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Titolo:
Roles for lipoprotein lipase in Alzheimer's disease: An association study
Autore:
Baum, L; Wiebusch, H; Pang, CP;
Indirizzi:
Chinese Univ Hong Kong, Dept Ophthalmol & Visual Sci, Hong Kong, Hong Kong, Peoples R China Chinese Univ Hong Kong Hong Kong Hong Kong Peoples R China oples R China Nova Mol Inc, Montreal, PQ, Canada Nova Mol Inc Montreal PQ CanadaNova Mol Inc, Montreal, PQ, Canada
Titolo Testata:
MICROSCOPY RESEARCH AND TECHNIQUE
fascicolo: 4, volume: 50, anno: 2000,
pagine: 291 - 296
SICI:
1059-910X(20000815)50:4<291:RFLLIA>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
RECEPTOR-RELATED PROTEIN; FAMILIAL COMBINED HYPERLIPIDEMIA; MYOCARDIAL-INFARCTION SURVIVORS; FREQUENTLY OCCURRING MUTATION; APOLIPOPROTEIN-E GENOTYPE; CORONARY-ARTERY DISEASE; LATE-ONSET; GENETIC ASSOCIATION; HDL CHOLESTEROL; DEFICIENT MICE;
Keywords:
LPL; lipoprotein lipase; AD; Alzheimer's disease; dementia; hippocampus;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Pang, CP Chinese Univ Hong Kong, Hong Kong Eye Hosp, Dept Ophthalmol & Visual Sci, 3F,147K Argyle St, Hong Kong, Hong Kong, Peoples R China Chinese Univ Hong Kong 3F,147K Argyle St Hong Kong Hong Kong Peoples R China
Citazione:
L. Baum et al., "Roles for lipoprotein lipase in Alzheimer's disease: An association study", MICROSC RES, 50(4), 2000, pp. 291-296

Abstract

Lipoprotein lipase (LPL) assists lipid transport by transferring lipids between lipoprotein particles and cells. LPL binds apolipoprotein E (apoE) lipoprotein particles and a major apoE receptor, low density lipoprotein receptor related protein (LRP). Because apoE and LRP polymorphisms alter Alzheimer's disease (AD) risk, and LPL itself is found in AD amyloid plaques, we examined whether LPL variants also affect AD risk. In case-control studies in the United States and Canada, the frequencies of two LPL alleles known to affect LPL enzymatic activity were measured in Caucasian AD or elderly normal (N) subjects. Pathologically confirmed subjects in both studies exhibited similar trends toward fewer 447Ter and more 291Ser alleles in AD. Combining results from both countries gave allele frequencies for 447Ter of 13.7% (26/190) in N and 9.4% (80/852) in AD (P = 0.10), and for 291Ser of 0.0% (0/184) in N and 1.3% (8/636) in AD (P = 0.21). The trend appeared even greater for homozygous 447Ter subjects: 4.2% (4/95) of N vs. 1.4% (6/426) of AD (P = 0.09). These trends are consistent with a putative protective effectof 447Ter and causative effect of 291Ser on AD. Furthermore, brains of AD patients with 447Ter showed trends toward fewer plaques, tangles, and glia,and more neurons and cortical thickness than AD patients without 447Ter. Hippocampal plaques were significantly reduced. LPL might affect hippocampalfunction and thus dementia via its role as supplier of membrane componentsor antioxidants to neurons. Alternatively, LPL may play a part in plaque formation through its interaction with apoE and LRP. (C) 2000 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 17:53:55