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Article ; Online: Alzheimer's disease genetics: current knowledge and future challenges.

Hollingworth, Paul / Harold, Denise / Jones, Lesley / Owen, Michael J / Williams, Julie

International journal of geriatric psychiatry

2010 Volume 26, Issue 8, Page(s) 793–802

Abstract: Alzheimer's disease (AD) is highly heritable, but genetically complex. Recently, three large-scale genome-wide association studies have made substantial breakthroughs in disentangling the genetic architecture of the disease. These studies combined ... ...

Abstract	Alzheimer's disease (AD) is highly heritable, but genetically complex. Recently, three large-scale genome-wide association studies have made substantial breakthroughs in disentangling the genetic architecture of the disease. These studies combined include data from over 43 000 independent individuals and provide compelling evidence that variants in four novel susceptibility genes (CLU, PICALM, CR1, BIN1) are associated with disease risk. These findings are tremendously exciting, not only in providing new avenues for exploration, but also highlighting the potential for further gene discovery when larger samples are analysed. Here we discuss progress to date in identifying risk genes for dementia, ways forward and how current findings are refining previous ideas and defining new putative primary disease mechanisms.
MeSH term(s)	Alzheimer Disease/genetics ; Genetic Markers/genetics ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans
Chemical Substances	Genetic Markers
Language	English
Publishing date	2010-10-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	806736-3
ISSN	1099-1166 ; 0885-6230
ISSN (online)	1099-1166
ISSN	0885-6230
DOI	10.1002/gps.2628
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Article ; Online: An association study of common variation at the MAPT locus with late-onset Alzheimer's disease.

Abraham, Richard / Sims, Rebecca / Carroll, Liam / Hollingworth, Paul / O'Donovan, Michael C / Williams, Julie / Owen, Michael J

American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics

2009 Volume 150B, Issue 8, Page(s) 1152–1155

Abstract: The MAPT gene that encodes Tau is located on chromosome 17q21, in a region, which has evolved to form two major haplotypes, H1 and H2. There is strong evidence that the H1 haplotype, and a sub-haplotype (H1C), are overrepresented and associated with ... ...

Abstract	The MAPT gene that encodes Tau is located on chromosome 17q21, in a region, which has evolved to form two major haplotypes, H1 and H2. There is strong evidence that the H1 haplotype, and a sub-haplotype (H1C), are overrepresented and associated with increased risk for the sporadic tauopathies, progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD). Both PSP and CBD cases display Tau pathology similar to Late-Onset Alzheimer's Disease (LOAD). However, numerous association studies investigating the genetic involvement of MAPT in LOAD have generated conflicting results. Here we have used a large LOAD case-control sample to genotype SNPs that have been shown to define H1/H2 status and intra-H1 variability. Single marker association analyses found no evidence that any of the SNPs are associated with risk of LOAD. When gender and APOE4 status were taken into account we observed suggestive association for SNP rs242557 (P = 0.02). Stratification of the sample revealed association with rs242557 only in APOE4 positive individuals (P = 0.01 recessive model), however this result would not survive multiple correction. There was no significant difference in H1/H2 haplotype distribution between cases and controls. We also tested the association of specific sub-haplotypes on the H1 background and likewise results were negative. No effect was observed on disease age of onset for any of the markers studied. In summary, we find no evidence for allelic or haplotypic association, with SNPs in the MAPT gene and LOAD. SNP rs242557 is nominally significant in the APOE4 positive individuals. None of the SNPs studied modified AAO for LOAD.
MeSH term(s)	Age of Onset ; Aged ; Aged, 80 and over ; Alzheimer Disease/epidemiology ; Alzheimer Disease/genetics ; Case-Control Studies ; Female ; Genetic Association Studies/methods ; Genetic Variation ; Genotype ; Haplotypes ; Humans ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Sex Factors ; tau Proteins/genetics
Chemical Substances	MAPT protein, human ; tau Proteins
Language	English
Publishing date	2009-03-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2108616-3
ISSN	1552-485X ; 1552-4841 ; 0148-7299
ISSN (online)	1552-485X
ISSN	1552-4841 ; 0148-7299
DOI	10.1002/ajmg.b.30951
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Article ; Online: A genome-wide study shows a limited contribution of rare copy number variants to Alzheimer's disease risk.

