# US 2014/0193440 A1 · Markers of alzheimers disease

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- Number: US 2014/0193440 A1
- Document ID: US20140193440A1
- Status: Published application
- Kind: A1
- Application number: 14/149,362
- Filed: 2014-01-07
- Published: 2014-07-10
- Earliest claimed: 2005-06-30
- Applicants: ImmunoClin Ltd.
- Inventors: Mario Clerici; Giorgio Annoni; Beatrice Arosio
- Web page: https://patentgrep.com/patent/US20140193440A1

## CPC

- C12Q 1/6883: for diseases caused by alterations of genetic material
- C12Q 2600/156: Polymorphic or mutational markers
- C12Q 2600/172: Haplotypes
- C12Q: MEASURING OR TESTING PROCESSES INVOLVING ENZYMES, NUCLEIC ACIDS OR MICROORGANISMS (immunoassay G01N33/53); COMPOSITIONS OR TEST PAPERS THEREFOR; PROCESSES OF PREPARING SUCH COMPOSITIONS; CONDITION-RESPONSIVE CONTROL IN MICROBIOLOGICAL OR ENZYMOLOGICAL PROCESSES

## Abstract

An inflammatory process is suggested to be involved in the pathogenesis of Alzheimer's disease (AD), a neurodegenerative disorder characterized by the presence of neuritic plaques within the cerebral cortex that are mainly composed of a small insoluble protein of 40-42 aminoacids (amyloid protein). Amyloid-specific Interleukin-10 (IL-10) generation is found to be selectively and significantly reduced in AD patients (p=0.023). The genotype associated with high IL-10 production is extremely infrequent in AD individuals (2% vs. 28%). The presence of low/intermediate-IL-10-producing genotypes (GCC/ATA; ATA/ATA) was associated with an earlier age at disease onset and (ACC/ACC; ACC/ATA) with an accelerated rate of disease progression/severity and with amyloid-specific impairment of IL-10 production. This relationship is independent of ApoE gene polymorphism. These results support the use of anti-inflammatory compounds in the therapy of this disease.

## Claims

### Claim at position 1

1-17. (canceled)

### Claim 18

A method for treating a human subject suspected of being at risk for or having Alzheimer's disease, the method comprising:
analyzing a DNA bearing sample taken from said subject to determine the allelic variants present at one or more of the SNP loci at positions −1082 of the gene encoding IL-10, and detecting the G to A substitution at position −1082,
wherein, if the presence of a polymorphism selected from the group consisting of a G to A substitution at position −1082 of the gene encoding IL-10 is determined to be present in the DNA bearing sample, the human subject is treated by administration of pharmaceutical compositions which directly, as an intermediate, as a pre-cursor or pre-pro-cursor, stimulate the synthesis of IL-10 ab initio or by administration of pharmacological compositions that enhance or inhibit antigen specific production of IL-10.

### Claim 19 (depends on 18)

The method according to claim 18 which further comprises analyzing the sample to determine the presence of a −174C allele for the gene encoding IL-6 and Apo-E carrier status, wherein if the presence of a −174C allele for the gene encoding IL-6 is determined to be present in the DNA bearing sample, the human subject is further treated by administration of pharmaceutical compositions which inhibit or block the action of IL-6 in the human subject.

### Claim 20

A method of treating a human subject suspected of being at risk for or having Alzheimer's disease, the method comprising:
analyzing a DNA sample from said subject to determine the allelic variants present at SNP loci position −1082 of the gene encoding IL-10, and detecting the G to A substitution at position −1082, the presence of a −174C allele for the gene encoding IL-6, and Apo-E 4 carrier status, wherein, if the presence of a polymorphism selected from the group consisting of a G to A substitution at position −1082, the presence of a −174C allele for the gene encoding IL-6, and the presence of a Apo-E 4 allele is determined to be present in the DNA sample, the human subject is treated by administration of pharmaceutical compositions which inhibit or block the action of IL-6 in the human subject and further pharmaceutical compositions which directly, as an intermediate, as a pre-cursor or pre-pro-cursor, stimulate the synthesis of IL-10 ab initio or by administration of pharmacological compositions that enhance or inhibit antigen specific production of IL-10.