Polymorphisms of pro-inflammatory genes and Alzheimer's disease risk: a pharmacogenomic approach.
Clinically and pathologically Alzheimer's disease (AD) represents a sequential progressive neurodegenerative disorder. AD is etiologically heterogeneous and accounts for a majority of dementia in western societies. Inflammation clearly occurs in pathologically vulnerable regions of the AD brain and the search for genetic factors influencing the pathogenesis of AD has lead to the identification of numerous gene polymorphisms that might act as susceptibility modifiers. Accordingly, several reports have indicated that the risk of AD is substantially influenced by several genetic polymorphisms in the promoter region, or other untranslated regions, of genes encoding inflammatory mediators, although not all the studies were replied. Here, we review several data suggesting that inflammatory genetic variation may contribute to AD susceptibility. All together this information may represent the basis both for future recognition of individuals at risk and for the pharmacogenomic driving of drug responsiveness.
Candore
Giuseppina
G
Gruppo di Studio sull' Immunosenescenza, Dipartimento di Biopatologia e Metodologie Biomediche, Università di Palermo, Corso Tukory 211, 90134 Palermo, Italy. gcandore@unipa.it
Balistreri
Carmela Rita
CR
Grimaldi
Maria Paola
MP
Listì
Florinda
F
Vasto
Sonya
S
Chiappelli
Martina
M
Licastro
Federico
F
Colonna-Romano
Giuseppina
G
Lio
Domenico
D
Caruso
Calogero
C
D000544:Alzheimer Disease / Q000235:genetics* / Q000473:pathology; D000818:Animals; D016678:Genome; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology*; D010597:Pharmacogenetics; D011110:Polymorphism, Genetic; D012306:Risk
D018836:Inflammation Mediators