Chapman, Jade / Rees, Elliott / Harold, Denise / Ivanov, Dobril / Gerrish, Amy / Sims, Rebecca / Hollingworth, Paul / Stretton, Alexandra / Holmans, Peter / Owen, Michael J / O'Donovan, Michael C / Williams, Julie / Kirov, George

Human molecular genetics

2012 Volume 22, Issue 4, Page(s) 816–824

Abstract: We assessed the role of rare copy number variants (CNVs) in Alzheimer's disease (AD) using intensity data from 3260 AD cases and 1290 age-matched controls from the genome-wide association study (GWAS) conducted by the Genetic and Environmental Risk for ... ...

Abstract	We assessed the role of rare copy number variants (CNVs) in Alzheimer's disease (AD) using intensity data from 3260 AD cases and 1290 age-matched controls from the genome-wide association study (GWAS) conducted by the Genetic and Environmental Risk for Alzheimer's disease Consortium (GERAD). We did not observe a significant excess of rare CNVs in cases, although we did identify duplications overlapping APP and CR1 which may be pathogenic. We looked for an excess of CNVs in loci which have been highlighted in previous AD CNV studies, but did not replicate previous findings. Through pathway analyses, we observed suggestive evidence for biological overlap between single nucleotide polymorphisms and CNVs in AD susceptibility. We also identified that our sample of elderly controls harbours significantly fewer deletions >1 Mb than younger control sets in previous CNV studies on schizophrenia and bipolar disorder (P = 8.9 × 10(-4) and 0.024, respectively), raising the possibility that healthy elderly individuals have a reduced rate of large deletions. Thus, in contrast to diseases such as schizophrenia, autism and attention deficit/hyperactivity disorder, CNVs do not appear to make a significant contribution to the development of AD.
MeSH term(s)	Aged ; Alzheimer Disease/genetics ; Amyloid beta-Protein Precursor/genetics ; Case-Control Studies ; DNA Copy Number Variations ; Gene Duplication ; Genetic Loci ; Genetic Predisposition to Disease ; Genome, Human ; Genome-Wide Association Study ; Genotype ; Humans ; Polymorphism, Single Nucleotide ; Receptors, Complement 3b/genetics ; Risk Factors
Chemical Substances	Amyloid beta-Protein Precursor ; CR1 protein, human ; Receptors, Complement 3b
Language	English
Publishing date	2012-11-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/dds476
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Article: Diagnosing Alzheimer's disease--non-clinicians and computerised algorithms together are as accurate as the best clinical practice.

Foy, Catherine M L / Nicholas, Helen / Hollingworth, Paul / Boothby, Harry / Willams, Julie / Brown, Richard G / Al-Sarraj, Safa / Lovestone, Simon

International journal of geriatric psychiatry

2007 Volume 22, Issue 11, Page(s) 1154–1163

Abstract: Background: An accurate diagnosis of Alzheimer's disease and an exclusion of other dementias is important in many clinical studies. Obtaining such a clinical diagnosis in epidemiological studies and clinical trials that recruit large numbers of patients ...

Abstract	Background: An accurate diagnosis of Alzheimer's disease and an exclusion of other dementias is important in many clinical studies. Obtaining such a clinical diagnosis in epidemiological studies and clinical trials that recruit large numbers of patients is time consuming. Objectives: To construct an algorithm using a limited number of data points to generate a diagnosis of the commonest forms of dementia using information collected by non clinicians. Methods: We constructed a computer algorithm to generate a diagnosis of Alzheimer's disease (AD), Dementia with Lewy Bodies (DLB), frontotemporal dementia (FTD), vascular dementia or to flag the case as needing a clinical review based on a limited number of data points taken from a largely structured interview using widely used scales. The diagnosis generated in life by the algorithm in a prospective, longitudinal study was compared to definitive diagnosis at post mortem. Results: Post mortem diagnosis was available for 43 cases. The positive predictive value of the algorithm was greater than 95%. AD was diagnosed by the algorithm and at post mortem in 36 of the cases. Two cases with FTD were wrongly diagnosed as having AD by the algorithm, five cases were flagged as needing a clinical review due to concomitant medical conditions of whom four had AD and one, who had been diagnosed clinically as having AD, was diagnosed on post mortem with corticobasal degeneration. Conclusions: A combination of non-clinical researchers, a structured interview and a computerised algorithm is as effective at identifying AD as highly trained and skilled clinicians.
MeSH term(s)	Aged ; Algorithms ; Allied Health Personnel ; Alzheimer Disease/diagnosis ; Autopsy ; Decision Trees ; Dementia, Vascular/diagnosis ; Diagnosis, Computer-Assisted/methods ; Disease Progression ; Humans ; Interview, Psychological ; Lewy Body Disease/diagnosis ; Longitudinal Studies ; Prospective Studies
Language	English
Publishing date	2007-05-26
Publishing country	England
Document type	Evaluation Study ; Journal Article ; Multicenter Study ; Research Support, Non-U.S. Gov't
ZDB-ID	806736-3
ISSN	1099-1166 ; 0885-6230
ISSN (online)	1099-1166
ISSN	0885-6230
DOI	10.1002/gps.1810
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Article ; Online: A genome-wide association study for late-onset Alzheimer's disease using DNA pooling

