A method for reducing senescence-positive cells in a subject includes a step of identify a subject having increased expression of p16INK4a or at risk for increased of p16INK4a. A fasting-mimicking diet is administered to the subject for a first time period.

The present disclosure provides compositions and methods based on the use of 15-PGDH as a therapeutic target in rejuvenation of aging non-skeletal muscle tissues and/or organs. The 15-PGDH inhibitor SW033291 administered intraperitoneally for 4 weeks resulted in restoration of follicular structure and re-establishment of the marginal zone in spleens of 25 month old mice. Treatment of 25 month old mice with SW033291 also reduced the levels of IL10, IL6, BTC, GM-CSF, IL 13 back to levels similar 0 to 4 month old mice.

The present invention relates to a marker that can be used as aging biomarker. More specifically, the present invention relates to the analysis of nucleolar size as a biomarker for aging and metabolic health and its relation to the virtual age, or the life expectancy of animals, including humans. The aging biomarker of the invention can be used to study the effect of medication, food compounds and/or special diets on the wellness and virtual age, or the life expectancy of animals, including humans.

The present invention relates to a real-time fluorescence imaging sensor for measuring glutathione in the endoplasmic reticulum (ER) and a method for producing same. More specifically, the present invention relates to a new compound for measuring glutathione in the endoplasmic reticulum (ER), a method for producing the new compound, a real-time imaging sensor for measuring glutathione in the endoplasmic reticulum (ER) comprising the new compound, a method for producing same, and a method for measuring glutathione in the endoplasmic reticulum (ER) by using the imaging sensor.

Provided are age-modified cells and method for making age modified cells by reducing or increasing the level of genomic nucleic acid methylation in the cells. The aging and/or maturation process can be accelerated or reduced and controlled for young, aged, mature and/or immature cells, such as a somatic cell, a stem cell, a stem cell-derived somatic cell, including an induced pluripotent stem cell-derived cell, by reducing or increasing the level of genomic nucleic acid methylation in the cells. Methods described by the present disclosure can produce age-appropriate cells from a somatic cell or a stem cell, such as an old cell, young cell, immature cell, and/or a mature cell. Such age-modified cells constitute model systems for the study of late-onset diseases and/or disorders.

The instant invention relates to novel compounds useful for visualizing cell senescence, their preparation and use. In particular, this invention relates to novel fucose and amino-quinoline derivatives useful as senescence traces and their preparation.

Provided is a novel biomarker for the diagnosis of aging or amyotrophy. Provided are a method for determining the state of aging or amyotrophy, a method for determining the efficacy of therapeutic or preventive effects on aging or amyotrophy, and a method of screening for a therapeutic or preventive agent for aging or amyotrophy. The biomarker is a free MuSK protein or an mRNA for a secreted MuSK.

The present invention relates to a fluorescence sensor capable of real-time imaging for measuring a cellular thiol level. The present invention reveals that the fluorescence intensity of the fluorescent real-time SH group-tracer (FreSH-Tracer) of the present invention increases or decreases continuously, ratiometrically or reversibly depending on the thiol level in living cells, and thus can be usefully used as a biosensor which is remarkably susceptible to quantitative or qualitative real-time detection of the cellular thiol level in living cells.

The present invention relates to a CFI bioactivity assay designed to quantitatively measure (a) CFI bioactivity of plasma or other body fluids; and (b) bioactivity of CFI in plasma or other body fluids of a human patient afflicted by a disease that involves amyloid deposition in tissues, in particular Alzheimer disease, AMD, glaucoma, or beta-amyloid cataract formation.

The invention relates to a method for in vitro investigating mitochondrial replication dysfunction in a biological sample removed from a subject susceptible of suffering from physiological ageing or physiopathological conditions related to physiological ageing, or physiopathological ageing or associated symptoms or conditions, in particular premature ageing or accelerated ageing, or of a progeroid syndrome, such as Cockayne syndrome (CS), or neurodegenerative disorders or symptoms thereof, in which the levels of at least one species selected in the group of: POLG1 protein, POLG1 RNA, POLG2 protein, protease(s) which have POLG as a target, in particular serine protease(s) such as HTRA3 protein, HTRA2 protein and, HTRA3 RNA or HTRA2 RNA, or any combination of these species, are investigated. The invention also relates to kits and uses thereof, therapeutic methods against progeroid-like syndromes or symptoms and screening method for identifying particular protease inhibitor(s) and/or nitroso-redox stress scavenger compound(s) having relevance for the symptoms discussed herein.