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Identification of genetic markers of biological age and metabolism

a technology applied in the field of identification of genetic markers of biological age and metabolism, can solve the problems of complex organismal senescence, lack of biological age molecular markers, and difficulty in elucidating mechanisms and testing interventions

Inactive Publication Date: 2008-10-16
WEINDRUCH RICHARD H +2
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Benefits of technology

[0016]Other objects, features and advantage of the present invention will become apparent to one of skill in the art after review of the specification and claims.

Problems solved by technology

Factors which contribute to the difficulty of elucidating mechanisms and testing interventions include the complexity of organismal senescence and the lack of molecular markers of biological age (biomarkers).
In mammals, there has been limited success in the identification of genes that control aging rates.

Method used

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  • Identification of genetic markers of biological age and metabolism
  • Identification of genetic markers of biological age and metabolism

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1. In General

[0036]In order to test our hypothesis, we performed gene expression profiling of over 6300 genes in skeletal muscle, neocortex tissue, and cerebellum tissue and 19,000 genes in skeletal muscle and heart tissue of 5-month and 30-month old C57B16 mice, using high density oligonucleotide arrays. We found that a number of genes demonstrated alterations in gene expression profile as a function of chronological age and that these genes were broadly divided into a few classes listed in the Tables, such as stress response, energy metabolism, biosynthesis, protein metabolism and neuronal growth.

[0037]In order to validate the use of gene expression profiles as biomarkers of biological age, we investigated the role of caloric restriction, the only intervention known to retard the aging process in mammals, on gene expression profiles. Our analysis demonstrated that 30-month old calorically restricted animals display either complete or partial prevention of most aging associated alt...

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Abstract

A method of measuring the biological age of a multicellular organism is disclosed. In one embodiment this method comprises the steps of obtaining a sample of nucleic acid isolated from the organism's organ, tissue or cell and determining the expression pattern of a panel of sequences within the nucleic acid that have been predetermined by either increase or decrease in response to biological aging of the organ, tissue or cell. A method of obtaining biomarkers of aging is also disclosed. This method comprises the step of comparing a gene expression profile of a young multicellular organism subject's organ, tissue or cells; a gene expression profile from a chronologically aged subject's organ, tissue or cell; and a gene expression profile from a chronologically aged but biologically younger subject's organ, tissue or cell and identifying gene expression alterations that are observed when comparing the young subjects and the chronologically aged subjects and are not observed or reduced in magnitude when comparing the young subjects and the chronologically aged but biologically younger subjects.

Description

CROSS-REFERENCE TO RELATED APPLICATION[0001]This application claims priority to provisional application 60 / 148,540, filed Aug. 12, 1999, U.S. provisional application 60 / 178,232, filed Jan. 26, 2000 and 60 / 211,923 filed Jun. 16, 2000. These provisional applications are incorporated by reference as if fully set forth herein.STATEMENT REGARDING FEDERALLY SPONSORED RESEARCH AND DEVELOPMENT[0002]This invention was made with United States government support awarded by the following agencies: NIH Grant No: AG 11915. The United States has certain rights in this invention.BACKGROUND OF THE INVENTION[0003]A common feature of most multicellular organisms is the progressive and irreversible physiological decline that characterizes senescence. Although genetic and environmental factors can influence the aging process, the molecular basis of senescence remains unknown. Postulated mechanisms include cumulative damage to DNA leading to genomic instability, epigenetic alterations that lead to altere...

Claims

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Application Information

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Patent Type & Authority Applications(United States)
IPC IPC(8): C12Q1/68
CPCC12Q1/6809C12Q2600/158C12Q1/6883
Inventor WEINDRUCH, RICHARD H.PROLLA, TOMAS A.LEE, CHEOL-KOO
Owner WEINDRUCH RICHARD H
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