Hillmer Axel M / Cichon Sven / Dowzell Kimberley / Georgieva Lyudmila / Morgan Angharad / Hollingworth Paul / Sims Rebecca / Moskvina Valentina / Abraham Richard / O'Donovan Michael C / Williams Julie / Owen Michael J / Kirov George

BMC Medical Genomics, Vol 1, Iss 1, p

2008 Volume 44

Abstract: Abstract Background Late-onset Alzheimer's disease (LOAD) is an age related neurodegenerative disease with a high prevalence that places major demands on healthcare resources in societies with increasingly aged populations. The only extensively ... ...

Abstract	Abstract Background Late-onset Alzheimer's disease (LOAD) is an age related neurodegenerative disease with a high prevalence that places major demands on healthcare resources in societies with increasingly aged populations. The only extensively replicable genetic risk factor for LOAD is the apolipoprotein E gene. In order to identify additional genetic risk loci we have conducted a genome-wide association (GWA) study in a large LOAD case – control sample, reducing costs through the use of DNA pooling. Methods DNA samples were collected from 1,082 individuals with LOAD and 1,239 control subjects. Age at onset ranged from 60 to 95 and Controls were matched for age (mean = 76.53 years, SD = 33), gender and ethnicity. Equimolar amounts of each DNA sample were added to either a case or control pool. The pools were genotyped using Illumina HumanHap300 and Illumina Sentrix HumanHap240S arrays testing 561,494 SNPs. 114 of our best hit SNPs from the pooling data were identified and then individually genotyped in the case – control sample used to construct the pools. Results Highly significant association with LOAD was observed at the APOE locus confirming the validity of the pooled genotyping approach. For 109 SNPs outside the APOE locus, we obtained uncorrected p-values ≤ 0.05 for 74 after individual genotyping. To further test these associations, we added control data from 1400 subjects from the 1958 Birth Cohort with the evidence for association increasing to 3.4 × 10 -6 for our strongest finding, rs727153. rs727153 lies 13 kb from the start of transcription of lecithin retinol acyltransferase (phosphatidylcholine – retinol O-acyltransferase, LRAT ). Five of seven tag SNPs chosen to cover LRAT showed significant association with LOAD with a SNP in intron 2 of LRAT , showing greatest evidence of association (rs201825, p-value = 6.1 × 10 -7 ). Conclusion We have validated the pooling method for GWA studies by both identifying the APOE locus and by observing a strong enrichment for significantly associated SNPs. We ...
Keywords	Internal medicine ; RC31-1245 ; Genetics ; QH426-470
Subject code	616
Language	English
Publishing date	2008-09-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
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Article ; Online: Deep sequencing of the Nicastrin gene in pooled DNA, the identification of genetic variants that affect risk of Alzheimer's disease.

Lupton, Michelle K / Proitsi, Petroula / Danillidou, Makrina / Tsolaki, Magda / Hamilton, Gillian / Wroe, Richard / Pritchard, Megan / Lord, Kathryn / Martin, Belinda M / Kloszewska, Iwona / Soininen, Hilkka / Mecocci, Patrizia / Vellas, Bruno / Harold, Denise / Hollingworth, Paul / Lovestone, Simon / Powell, John F

PloS one

2011 Volume 6, Issue 2, Page(s) e17298

Abstract: Nicastrin is an obligatory component of the γ-secretase; the enzyme complex that leads to the production of Aβ fragments critically central to the pathogenesis of Alzheimer's disease (AD). Analyses of the effects of common variation in this gene on risk ... ...

