skip (more of a protocol)
5 (review paper)
The samples were grouped and named as young (age, 23–40 years; n = 20),
old (age, 50–89 years; n=27), and centenarian (age, 99–107 years; n=49)"
90 years of age (median age 96 years; range 90-103) and 100 (80 female/
20 male) younger controls (median age 32 years, range 19-44)."
1 DID NOT ANALYZE SNPS
1 (links APOE with cardiovascular issues)
favorable pattern of lipoprotein levels and sizes, as well as lower prevalence of hypertension and greater insulin
2.931). 100+ years old: 3.263 (1.860–5.722)"
pyrophosphate DNA sequencing using a PSQ 96 system"""
and B4a haplogroups"
risk factors, the C allele of rs1333049 remained significantly associated with a reduced likelihood to reach longevity. Detailed OR information is as follow: .64 (0.39–0.89)"
Discard - no specific gene mentioned
between the IL-6 polymorphism and longevity. In exploratory analyses, we observed a possible interaction among anti-inflammatory drugs, interleukin-6 −174 C/C genotype, and longevity"
between the fibrinogen promoter polymorphism and longevity."
(−1082A, −819C, and −592C) was observed in the elderly (Pc < 0.05). The observations imply that longevity might be associated with anti-inflammatory cytokine gene profiles."""
genetic and environmental history. So, in our opinion, HLA genes might be considered survival genes, not
octo/nonagenarian subjects who were heterozygous for PON1 192 R allele, (OR 1.3... p = 0.04) with a stepwise increase for RR homozygous subjects (OR 1.7... p = 0.02), compared to QQ subjects... The PON1 192R/Q and PON55L/M loci were in strong linkage