{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,3]],"date-time":"2025-12-03T17:46:24Z","timestamp":1764783984866,"version":"build-2065373602"},"reference-count":62,"publisher":"Bentham Science Publishers Ltd.","issue":"1","license":[{"start":{"date-parts":[[2017,6,13]],"date-time":"2017-06-13T00:00:00Z","timestamp":1497312000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/legalcode"}],"content-domain":{"domain":["openbiochemistryjournal.com","benthamopen.com"],"crossmark-restriction":true},"short-container-title":["TOBIOCJ"],"published-print":{"date-parts":[[2017,6,13]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>\n                      Some studies have indicated that human paraoxonase 1 (\n                      <jats:italic>PON1<\/jats:italic>\n                      ) activity shows a polymorphic distribution. The aim of this study was to determine the distribution of\n                      <jats:italic>PON1<\/jats:italic>\n                      polymorphism in patients with Alzheimer\u2019s disease in Gorgan and compare it with a healthy control group.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Method:<\/jats:title>\n                    <jats:p>\n                      The study included 100 healthy individuals and 50 patients. Enzyme activity and genetic polymorphism of\n                      <jats:italic>PON1<\/jats:italic>\n                      were determined.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Result:<\/jats:title>\n                    <jats:p>\n                      There were significant differences in distribution of genotypes and alleles among patients and control group. The most common genotype was CT in patients and control group, while the most frequent alleles were T and C in patients and controls, respectively. There was a statistically significant variation between serum\n                      <jats:italic>PON1<\/jats:italic>\n                      activity and \u2013108C&gt; T polymorphism. The highest\n                      <jats:italic>PON1<\/jats:italic>\n                      enzyme activities in the patients and controls were found in CC, while lower enzyme activities were seen in CT and TT genotypes in both genders and age groups.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>\n                      Onset of Alzheimer\u2019s disease may depend on different polymorphisms of the\n                      <jats:italic>PON1<\/jats:italic>\n                      enzyme. Late or early-onset of Alzheimer\u2019s disease may also depend on age and gender distribution, especially for arylesterase enzyme. Further studies on polymorphism of the enzyme are necessary for interpretation of possible polymorphic effects of enzyme on\n                      <jats:italic>PON1<\/jats:italic>\n                      activity in humans.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.2174\/1874091x01711010047","type":"journal-article","created":{"date-parts":[[2017,6,13]],"date-time":"2017-06-13T02:27:16Z","timestamp":1497320836000},"page":"47-55","update-policy":"https:\/\/doi.org\/10.2174\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Alzheimer\u2019s Disease and Paraoxonase 1 (PON1) Gene Polymorphisms"],"prefix":"10.2174","volume":"11","author":[{"given":"Mohsen","family":"Saeidi","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Raheleh","family":"Shakeri","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Abdoljalal","family":"Marjani","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Safoura","family":"Khajeniazi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"965","reference":[{"key":"ref1","first-page":"130","volume":"50","author":"Armstrong R.A.","year":"2012","unstructured":"Armstrong RA. \n                    \u03b2-amyloid (A\u03b2) deposition in cognitively normal brain, dementia with Lewy bodies, and Alzheimers disease: a study using principal components analysis. \n                    Folia Neuropathol  \n                    2012; \n                    50\n                    (2)\n                    : 130-9.","journal-title":"Folia Neuropathol."},{"key":"ref2","doi-asserted-by":"publisher","first-page":"187","DOI":"10.1159\/000330363","volume":"9","author":"Biscaro B.","year":"2012","unstructured":"Biscaro B, Lindvall O, Tesco G, Ekdahl CT, Nitsch RM. \n                    Inhibition of microglial activation protects hippocampal neurogenesis and improves cognitive deficits in a transgenic mouse model for Alzheimers disease. \n                    Neurodegener Dis  \n                    2012; \n                    9\n                    (4)\n                    : 187-98.","journal-title":"Neurodegener. 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