US20100105101A1 - Methods for the diagnosis and risk assessment of plasmalogen deficiency mediated diseases of aging - Google Patents

Methods for the diagnosis and risk assessment of plasmalogen deficiency mediated diseases of aging Download PDF

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US20100105101A1
US20100105101A1 US12/595,178 US59517808A US2010105101A1 US 20100105101 A1 US20100105101 A1 US 20100105101A1 US 59517808 A US59517808 A US 59517808A US 2010105101 A1 US2010105101 A1 US 2010105101A1
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cancer
plasmenyl
plasmanyl
sample
plasmalogen
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Dayan Goodenowe
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Med-Life Discoveries Lp
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Phenomenome Discoveries Inc
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    • G—PHYSICS
    • G01—MEASURING; TESTING
    • G01N—INVESTIGATING OR ANALYSING MATERIALS BY DETERMINING THEIR CHEMICAL OR PHYSICAL PROPERTIES
    • G01N33/00—Investigating or analysing materials by specific methods not covered by groups G01N1/00 - G01N31/00
    • G01N33/48—Biological material, e.g. blood, urine; Haemocytometers
    • G01N33/483—Physical analysis of biological material
    • G01N33/487—Physical analysis of biological material of liquid biological material
    • G01N33/49—Blood
    • G—PHYSICS
    • G01—MEASURING; TESTING
    • G01N—INVESTIGATING OR ANALYSING MATERIALS BY DETERMINING THEIR CHEMICAL OR PHYSICAL PROPERTIES
    • G01N33/00—Investigating or analysing materials by specific methods not covered by groups G01N1/00 - G01N31/00
    • G01N33/48—Biological material, e.g. blood, urine; Haemocytometers
    • G01N33/50—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing
    • G01N33/53—Immunoassay; Biospecific binding assay; Materials therefor
    • G01N33/574—Immunoassay; Biospecific binding assay; Materials therefor for cancer
    • G01N33/57484—Immunoassay; Biospecific binding assay; Materials therefor for cancer involving compounds serving as markers for tumor, cancer, neoplasia, e.g. cellular determinants, receptors, heat shock/stress proteins, A-protein, oligosaccharides, metabolites
    • G—PHYSICS
    • G01—MEASURING; TESTING
    • G01N—INVESTIGATING OR ANALYSING MATERIALS BY DETERMINING THEIR CHEMICAL OR PHYSICAL PROPERTIES
    • G01N33/00—Investigating or analysing materials by specific methods not covered by groups G01N1/00 - G01N31/00
    • G01N33/48—Biological material, e.g. blood, urine; Haemocytometers
    • G01N33/50—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing
    • G01N33/68—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing involving proteins, peptides or amino acids
    • G01N33/6893—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing involving proteins, peptides or amino acids related to diseases not provided for elsewhere
    • G01N33/6896—Neurological disorders, e.g. Alzheimer's disease
    • G—PHYSICS
    • G01—MEASURING; TESTING
    • G01N—INVESTIGATING OR ANALYSING MATERIALS BY DETERMINING THEIR CHEMICAL OR PHYSICAL PROPERTIES
    • G01N33/00—Investigating or analysing materials by specific methods not covered by groups G01N1/00 - G01N31/00
    • G01N33/48—Biological material, e.g. blood, urine; Haemocytometers
    • G01N33/50—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing
    • G01N33/92—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing involving lipids, e.g. cholesterol, lipoproteins, or their receptors
    • H—ELECTRICITY
    • H01—ELECTRIC ELEMENTS
    • H01J—ELECTRIC DISCHARGE TUBES OR DISCHARGE LAMPS
    • H01J49/00—Particle spectrometers or separator tubes
    • H01J49/0027—Methods for using particle spectrometers
    • H01J49/0031—Step by step routines describing the use of the apparatus
    • H—ELECTRICITY
    • H01—ELECTRIC ELEMENTS
    • H01J—ELECTRIC DISCHARGE TUBES OR DISCHARGE LAMPS
    • H01J49/00—Particle spectrometers or separator tubes
    • H01J49/26—Mass spectrometers or separator tubes
    • H01J49/34—Dynamic spectrometers
    • H01J49/36—Radio frequency spectrometers, e.g. Bennett-type spectrometers, Redhead-type spectrometers
    • H01J49/38—Omegatrons ; using ion cyclotron resonance
    • G—PHYSICS
    • G01—MEASURING; TESTING
    • G01N—INVESTIGATING OR ANALYSING MATERIALS BY DETERMINING THEIR CHEMICAL OR PHYSICAL PROPERTIES
    • G01N2560/00—Chemical aspects of mass spectrometric analysis of biological material
    • G—PHYSICS
    • G01—MEASURING; TESTING
    • G01N—INVESTIGATING OR ANALYSING MATERIALS BY DETERMINING THEIR CHEMICAL OR PHYSICAL PROPERTIES
    • G01N2800/00—Detection or diagnosis of diseases
    • G01N2800/50—Determining the risk of developing a disease
    • G—PHYSICS
    • G01—MEASURING; TESTING
    • G01N—INVESTIGATING OR ANALYSING MATERIALS BY DETERMINING THEIR CHEMICAL OR PHYSICAL PROPERTIES
    • G01N2800/00—Detection or diagnosis of diseases
    • G01N2800/70—Mechanisms involved in disease identification
    • G01N2800/7042—Aging, e.g. cellular aging