Abstract	Nicastrin is an obligatory component of the γ-secretase; the enzyme complex that leads to the production of Aβ fragments critically central to the pathogenesis of Alzheimer's disease (AD). Analyses of the effects of common variation in this gene on risk for late onset AD have been inconclusive. We investigated the effect of rare variation in the coding regions of the Nicastrin gene in a cohort of AD patients and matched controls using an innovative pooling approach and next generation sequencing. Five SNPs were identified and validated by individual genotyping from 311 cases and 360 controls. Association analysis identified a non-synonymous rare SNP (N417Y) with a statistically higher frequency in cases compared to controls in the Greek population (OR 3.994, CI 1.105-14.439, p = 0.035). This finding warrants further investigation in a larger cohort and adds weight to the hypothesis that rare variation explains some of genetic heritability still to be identified in Alzheimer's disease.
MeSH term(s)	Aged ; Aged, 80 and over ; Alzheimer Disease/genetics ; Amyloid Precursor Protein Secretases/genetics ; Case-Control Studies ; DNA/analysis ; Gene Frequency ; Genetic Predisposition to Disease ; Genetic Variation/physiology ; High-Throughput Nucleotide Sequencing/methods ; Humans ; Membrane Glycoproteins/genetics ; Meta-Analysis as Topic ; Middle Aged ; Polymorphism, Single Nucleotide/physiology ; Risk Factors ; Specimen Handling/methods ; Validation Studies as Topic
Chemical Substances	Membrane Glycoproteins ; nicastrin protein ; DNA (9007-49-2) ; Amyloid Precursor Protein Secretases (EC 3.4.-)
Language	English
Publishing date	2011-02-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0017298
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Article ; Online: A genome-wide association study for late-onset Alzheimer's disease using DNA pooling.

Abraham, Richard / Moskvina, Valentina / Sims, Rebecca / Hollingworth, Paul / Morgan, Angharad / Georgieva, Lyudmila / Dowzell, Kimberley / Cichon, Sven / Hillmer, Axel M / O'Donovan, Michael C / Williams, Julie / Owen, Michael J / Kirov, George

BMC medical genomics

2008 Volume 1, Page(s) 44

Abstract: Background: Late-onset Alzheimer's disease (LOAD) is an age related neurodegenerative disease with a high prevalence that places major demands on healthcare resources in societies with increasingly aged populations. The only extensively replicable ... ...

Abstract	Background: Late-onset Alzheimer's disease (LOAD) is an age related neurodegenerative disease with a high prevalence that places major demands on healthcare resources in societies with increasingly aged populations. The only extensively replicable genetic risk factor for LOAD is the apolipoprotein E gene. In order to identify additional genetic risk loci we have conducted a genome-wide association (GWA) study in a large LOAD case - control sample, reducing costs through the use of DNA pooling. Methods: DNA samples were collected from 1,082 individuals with LOAD and 1,239 control subjects. Age at onset ranged from 60 to 95 and Controls were matched for age (mean = 76.53 years, SD = 33), gender and ethnicity. Equimolar amounts of each DNA sample were added to either a case or control pool. The pools were genotyped using Illumina HumanHap300 and Illumina Sentrix HumanHap240S arrays testing 561,494 SNPs. 114 of our best hit SNPs from the pooling data were identified and then individually genotyped in the case - control sample used to construct the pools. Results: Highly significant association with LOAD was observed at the APOE locus confirming the validity of the pooled genotyping approach.For 109 SNPs outside the APOE locus, we obtained uncorrected p-values </= 0.05 for 74 after individual genotyping. To further test these associations, we added control data from 1400 subjects from the 1958 Birth Cohort with the evidence for association increasing to 3.4 x 10-6 for our strongest finding, rs727153.rs727153 lies 13 kb from the start of transcription of lecithin retinol acyltransferase (phosphatidylcholine - retinol O-acyltransferase, LRAT). Five of seven tag SNPs chosen to cover LRAT showed significant association with LOAD with a SNP in intron 2 of LRAT, showing greatest evidence of association (rs201825, p-value = 6.1 x 10-7).<br />Conclusion: We have validated the pooling method for GWA studies by both identifying the APOE locus and by observing a strong enrichment for significantly associated SNPs. We provide evidence for LRAT as a novel candidate gene for LOAD. LRAT plays a prominent role in the Vitamin A cascade, a system that has been previously implicated in LOAD.
Language	English
Publishing date	2008-09-29
Publishing country	England
Document type	Journal Article
ZDB-ID	2411865-5
ISSN	1755-8794 ; 1755-8794
ISSN (online)	1755-8794
ISSN	1755-8794
DOI	10.1186/1755-8794-1-44
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Article ; Online: Association of serotonin and dopamine gene pathways with behavioral subphenotypes in dementia.

