TY - JOUR
T1 - Apolipoprotein e genotype in patients with focal cerebral atrophy
AU - Filippini, V.
AU - Daniele, A.
AU - Masuüo, C.
AU - Silveri, M. C.
AU - Seripa, D.
AU - Fazio, V.
AU - Gainotti, G.
PY - 1997
Y1 - 1997
N2 - While the distribution of Apolipoprotein E (ApoE) alleles in Alzheimer's Disease (AD) has been extensively investigated, the ApoE allele frequency in neurodegenerative disorders associated with focal cerebral atrophy (FCA) needs further investigatipn. ApoE genotype was determined in 9 patients with neurodegenerative syndromes with FCA (Pick's disease, primary progressive aphasia, progressive amnesia without dementia). Genomic DNA was extracted from blcod and amplified by a modified one-stage PCR, using primers that amplify 227 bp in ApoE exon 4, followed by Hhal or Tagf restriction enzyme digesticns, gel electrophoresis fractionation, and DNA staining. As compared with normal controls, in the FCA group, there was a three-fold increase of ET allele frequency (E-> = 0.17; £3 = 0.72; £4 = 0.11). These preliminary findings seem to be at variance with the results of a previous investigation showing that in patients with lobar atrophy the frequency of £3, £3, £4 does not differ from normal controls (Piclfering-Brown et al., Neuroscience Letters 188, 205, 1995). Our pilot study on a small series of patients with FCA may suggest differential patterns of ApoE allelic distribution in neurodegenerative disorders associated with FCA, as compared with sporadic AD.
AB - While the distribution of Apolipoprotein E (ApoE) alleles in Alzheimer's Disease (AD) has been extensively investigated, the ApoE allele frequency in neurodegenerative disorders associated with focal cerebral atrophy (FCA) needs further investigatipn. ApoE genotype was determined in 9 patients with neurodegenerative syndromes with FCA (Pick's disease, primary progressive aphasia, progressive amnesia without dementia). Genomic DNA was extracted from blcod and amplified by a modified one-stage PCR, using primers that amplify 227 bp in ApoE exon 4, followed by Hhal or Tagf restriction enzyme digesticns, gel electrophoresis fractionation, and DNA staining. As compared with normal controls, in the FCA group, there was a three-fold increase of ET allele frequency (E-> = 0.17; £3 = 0.72; £4 = 0.11). These preliminary findings seem to be at variance with the results of a previous investigation showing that in patients with lobar atrophy the frequency of £3, £3, £4 does not differ from normal controls (Piclfering-Brown et al., Neuroscience Letters 188, 205, 1995). Our pilot study on a small series of patients with FCA may suggest differential patterns of ApoE allelic distribution in neurodegenerative disorders associated with FCA, as compared with sporadic AD.
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M3 - Article
AN - SCOPUS:33746329636
VL - 18
SP - 67
JO - Italian Journal of Neurological Sciences
JF - Italian Journal of Neurological Sciences
SN - 0392-0461
IS - 4
ER -