Definitions

  • the present invention relates to methods for the diagnosis of plasmalogen deficiency mediated diseases of aging.
  • the present invention describes the relationship between plasmalogen biosynthesis dysfunction and the biochemical and clinical manifestations of age related disorders. Specifically the present invention describes an increased prevalence of colon cancer, prostate cancer, lung cancer, breast cancer, ovarian cancer, kidney cancer, cognitive impairment and dementia in subjects with decreased levels of plasmalogens.
  • Cancer is a state where the cells have lost their tissue identity and have reverted back to a primitive cell form that grows rapidly and without regulation. Invasive carcinoma is the final step in this sequence. It is a cancer which has invaded beyond the original tissue layer and is also able to spread to other parts of the body (metastasize), starting growth of the cancer there and destroying the affected organs. It can be treated, but not always successfully. However, if left untreated it is almost always fatal.
  • cancer cells can utilize both respiration and glycolysis for energy.
  • much work is now focused on developing drugs that inhibit the glycolysis pathway.
  • One of the defining features of aerobic glycolysis in cancer is an enhanced mitochondrial citrate export and the use of cytosolic citrate to form acetyl-CoA. Therefore, the direct findings presented above, that an impairment in plasmalogen biosynthesis result in both increased membrane cholesterol levels and increased cytosolic acetyl-CoA utilization, strongly implicate plasmalogen biosynthesis impairment in cancer etiology.
  • the present invention provides a method for identifying an individual who would benefit from an age-related plasmalogen deficiency-targeted therapy comprising: analyzing a blood sample from a test subject to obtain quantifying data on all or a subset of the metabolites listed in Table 5, or closely related entities; comparing the data obtained on said metabolites in said test subject with reference data obtained from the analysis of a plurality of age-related plasmalogen deficiency humans or from a plurality of non-age-related plasmalogen deficiency humans; and using said comparison to determine the probability that the test subject would benefit from an age-related plasmalogen deficiency-targeted therapy.
  • the present invention provides a method for monitoring the effect of an age-related plasmalogen deficiency-targeted therapy comprising: analyzing a plurality of blood samples from a test subject prior to the initiation, during administration, or following administration of such therapy to obtain quantifying data on all or a subset of the metabolites listed in Table 5, or closely related entities; comparing the data obtained on said metabolites in said samples to each other or to reference data obtained from the analysis of a plurality of age-related plasmalogen deficiency humans or from a plurality of non-age-related plasmalogen deficiency humans; and using said comparison to determine the probability that the test subject would benefit from the continued treatment of an age-related plasmalogen deficiency-targeted therapy.
  • FIG. 1 shows the biosynthesis pathway for plasmalogens.
  • FIG. 9 shows the distribution of plasmalogen concentrations in prostate cancer patients.
  • FIG. 17 shows the etiology of dementia.
  • FIG. 20 shows the distribution of plasmenyl 16:0/22:6 in autopsy-confirmed non-Alzheimer's subjects.
  • the present invention relates to methods for the diagnosis of plasmalogen deficiency mediated diseases of aging.
  • the present invention describes the relationship between plasmalogen biosynthesis dysfunction and the biochemical and clinical manifestations of age related disorders. Specifically the present invention describes an increased prevalence of colon cancer, prostate cancer, lung cancer, breast cancer, ovarian cancer, kidney cancer, cognitive impairment and dementia in subjects with decreased levels of plasmalogens.