Proitsi, Petroula / Lupton, Michelle K / Reeves, Suzanne J / Hamilton, Gillian / Archer, Nicola / Martin, Belinda M / Iyegbe, Conrad / Hollingworth, Paul / Lawlor, Brian / Gill, Michael / Brayne, Carol / Rubinsztein, David C / Owen, Michael J / Williams, Julie / Lovestone, Simon / Powell, John F

Neurobiology of aging

2010 Volume 33, Issue 4, Page(s) 791–803

Abstract: Genetic association studies investigating the association between genes of serotonergic and dopaminergic systems and behavioral and psychological symptoms in dementia (BPSD) are contradictory. We have utilized 1008 probable Alzheimer's disease (AD) ... ...

Abstract	Genetic association studies investigating the association between genes of serotonergic and dopaminergic systems and behavioral and psychological symptoms in dementia (BPSD) are contradictory. We have utilized 1008 probable Alzheimer's disease (AD) patients from the UK and used the 12-item Neuropsychiatric Inventory. We applied a multiple indicators-multiple causes (MIMIC) approach to investigate the effect of 11 polymorphisms on the 4 behavioral subphenotypes "psychosis", "moods", "agitation", and "behavioural dyscontrol". Significant associations were observed between the serotonin transporter gene (SERT) polymorphism STin2 and "psychosis"; the dopamine transporter gene (DAT) 3' variable number tandem repeats (VNTR) and "agitation"; and the dopamine receptor 4 (DRD4) VNTR and "moods" factors. Direct associations were identified between the dopamine receptor 3 (DRD3) BalI polymorphism and depression; the dopamine receptor 1 (DRD1) and dopamine transporter gene 3' VNTR polymorphisms and aberrant motor behavior; the DRD4 VNTR and sleep disturbances; and the SERT gene VNTR 5HTTLPR and apathy items. Significant interactions observed between polymorphisms suggested epistatic effects and interactions between polymorphisms and medications highlighted potential treatment response. This multiple indicators multiple causes (MIMIC) model efficiently captured the complexity of the interrelations between genetic variation, behavioral symptoms, and clinical variables.
MeSH term(s)	Aged ; Aged, 80 and over ; Apolipoprotein E4/genetics ; Behavioral Symptoms/etiology ; Behavioral Symptoms/genetics ; Catechol O-Methyltransferase/genetics ; Chi-Square Distribution ; Cohort Studies ; DNA Mutational Analysis ; Dementia/complications ; Dementia/genetics ; Dementia/psychology ; Dopamine/genetics ; Dopamine Plasma Membrane Transport Proteins ; Female ; Genetic Association Studies ; Genetic Predisposition to Disease/genetics ; Genotype ; Humans ; Male ; Middle Aged ; Minisatellite Repeats/genetics ; Models, Biological ; Monoamine Oxidase/genetics ; Polymorphism, Genetic/genetics ; Psychiatric Status Rating Scales ; Receptors, Dopamine ; Risk Factors ; Serotonin/genetics ; Serotonin Plasma Membrane Transport Proteins ; Signal Transduction/genetics ; United Kingdom
Chemical Substances	Apolipoprotein E4 ; Dopamine Plasma Membrane Transport Proteins ; Receptors, Dopamine ; Serotonin Plasma Membrane Transport Proteins ; Serotonin (333DO1RDJY) ; Monoamine Oxidase (EC 1.4.3.4) ; Catechol O-Methyltransferase (EC 2.1.1.6) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2010-08-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604505-4
ISSN	1558-1497 ; 0197-4580
ISSN (online)	1558-1497
ISSN	0197-4580
DOI	10.1016/j.neurobiolaging.2010.06.011
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Article ; Online: Education, occupation and retirement age effects on the age of onset of Alzheimer's disease.

Lupton, Michelle K / Stahl, Daniel / Archer, Nicola / Foy, Catherine / Poppe, Michaela / Lovestone, Simon / Hollingworth, Paul / Williams, Julie / Owen, Micheal J / Dowzell, Kimberley / Abraham, Richard / Sims, Rebecca / Brayne, Carol / Rubinsztein, David / Gill, Michael / Lawlor, Brian / Lynch, Aoibhinn / Powell, John F

International journal of geriatric psychiatry

2009 Volume 25, Issue 1, Page(s) 30–36

Abstract: Objective: To determine the effects of early life education, mid life employment and later life retirement age on the age of onset (AOO) of Alzheimer's disease (AD).: Methods: Multiple regression analyses were carried out using data for 1320 probable ...

