprotein D (ApoD) is a secreted glycoprotein that is markedly induced in several pathological and stressful conditions in the nervous system. In the central nervous system, ApoD expression is upregulated during aging, after traumatic brain injury, and in several human neuropathologies such as Alzheimer's disease (AD), where it is found associated with amyloid-β (Aβ) plaques. Recent studies have indicated that ApoD has an important function as a neuroprotective and antioxidant protein. The aim of this work is to study the effect of the peptide fragment Aβ25-35, which is believed to play a major role in the neurodegenerative process of AD, in ApoD expression in a mouse hippocampal cell line. In addition, we studied whether direct addition of exogenous human recombinant ApoD protein has neuroprotective effect against Aβ25-35 treatment on neuronal cells. Our results demonstrate that Aβ25-35 induces ApoD expression in hippocampal cells in response to stress-induced growth arrest. This observed relationship between Aβ and ApoD expression could explain the elevated levels of ApoD found in AD brain, where it may be a neuroprotective molecule in the course of AD, probably related to its lipid transport function or a direct antioxidant property. However, the addition of exogenous human recombinant ApoD does not exert any protective effect, most likely due to its major structural modifications.