  • One embodiment of the present invention detects and measures a panel of metabolites in which a subset were found to have statistically significantly differential abundances between AO-PBD and normal serum.
  • the panel of metabolites is one or more than one metabolites listed in Table 5.
  • Common mass separation and detection systems can include quadrupole, quadrupole ion trap, linear ion trap, time-of-flight (TOF), magnetic sector, ion cyclotron (FTMS), Orbitrap, and derivations and combinations thereof.
  • TOF time-of-flight
  • FTMS ion cyclotron
  • Orbitrap derivations and combinations thereof.
  • the advantage of FTMS over other MS-based platforms is its high resolving capability that allows for the separation of metabolites differing by only hundredths of a Dalton, many which would be missed by lower resolution instruments.
  • the ionization of the metabolites which occurs during analysis of the sample, the metabolite will cause either a loss or gain of one or more hydrogen atoms and a loss or gain of an electron.
  • the accurate neutral mass will be referred to herein.
  • the step of analyzing the sample can be as described above.
  • the one or more than one reference sample may be a first reference sample obtained from a non-AO-PBD control individual.
  • the “internal control metabolite” refers to an endogenous metabolite naturally present in the patient. Any suitable endogenous metabolite that does not vary over the disease states can be used as the internal control metabolite.
  • the internal control metabolite may be phosphatidylethanolamine 16:0/18:0 (PtdEtn 16:0/18:0, M01), as shown in Table 5; this internal control metabolite has a molecular formula of C 39 H 78 NO 8 P, and a structure characterized as
  • High throughput screening was performed with a linear ion trap mass spectrometer (Q-trap 4000, Applied Biosystem) coupled with Agilent 1100 LC system.
  • Sample was prepared by adding 15 uL of internal standard (5 ⁇ g/mL of (24-13C)-Cholic Acid in methanol) to 120 uL ethyl acetate fraction of each sample. 100 ul sample was injected by flow injection analysis (FIA), and monitored under negative APCI mode. The method was based on multiple reaction monitoring (MRM) scan mode of one parent/daughter transition for each metabolite and one internal standard. Each transition was scanned for 70 ms for a total cycle time of 2.475 sec.
  • MRM multiple reaction monitoring
  • Plasmenyl 16:0/18:2 is a prototypical white matter plasmalogen containing a simple di-unsaturated fatty acid at sn-2 (linoleic acid) and plasmenyl 16:0/22:6 is a prototypical gray matter plasmalogen containing a polyunsaturated fatty acid at sn-2 (DHA).
  • DHA polyunsaturated fatty acid
  • Plasmenyl 16:0/18:2 and 16:0/22:6 are significantly lower in all of the cancers and in probable Alzheimer's, but not in any of the multiple sclerosis groups. In fact, plasmenyl 16:0/22:6 is actually statistically elevated in secondary progressive and primary progressive MS. The other important observation from these two graphs is that there is a significant decrease in plasmalogens in the age 60-69 age group versus the age 50-59 group.
  • the prodromal biochemical phase would be expected to be longer than the prodromal clinical phase. This is supported by the fact that amyloid plaques begin to accumulate in 40-49 year olds 14 but Alzheimer's does not begin to clinically manifest until late 60's early 70's. Based upon these two studies and our own evidence that serum plasmalogens decrease before clinical symptoms occur, the etiology of dementia can be expressed according to FIG. 17 .
  • AO-PBD shows a separate and distinct etiology from both cancer and dementia. Whereas the prevalence of cancer and dementia continue to increase with increasing age to at least age 90, the prevalence of AO-PBD peaks at age 60-69 and then decreases from age 70 onward. Furthermore although AO-PBD exhibits a similar biochemical profile to RCDP, it should not be confused with RCDP. The three forms of RDCP are all genetic disorders that affect children. Although, the underlying cause of AO-PBD is at this time unknown, it is certainly not an inborn error of metabolism.

