Abstract
Alzheimer’s disease (AD), the most common cause of dementia, is generally sporadic. However, a proportion of cases, defined as familial AD, has an early onset and is transmitted in an autosomal dominant fashion.1 A locus segregating with familial AD has been mapped on the chromosome 21,2 close to the amyloid precursor gene,3 but this clinical entity could be also rather heterogeneous.4 Chromosome 21 also contains genes involved in the very common Down’s syndrome (DS), which has many pathological and clinical aspects similar to AD. Cu/Zn superoxide dismutase (Cu/Zn SOD), a key enzyme in the metabolism of oxygen-free radicals, is encoded by the SOD-1 gene, which is also located on the chromosome 21 in its distal portion.5 Since patients with DS show an increase by almost 50% in SOD-1 activity due to the higher than normal level of SOD-1 protein,6 it has been suggested that abnormalities in the formation of free radicals may be involved in more than one clinical aspect of DS7 and similar interest has been developed in AD.8-10
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Postiglione, A. et al. (1995). Enzymatic and Genetic Analysis of Cu/Zn Superoxide Dismutase in Non-Familial Alzheimer’s Disease. In: Hanin, I., Yoshida, M., Fisher, A. (eds) Alzheimer’s and Parkinson’s Diseases. Advances in Behavioral Biology, vol 44. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9145-7_46
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DOI: https://doi.org/10.1007/978-1-4757-9145-7_46
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