Association between 5-HT(2A) receptor polymorphism and psychotic symptoms in Alzheimer's disease
The aim of this study is to analyze the segregation of the 102T/C polymorphism in the serotonin 2A receptor gene in patients affected by sporadic and familial Alzheimer's disease (FAD) with and without psychotic symptoms. The polymorphism was analyzed in 275 subjects. A semistructured interview...
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| Veröffentlicht in: | Biological psychiatry (1969) 2001-09, Vol.50 (6), p.472-475 |
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| container_issue | 6 |
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| container_title | Biological psychiatry (1969) |
| container_volume | 50 |
| creator | Nacmias, B Tedde, A Forleo, P Piacentini, S Guarnieri, B M Bartoli, A Ortenzi, L Petruzzi, C Serio, A Marcon, G Sorbi, S |
| description | The aim of this study is to analyze the segregation of the 102T/C polymorphism in the serotonin 2A receptor gene in patients affected by sporadic and familial Alzheimer's disease (FAD) with and without psychotic symptoms.
The polymorphism was analyzed in 275 subjects. A semistructured interview was used to obtain information about delusions, hallucinations, and other specific behavioral signs occurring during the disease.
Fifty-two percent of AD patients with psychotic symptoms were homozygous for the C102 allele, as compared with 6.9% of AD patients without psychosis. Similarly, the C102/C102 genotype was significantly more frequent in FAD patients with psychosis than in FAD patients without (46.5% vs. 7.8%).
Our data strongly confirm and extend to FAD previous studies suggesting that the genetic variation at this locus is associated with prominent psychotic features in AD and that the 102C allele could play an important role in late-onset AD. |
| format | Article |
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The polymorphism was analyzed in 275 subjects. A semistructured interview was used to obtain information about delusions, hallucinations, and other specific behavioral signs occurring during the disease.
Fifty-two percent of AD patients with psychotic symptoms were homozygous for the C102 allele, as compared with 6.9% of AD patients without psychosis. Similarly, the C102/C102 genotype was significantly more frequent in FAD patients with psychosis than in FAD patients without (46.5% vs. 7.8%).
Our data strongly confirm and extend to FAD previous studies suggesting that the genetic variation at this locus is associated with prominent psychotic features in AD and that the 102C allele could play an important role in late-onset AD.</description><identifier>ISSN: 0006-3223</identifier><identifier>PMID: 11566166</identifier><language>eng</language><publisher>United States</publisher><subject>Aged ; Alzheimer Disease - genetics ; Alzheimer Disease - psychology ; Apolipoproteins E - genetics ; Female ; Gene Amplification ; Gene Expression - genetics ; Gene Frequency ; Genotype ; Homozygote ; Humans ; Male ; Point Mutation - genetics ; Polymorphism, Genetic - genetics ; Psychotic Disorders - etiology ; Psychotic Disorders - genetics ; Psychotic Disorders - metabolism ; Receptors, Serotonin - genetics ; Receptors, Serotonin - metabolism</subject><ispartof>Biological psychiatry (1969), 2001-09, Vol.50 (6), p.472-475</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11566166$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nacmias, B</creatorcontrib><creatorcontrib>Tedde, A</creatorcontrib><creatorcontrib>Forleo, P</creatorcontrib><creatorcontrib>Piacentini, S</creatorcontrib><creatorcontrib>Guarnieri, B M</creatorcontrib><creatorcontrib>Bartoli, A</creatorcontrib><creatorcontrib>Ortenzi, L</creatorcontrib><creatorcontrib>Petruzzi, C</creatorcontrib><creatorcontrib>Serio, A</creatorcontrib><creatorcontrib>Marcon, G</creatorcontrib><creatorcontrib>Sorbi, S</creatorcontrib><title>Association between 5-HT(2A) receptor polymorphism and psychotic symptoms in Alzheimer's disease</title><title>Biological psychiatry (1969)</title><addtitle>Biol Psychiatry</addtitle><description>The aim of this study is to analyze the segregation of the 102T/C polymorphism in the serotonin 2A receptor gene in patients affected by sporadic and familial Alzheimer's disease (FAD) with and without psychotic symptoms.
The polymorphism was analyzed in 275 subjects. A semistructured interview was used to obtain information about delusions, hallucinations, and other specific behavioral signs occurring during the disease.
Fifty-two percent of AD patients with psychotic symptoms were homozygous for the C102 allele, as compared with 6.9% of AD patients without psychosis. Similarly, the C102/C102 genotype was significantly more frequent in FAD patients with psychosis than in FAD patients without (46.5% vs. 7.8%).