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US12/595,178 2007-04-13 2008-04-09 Methods for the diagnosis and risk assessment of plasmalogen deficiency mediated diseases of aging Abandoned US20100105101A1 (en)

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US91154807P 2007-04-13 2007-04-13
PCT/CA2008/000659 WO2008124916A1 (fr) 2007-04-13 2008-04-09 Procédés pour le diagnostic et l'évaluation de risque de maladies dues au vieillissement induites par la déficience en plasmalogène
US12/595,178 US20100105101A1 (en) 2007-04-13 2008-04-09 Methods for the diagnosis and risk assessment of plasmalogen deficiency mediated diseases of aging

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WO2012099881A2 (fr) * 2011-01-17 2012-07-26 The John Hopkins University Protéines mutantes en tant que biomarqueurs spécifiques du cancer

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TWI475989B (zh) 2008-12-22 2015-03-11 Phenomenome Discoveries Inc 縮醛磷脂類化合物，含彼之醫藥組成物以及治療老化疾病的方法
CA2747582A1 (fr) * 2009-01-02 2010-07-08 Nestec S.A. Procedes pour augmenter les niveaux de plasmologenes endogenes
WO2010100060A2 (fr) 2009-03-04 2010-09-10 Nestec S.A. Procédé d'augmentation des taux de plasmalogène endogène chez des mammifères
CA2797960A1 (fr) 2009-10-01 2011-04-07 Phenomenome Discoveries Inc. Biomarqueurs seriques du cancer du pancreas et leurs utilisations en vue de la detection et du diagnostic de la maladie
JP6025568B2 (ja) * 2010-12-28 2016-11-16 株式会社藤野ブレインリサーチ 認知症を血液サンプルで判定するための検査方法
AU2018255514A1 (en) * 2017-04-17 2019-10-17 Med-Life Discoveries Lp Cyclic plasmenylethanolamines
CN115515600B (zh) * 2020-04-28 2024-06-25 株式会社流变机能食品研究所 免疫功能兴奋用组合物
CN113244246B (zh) * 2021-05-11 2022-05-06 江南大学 一种微生物源缩醛磷脂在治疗结肠癌中的应用

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Cited By (2)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
WO2012099881A2 (fr) * 2011-01-17 2012-07-26 The John Hopkins University Protéines mutantes en tant que biomarqueurs spécifiques du cancer
WO2012099881A3 (fr) * 2011-01-17 2012-10-26 The John Hopkins University Protéines mutantes en tant que biomarqueurs spécifiques du cancer

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WO2008124916A1 (fr) 2008-10-23
HK1134136A1 (en) 2010-04-16
EP2145181A4 (fr) 2011-01-12
AU2008238553A1 (en) 2008-10-23
JP2010523986A (ja) 2010-07-15
EP2145181B1 (fr) 2012-12-26
CN101675337A (zh) 2010-03-17
AU2008238553B2 (en) 2014-06-19
JP5220842B2 (ja) 2013-06-26
CA2680748C (fr) 2012-08-28
CA2680748A1 (fr) 2008-10-23
EP2145181A1 (fr) 2010-01-20
WO2008124916A8 (fr) 2009-01-15
US10302624B2 (en) 2019-05-28
US20160320366A1 (en) 2016-11-03

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