Leonard Guarente,1,2, * David A. Sinclair,2,3 and Guido Kroemer2,4,5,6, *
1 Department of Biology, Massachusetts Institute for Technology, Cambridge, MA 02139
2 Academy for Healthspan and Lifespan Research (AHLR), New York, NY, USA
3 Blavatnik Institute, Genetics Department, Harvard Medical School, Boston, MA 02115, USA
4 Centre de Recherche des Cordeliers, Equipe labellise´ e par la Ligue contre le cancer, Universite´ Paris Cite´ , Sorbonne Universite´ , Inserm U1138, Institut Universitaire de France, Paris, France
5 Metabolomics and Cell Biology Platforms, Institut Gustave Roussy, Villejuif, France
6 Institut du Cancer Paris CARPEM, Department of Biology, Hoˆ pital Europe´ en Georges Pompidou, AP-HP, Paris, France
*Correspondence: 该Email地址已收到反垃圾邮件插件保护。要显示它您需要在浏览器中启用JavaScript。 (L.G.), 该Email地址已收到反垃圾邮件插件保护。要显示它您需要在浏览器中启用JavaScript。 (G.K.)
https://doi.org/10.1016/j.cmet.2023.12.007
SUMMARY
Here, we summarize the current knowledge on eight promising drugs and natural compounds that have been tested in the clinic: metformin, NAD+ precursors, glucagon-like peptide-1 receptor agonists, TORC1 inhibitors, spermidine, senolytics, probiotics, and anti-inflammatories. Multiple clinical trials have commenced to evaluate the efficacy of such agents against age-associated diseases including diabetes, cardiovascular disease, cancer, and neurodegenerative diseases. There are reasonable expectations that drugs able to decelerate or reverse aging processes will also exert broad disease-preventing or -attenuating effects. Hence, the outcome of past, ongoing, and future disease-specific trials may pave the way to the development of new anti-aging medicines. Drugs approved for specific disease indications may subsequently be repurposed for the treatment of organism-wide aging consequences.
Javier Ganz,1,2,3,8,9 Lovelace J. Luquette,4,8 Sara Bizzotto,1,2,3,5,8 Michael B. Miller,1,3,6 Zinan Zhou,1,2,3 Craig L. Bohrson,4
Hu Jin,4 Antuan V. Tran,4 Vinayak V. Viswanadham,4 Gannon McDonough,6 Katherine Brown,6 Yasmine Chahine,1
Brian Chhouk,1 Alon Galor,4 Peter J. Park,4,7,* and Christopher A. Walsh1,2,3,10,*
1 Division of Genetics and Genomics, Manton Center for Orphan Disease Research, Department of Pediatrics, and Howard Hughes Medical Institute, Boston Childrens Hospital, Boston, MA 02115, USA
2 Departments of Pediatrics and Neurology, Harvard Medical School, Boston, MA 02115, USA
3 Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA
4 Department of Biomedical Informatics, Harvard Medical School, Boston, MA 02115, USA
5 Sorbonne Universite´ , Institut du Cerveau (Paris Brain Institute) ICM, Inserm, CNRS, Hoˆ pital de la Pitie´ Salpeˆ trie`re, 75013 Paris, France
6 Department of Pathology, Brigham and Womens Hospital, Harvard Medical School, Boston, MA 02115, USA
7 Division of Genetics, Brigham and Womens Hospital, Boston, MA 02115, USA
8 These authors contributed equally
9 Present address: Merck Research Laboratories, Cambridge, MA 02142, USA
10 Lead contact
*Correspondence: 该Email地址已收到反垃圾邮件插件保护。要显示它您需要在浏览器中启用JavaScript。 (P.J.P.), 该Email地址已收到反垃圾邮件插件保护。要显示它您需要在浏览器中启用JavaScript。 (C.A.W.)
https://doi.org/10.1016/j.cell.2024.02.025
Characterizing somatic mutations in the brain is important for disentangling the complex mechanisms of aging, yet little is known about mutational patterns in different brain cell types. Here, we performed wholegenome sequencing (WGS) of 86 single oligodendrocytes, 20 mixed glia, and 56 single neurons from neurotypical individuals spanning 0.4–104 years of age and identified >92,000 somatic single-nucleotide variants (sSNVs) and small insertions/deletions (indels). Although both cell types accumulate somatic mutations linearly with age, oligodendrocytes accumulated sSNVs 81% faster than neurons and indels 28% slower than neurons. Correlation of mutations with single-nucleus RNA profiles and chromatin accessibility from the same brains revealed that oligodendrocyte mutations are enriched in inactive genomic regions and are distributed across the genome similarly to mutations in brain cancers. In contrast, neuronal mutations are enriched in open, transcriptionally active chromatin. These stark differences suggest an assortment of active mutagenic processes in oligodendrocytes and neurons.
擅长：1. 烧伤/烫伤/手术疤痕美学修复; 2. 创面/伤口/溃疡/皮肤缺损美学修复; 3. 全身体表肿瘤/包块手术治疗。
擅长疾病：1.面部轮廓整形;2.面部年轻化;3.身体塑形;4.先天性和创伤后畸形修复、体表肿瘤切除及器官再造。如：黄褐斑、瘢痕疙瘩、减肥 。教授，整形外科副主任，医学博士后，毕业于西安第四军医大学临床医学系，毕业后留校。
在成人大面积烧伤的休克复苏、感染防治、多器官功能障碍综合征的防治、严重电烧伤和吸入性损伤的救治以及小儿重度和特重度烧伤的救治等方面有较高造诣。获黑龙江省科技进步三等奖2项，哈尔滨市科技进步二等奖1项，三等奖2项。
担任欧洲糖尿病学会会员、美国糖尿病学会会员、欧洲糖尿病学会糖尿病足研究组发起会员、中华医学会糖尿病学分会第2届足病学组组长、中国人民解放军内分泌学会副主任委员、北京内分泌学会副主任委员、北京糖尿病防治协会副理事长、北京市朝阳区预防医学会副会长、国家卫生部全国慢性病综合防治示范点专家组成员、中国疾病控制中心慢病中心糖尿病专家、第四军医大学兼职教授，悉尼大学客座教授，第四军医大学硕士研究生导师，中南大学湘雅三医院硕士研究生导师主任医师。
擅长诊治各种危急重症烧伤、烧伤后疤痕挛缩、功能畸形整复、各类急慢性伤口、复杂难愈性创面、伤口早期微创美容及早期抗疤治疗等
浙江大学临床医学二系教授，浙江大学医学院附属第二医院主任医师，毕业于日本金泽医科大学。
伤口世界平台生态圈，以“关爱人间所有伤口患者”为愿景，连接、整合和拓展线上和线下的管理慢性伤口的资源，倡导远程、就近和居家管理慢性伤口，解决伤口专家的碎片化时间的价值创造、诊疗经验的裂变复制、和患者的就近、居家和低成本管理慢性伤口的问题。
2019广东省医疗行业协会伤口管理分会年会
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