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A Peri, Clinical Physiopathology, University of Florence, Florence, 50139, Italy
M Serio, Clinical Physiopathology, University of Florence, Florence, Italy

Correspondence: Alessandro Peri, Email: a.peri{at}dfc.unifi.it

Abstract

The endocrine and the nervous system are closely correlated throughout life, starting from the embryo and until the late stages of life. Alzheimer’s disease (AD) is the most common neurodegenerative disease associated with ageing. Unfortunately, an effective way to prevent or to cure this disease does not exist, so far. There is evidence that estrogens exert neuroprotective properties, although their efficacy against AD is still matter of debate. In 2000 a new neuroprotective gene, i.e. seladin-1 (for Selective Alzheimer’s Disease indicator-1) was identified and found to be down regulated in AD vulnerable brain regions. Seladin-1 inhibits the activation of caspase-3, a key modulator of apoptosis. This protein has also enzymatic activity. In fact, it has been demonstrated that the seladin-1 gene encodes 3-beta-hydroxysterol delta-24-reductase, that catalyzes the synthesis of cholesterol from desmosterol. In recent years it has been demonstrated that an appropriate amount of membrane cholesterol determines the generation of a barrier against toxic insults and prevents the production of β-amyloid, the histopathological hallmark of AD. This review will summarize the studies that have been focused on the characterization of the biological properties of seladin-1 since its first identification. In particular, the relationship between seladin-1-mediated neuroprotection and estrogens, IGF-I and thyroid hormones, will be described and discussed.

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