Serum Analysis of Amyloid Beta- Protein 1-40 in Healthy Subjects, Autistic Children and Alzheimer’s Patients
نویسنده
چکیده
Department of Biology, Utah State University, Logan, Utah (USA) UDK: 616.89:616.153.96-053.2 UDK: 616.892.3:616.153.96-053.2 Резиме Abstract Амилоид бета-протеин1-40 (АП40) е пептид со ниска молекуларна тежина произведен низ животот во текот на нормалниот метаболизам на клетката и неврогенеративните болести. Заради своите невротрофични и невротоксични ефекти, сегашната студија беше спроведена за да ги процени нивоата на серум на АП40 кај здравите субјекти, децата со аутизам и пациентите со Алцхајмерова болест. Серумот АП40 беше мерен со анализа на ензимо-поврзан имуносорбент (ЕЛИСА). АП40 е значително повисок кај нормалните деца споредени со нормалните постари контролни лица, кај нормалните деца споредени со децата со аутизам и кај децата со аутизам споредени со пациентите со Алцхајмерова болест (p вредноста беше помала од 0.05 за сите групи). Овој наод сугерира намалување на серумот АП40 во однос на возраста кај нормалното стареење, како и кај аутизмот и Алцхајмеровата болест. Овој пад можеби резултира од абнормалната обработка на претходникот на амилоид бета-протеинот (АПП) во текот на нормалното стареење и болестите поврзани со возраста како што се аутизмот кај децата и Алцхајмеровата болест кај постарите. Можното објаснување за овој пад може да ги вклучи зголемените интеракции на АП40 во однос на возраста кај цитоскелетните протеини за таложење во мозочното ткиво, зголемената серин протеаза Amyloid beta-protein1-40 (AP40) is a low molecular weight peptide produced throughout life during normal cell metabolism and neurodegenerative diseases. Owing to its neurotrophic and neurotoxic effects, the present study was conducted to evaluate serum levels of AP40 in healthy subjects, autistic children and Alzheimer’s disease patients. Serum AP40 was measured by enzyme-linked immunosorbent assay (ELISA). AP40 was significantly higher in normal children compared to normal older controls, in normal children compared to autistic children, and in autistic children compared to Alzheimer’s patients (p value was less than 0.05 for all groups). This finding suggests an age-related decline of serum AP40 in normal aging, as well as in autism and Alzheimer’s disease. This decline may result from abnormal processing of amyloid beta-protein precursor (APP) during normal aging and age-related diseases such as autism in children and Alzheimer’s disease in elderly. Possible explanations for this decline may include age-related increased interactions of AP40 with cytoskeletal proteins for brain tissue deposition, increased serine proteases for APP metabolism or
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