Abstract	Objective: To determine the effects of early life education, mid life employment and later life retirement age on the age of onset (AOO) of Alzheimer's disease (AD). Methods: Multiple regression analyses were carried out using data for 1320 probable AD cases, of which 382 were males with employment and retirement age data, using informant based information on education and employment. Results: No relation was found between years of education, best qualification obtained, or employment variables in males and the AOO of AD. A significant effect of later retirement age in delaying the AOO of AD was seen in males. Conclusions: In this study no effect of education or employment was seen, although this may be due to limited variance in the study population. The significant effect of retirement age may have several explanations, the most interesting of which would be the suggestion that active employment later in life allows an individual to prolong their cognitive assets above the threshold for dementia.
MeSH term(s)	Age Factors ; Age of Onset ; Aged ; Aged, 80 and over ; Alzheimer Disease/epidemiology ; Alzheimer Disease/etiology ; Alzheimer Disease/psychology ; Cohort Studies ; Educational Status ; Employment ; Female ; Humans ; Male ; Middle Aged ; Regression Analysis ; Retirement ; Risk Factors
Language	English
Publishing date	2009-05-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	806736-3
ISSN	1099-1166 ; 0885-6230
ISSN (online)	1099-1166
ISSN	0885-6230
DOI	10.1002/gps.2294
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Article: Four components describe behavioral symptoms in 1,120 individuals with late-onset Alzheimer's disease.

Hollingworth, Paul / Hamshere, Marian L / Moskvina, Valentina / Dowzell, Kimberley / Moore, Pamela J / Foy, Catherine / Archer, Nicola / Lynch, Aoibhinn / Lovestone, Simon / Brayne, Carol / Rubinsztein, David C / Lawlor, Brian / Gill, Mike / Owen, Michael J / Williams, Julie

Journal of the American Geriatrics Society

2006 Volume 54, Issue 9, Page(s) 1348–1354

Abstract: Objectives: To investigate behavioral components of Alzheimer's disease (AD) and to analyze behavioral components in relation to disease severity, apolipoprotein E genotype (APOE), sex, years of education, age at onset, and cognitive impairment.: ... ...

Abstract	Objectives: To investigate behavioral components of Alzheimer's disease (AD) and to analyze behavioral components in relation to disease severity, apolipoprotein E genotype (APOE), sex, years of education, age at onset, and cognitive impairment. Design: Cross-sectional study. Setting: Data were collected from community-dwelling individuals and those residing in nursing homes. Participants: A total of 1,120 individuals meeting National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer's Disease and Related Disorders Association criteria for late-onset probable AD. Measurements: Behavioral symptoms were assessed using the Neuropsychiatric Inventory. First-order polychoric correlations, controlling for disease severity, between the 12 symptom domain scores were estimated, and the resulting matrix underwent principal components analysis. Results: Four interpretable components were identified: behavioral dyscontrol (euphoria, disinhibition, aberrant motor behavior, and sleep and appetite disturbances), psychosis (delusions and hallucinations), mood (depression, anxiety, and apathy), and agitation (aggression and irritability). Scores on the four components were associated with severity of cognitive impairment. Higher behavioral dysfunction, agitation, and mood component scores were associated with lower age at onset. Behavioral dysfunction and mood component scores were associated with sex. None of the components were associated with age at assessment, years of education, or number of APOE epsilon4 alleles. Conclusion: Four behavioral components were identified that were comparable with those observed previously. Future analysis of these components will strengthen understanding of the underlying pathology of behavioral symptoms and AD.
MeSH term(s)	Age of Onset ; Aged ; Aged, 80 and over ; Alzheimer Disease/epidemiology ; Alzheimer Disease/genetics ; Alzheimer Disease/psychology ; Apolipoproteins E/genetics ; Behavioral Symptoms/diagnosis ; Behavioral Symptoms/etiology ; Cognition Disorders/etiology ; Cross-Sectional Studies ; Educational Status ; Female ; Genotype ; Humans ; Male ; Middle Aged ; Neuropsychological Tests ; Severity of Illness Index ; Sex Factors
Chemical Substances	Apolipoproteins E
Language	English
Publishing date	2006-09-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80363-7
ISSN	1532-5415 ; 0002-8614
ISSN (online)	1532-5415
ISSN	0002-8614
DOI	10.1111/j.1532-5415.2006.00854.x
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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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