Our data strongly confirm and extend to FAD previous studies suggesting that the genetic variation at this locus is associated with prominent psychotic features in AD and that the 102C allele could play an important role in late-onset AD.</description><subject>Aged</subject><subject>Alzheimer Disease - genetics</subject><subject>Alzheimer Disease - psychology</subject><subject>Apolipoproteins E - genetics</subject><subject>Female</subject><subject>Gene Amplification</subject><subject>Gene Expression - genetics</subject><subject>Gene Frequency</subject><subject>Genotype</subject><subject>Homozygote</subject><subject>Humans</subject><subject>Male</subject><subject>Point Mutation - genetics</subject><subject>Polymorphism, Genetic - genetics</subject><subject>Psychotic Disorders - etiology</subject><subject>Psychotic Disorders - genetics</subject><subject>Psychotic Disorders - metabolism</subject><subject>Receptors, Serotonin - genetics</subject><subject>Receptors, Serotonin - metabolism</subject><issn>0006-3223</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo10M1LwzAYBvAcFDen_4Lk5Meh0Hw0bY5lqBMGXnavafKORZom5u2Q-tc7cJ4eHvjxHJ4LsizLUhWCc7Eg14ifp1pzzq7IgrFKKabUkny0iNF6M_k40h6mb4CRVsVm98jbJ5rBQppipikOc4g5HTwGakZHE872ECdvKc7hRAJSP9J2-DmAD5AfkDqPYBBuyOXeDAi351yR3cvzbr0ptu-vb-t2W6RKqqJmpuFGNKBLZ4XUqq9ULet-r2TZMCd7LlnPuXPaAFeNlXvjDONGM60rAUasyP3fbMrx6wg4dcGjhWEwI8QjdjVjjRaSn-DdGR77AK5L2QeT5-7_EvELalRcZA</recordid><startdate>20010915</startdate><enddate>20010915</enddate><creator>Nacmias, B</creator><creator>Tedde, A</creator><creator>Forleo, P</creator><creator>Piacentini, S</creator><creator>Guarnieri, B M</creator><creator>Bartoli, A</creator><creator>Ortenzi, L</creator><creator>Petruzzi, C</creator><creator>Serio, A</creator><creator>Marcon, G</creator><creator>Sorbi, S</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20010915</creationdate><title>Association between 5-HT(2A) receptor polymorphism and psychotic symptoms in Alzheimer's disease</title><author>Nacmias, B ; Tedde, A ; Forleo, P ; Piacentini, S ; Guarnieri, B M ; Bartoli, A ; Ortenzi, L ; Petruzzi, C ; Serio, A ; Marcon, G ; Sorbi, S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p546-71a82a38e90dc3496b56747bf64081d4b241b22dd9ae268c4fada12a919953ea3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Aged</topic><topic>Alzheimer Disease - genetics</topic><topic>Alzheimer Disease - psychology</topic><topic>Apolipoproteins E - genetics</topic><topic>Female</topic><topic>Gene Amplification</topic><topic>Gene Expression - genetics</topic><topic>Gene Frequency</topic><topic>Genotype</topic><topic>Homozygote</topic><topic>Humans</topic><topic>Male</topic><topic>Point Mutation - genetics</topic><topic>Polymorphism, Genetic - genetics</topic><topic>Psychotic Disorders - etiology</topic><topic>Psychotic Disorders - genetics</topic><topic>Psychotic Disorders - metabolism</topic><topic>Receptors, Serotonin - genetics</topic><topic>Receptors, Serotonin - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nacmias, B</creatorcontrib><creatorcontrib>Tedde, A</creatorcontrib><creatorcontrib>Forleo, P</creatorcontrib><creatorcontrib>Piacentini, S</creatorcontrib><creatorcontrib>Guarnieri, B M</creatorcontrib><creatorcontrib>Bartoli, A</creatorcontrib><creatorcontrib>Ortenzi, L</creatorcontrib><creatorcontrib>Petruzzi, C</creatorcontrib><creatorcontrib>Serio, A</creatorcontrib><creatorcontrib>Marcon, G</creatorcontrib><creatorcontrib>Sorbi, S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Biological psychiatry (1969)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nacmias, B</au><au>Tedde, A</au><au>Forleo, P</au><au>Piacentini, S</au><au>Guarnieri, B M</au><au>Bartoli, A</au><au>Ortenzi, L</au><au>Petruzzi, C</au><au>Serio, A</au><au>Marcon, G</au><au>Sorbi, S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association between 5-HT(2A) receptor polymorphism and psychotic symptoms in Alzheimer's disease</atitle><jtitle>Biological psychiatry (1969)</jtitle><addtitle>Biol Psychiatry</addtitle><date>2001-09-15</date><risdate>2001</risdate><volume>50</volume><issue>6</issue><spage>472</spage><epage>475</epage><pages>472-475</pages><issn>0006-3223</issn><abstract>The aim of this study is to analyze the segregation of the 102T/C polymorphism in the serotonin 2A receptor gene in patients affected by sporadic and familial Alzheimer's disease (FAD) with and without psychotic symptoms.
The polymorphism was analyzed in 275 subjects. A semistructured interview was used to obtain information about delusions, hallucinations, and other specific behavioral signs occurring during the disease.
Fifty-two percent of AD patients with psychotic symptoms were homozygous for the C102 allele, as compared with 6.9% of AD patients without psychosis. Similarly, the C102/C102 genotype was significantly more frequent in FAD patients with psychosis than in FAD patients without (46.5% vs. 7.8%).
Our data strongly confirm and extend to FAD previous studies suggesting that the genetic variation at this locus is associated with prominent psychotic features in AD and that the 102C allele could play an important role in late-onset AD.</abstract><cop>United States</cop><pmid>11566166</pmid><tpages>4</tpages></addata></record> |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Aged Alzheimer Disease - genetics Alzheimer Disease - psychology Apolipoproteins E - genetics Female Gene Amplification Gene Expression - genetics Gene Frequency Genotype Homozygote Humans Male Point Mutation - genetics Polymorphism, Genetic - genetics Psychotic Disorders - etiology Psychotic Disorders - genetics Psychotic Disorders - metabolism Receptors, Serotonin - genetics Receptors, Serotonin - metabolism |
| title | Association between 5-HT(2A) receptor polymorphism and psychotic symptoms in Alzheimer's disease |
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