speed factor in the ALIGATOR analysis using GO terms. Of the significant genes we identified in this pathway, several are particularly interesting due to their link with AD. The alpha 1 laminin isoform is over-expressed in AD frontal cortex and presents as punctate deposits in the senile plaques, and in the astrocytes of grey and white matter (Palu and Liesi, 2002), providing a basis for linking LAMA1 to the aetiology of AD. Type 4 collagen (COL4A1 is part of the gene family coding for this protein) has also been localised within the senile plaques as punctuate deposits (Kiuchi et al., 2002); and integrins (e.g., ITGA2 gene product) have been identified immunohistochemically in cerebal amyloid plaques (Eikelenboom et al., 1994), again suggesting that variation in these relevant genes might be important. By the same logic, reduced levels of protein kinase C alpha (e.g., PRKCA gene product) have been linked to an altered amyloid precursor protein secretion in fibroblasts from AD patients (Benussi et al., 1998). The only gene (of those we identified in the focal adhesion pathway) to be directly tested for association with AD is PIK3R1 (Liolitsa et al., 2002). Here, the Met326Tyr polymorphism showed association with risk of late-onset
