Inglés Marta, Belenguer-Varea Angel, Serna Eva, Mas-Bargues Cristina, Tarazona-Santabalbina Francisco J, Borrás Consuelo, Vina Jose
Freshage Research Group, Department of Physiotherapy, Faculty of Physiotherapy, University of Valencia, CIBERFES-ISCIII, INCLIVA , Valencia, Spain.
Division of Geriatrics, Hospital Universitario de La Ribera, Alzira, Valencia, Spain.
J Gerontol A Biol Sci Med Sci. 2022 Oct 6;77(10):1931-1938. doi: 10.1093/gerona/glac119.
Centenarians exhibit extreme longevity and compression of morbidity and display a unique genetic signature. Centenarians' offspring seem to inherit centenarians' compression of morbidity, as measured by lower rates of age-related pathologies. We aimed to ascertain whether centenarians' offspring are less frail and whether they are endowed with a "centenarian genetic footprint" in a case-control study, matched 1:1 for gender, age ±5 years, and place of birth and residence. Cases must have a living parent aged 97 years or older, aged 65-80 years, community dwelling, not suffering from a terminal illness, or less than 6 months of life expectancy. Controls had to meet the same criteria as cases except for the age of death of their parents (not older than 89 years). Centenarians were individuals 97 years or older. Frailty phenotype was determined by Fried's criteria. We collected plasma and peripheral blood mononuclear cells from 63 centenarians, 88 centenarians' offspring, and 88 noncentenarians' offspring. miRNA expression and mRNA profiles were performed by the GeneChip miRNA 4.0 Array and GeneChip Clariom S Human Array, respectively. We found a lower incidence of frailty among centenarians' offspring when compared with their contemporaries' noncentenarians' offspring (p < .01). Both miRNA and mRNA expression patterns in centenarians' offspring were more like those of centenarians than those of noncentenarians' offspring (p < .01). In conclusion, centenarians' offspring are less frail than age-matched noncentenarians' offspring, and this may be explained by their unique genetic endowment.
百岁老人表现出超长的寿命和发病期的压缩，并呈现出独特的基因特征。百岁老人的后代似乎继承了百岁老人发病期的压缩，这通过与年龄相关的病理发生率较低来衡量。在一项病例对照研究中，我们旨在确定百岁老人的后代是否更不易衰弱，以及他们是否具有“百岁老人基因印记”，该研究在性别、年龄±5岁、出生地和居住地方面进行1:1匹配。病例必须有一位97岁或以上的在世父母，年龄在65 - 80岁之间，居住在社区，没有患绝症，预期寿命不少于6个月。对照组必须符合与病例相同的标准，但其父母的死亡年龄（不超过89岁）除外。百岁老人是指97岁及以上的个体。衰弱表型由弗里德标准确定。我们从63名百岁老人、88名百岁老人的后代和88名非百岁老人的后代中收集了血浆和外周血单核细胞。分别通过基因芯片miRNA 4.0阵列和基因芯片Clariom S人类阵列进行miRNA表达和mRNA谱分析。我们发现，与同龄人中非百岁老人的后代相比，百岁老人的后代衰弱发生率更低（p < 0.01）。百岁老人后代的miRNA和mRNA表达模式都比非百岁老人后代更类似于百岁老人（p < 0.01）。总之，百岁老人的后代比年龄匹配的非百岁老人的后代更不易衰弱，这可能是由他们独特的基因禀赋所解释的。
