| Class / Patent application number | Description | Number of patent applications / Date published |
|---|
| 800012000 | Alzheimers disease | 10 |
| 20090133135 | Diagnostic and Therapeutic Target SLC39A11 Proteins for Neurodegenerative Diseases - The present invention discloses a dysregulation of the SLC39A12 gene and the protein products thereof in Alzheimer's disease patients. Based on this finding, the invention provides methods for diagnosing and prognosticating Alzheimer's disease in a subject, and for determining whether a subject is at increased risk of developing Alzheimer's disease. Furthermore, this invention provides therapeutic and prophylactic methods for treating and preventing Alzheimer's disease and related neurodegenerative disorders using the SLC39A12 gene and its corresponding gene products. Screening methods for modulating agents of neurodegenerative diseases are also disclosed. | 05-21-2009 |
| 20090217395 | Promoter Mutations that Increase Amyloid Precursor Protein Expression - The present invention relates to mutations in the amyloid precursor protein (APP) promoter region, whereby the mutations cause a significant increase in APP expression. The increase in APP expression is related to Alzheimer's disease, and the mutations can be used in Alzheimer's disease diagnosis, or in the construction of transgenic animal models for studying Alzheimer's disease. | 08-27-2009 |
| 20120266263 | METHOD OF TREATING MEMORY DISORDERS AND ENHANCING MEMORY USING IGF-II COMPOUNDS - The present invention provides compositions of insulin-like growth factor II (IGF-II) peptides or nucleic acids for the treatment of memory disorders and to enhance memory in subjects in need thereof. | 10-18-2012 |
| 20120331573 | DYNACTIN SUBUNIT p62 BIOMARKER FOR NEUROLOGICAL CONDITIONS - Methods and kits for identifying neurological conditions in a patient by determining a level of expression of dynactin subunit p62 are disclosed. The neurological conditions may include, for example, Alzheimer's Disease (AD) without cerebral amyloid angiopathy (CAA). | 12-27-2012 |
| 20130133090 | TRANSGENIC MAMMALLS MODIFIED IN BRI PROTEIN EXPRESSION - Provided are non-human mammals comprising a knock-in nucleic acid sequence capable of causing an alteration of expression of wild-type Bri2 in the mammal or a knockout of wild-type Bri2. Also provided are the non-human mammals as a model for Alzheimer's disease. | 05-23-2013 |
| 20130263298 | MODELS FOR DIAGNOSIS, PREVENTION AND TREATMENT OF ALZHEIMER'S DISEASE - A transgenic fly whose genome is modified to express enhanced levels of glutamate-cysteine ligase (GCL) gene is provided. The fly displays phenotypes associated with Alzheimer's disease (AD). Further, a method for diagnosing AD is provided, which includes assessing enzymatic activities in mitochondrial enzymes. Glutathione pathway are investigated by creating Alzheimer's model | 10-03-2013 |
| 20130291135 | TRANSGENIC MODEL OF ALZHEIMER'S DISEASE - Evidence indicates dysregulation. of the immunoregulatory molecule CD45 occurs in Alzheimer's disease (AD). Transgenic mice overproducing amyloid-β peptide (Aβ) and deficient in CD45 (PSAPP/CD45 | 10-31-2013 |
| 20140259192 | TRANSGENIC ANIMAL COMPRISING A DELETION OR FUNCTIONAL DELETION OF THE 3'UTR OF AN ENDOGENOUS GENE - The present invention relates to the fields of knockout (KO) animal production. The invention is directed to a transgenic KO animal comprising a heterozygous or homozygous deletion or functional deletion of the gene's native 3′ untranslated region (3′UTR) at least in one of its endogenous gene loci, wherein the disrupted endogenous gene is transcribed into an m RNA without its native 3′UTR. Instead, a 3′UTR of choice, knocked in by the experimenter, is transcribed into an m RNA. The 3′UTR KO animals provide a new approach to study gene function as they enable to overexpress the gene products what are negatively regulated via their 3′UTR-s exclusively in those cells that already transcribe the gene, thereby avoiding the misexpression problem present in the animals produced by conventional transgenesis methods. The invention is further directed to KO animals, in which the gene with deletion of 3′UTR is GDNF, NGF or BDNF. | 09-11-2014 |
| 20140304845 | ALZHEIMER'S DISEASE SIGNATURE MARKERS AND METHODS OF USE - Methods, biomarkers, and expression signatures are disclosed for assessing the disease progression of Alzheimer's disease (AD). In one embodiment, BioAge (biological age), NdStress (neurodegenerative stress), Alz (Alzheimer), and Inflame (inflammation) are used as biomarkers of AD progression. In another aspect, the invention comprises a gene signature for evaluating disease progression. In still another embodiment, methods for evaluating disease progression are provided. In yet another embodiment, the invention can be used to identify animal models for use in the development and evaluation of therapeutics for the treatment of AD. | 10-09-2014 |
| 20140331341 | AUTOMATED HIGH-CONTENT LIVE ANIMAL DRUG SCREENING USING C. ELEGANS - The present invention relates to methods and compositions for high content drug screening in | 11-06-2014 |
| 20090133135 | Diagnostic and Therapeutic Target SLC39A11 Proteins for Neurodegenerative Diseases - The present invention discloses a dysregulation of the SLC39A12 gene and the protein products thereof in Alzheimer's disease patients. Based on this finding, the invention provides methods for diagnosing and prognosticating Alzheimer's disease in a subject, and for determining whether a subject is at increased risk of developing Alzheimer's disease. Furthermore, this invention provides therapeutic and prophylactic methods for treating and preventing Alzheimer's disease and related neurodegenerative disorders using the SLC39A12 gene and its corresponding gene products. Screening methods for modulating agents of neurodegenerative diseases are also disclosed. | 05-21-2009 |
| 20090217395 | Promoter Mutations that Increase Amyloid Precursor Protein Expression - The present invention relates to mutations in the amyloid precursor protein (APP) promoter region, whereby the mutations cause a significant increase in APP expression. The increase in APP expression is related to Alzheimer's disease, and the mutations can be used in Alzheimer's disease diagnosis, or in the construction of transgenic animal models for studying Alzheimer's disease. | 08-27-2009 |
| 20120266263 | METHOD OF TREATING MEMORY DISORDERS AND ENHANCING MEMORY USING IGF-II COMPOUNDS - The present invention provides compositions of insulin-like growth factor II (IGF-II) peptides or nucleic acids for the treatment of memory disorders and to enhance memory in subjects in need thereof. | 10-18-2012 |
| 20120331573 | DYNACTIN SUBUNIT p62 BIOMARKER FOR NEUROLOGICAL CONDITIONS - Methods and kits for identifying neurological conditions in a patient by determining a level of expression of dynactin subunit p62 are disclosed. The neurological conditions may include, for example, Alzheimer's Disease (AD) without cerebral amyloid angiopathy (CAA). | 12-27-2012 |
| 20130133090 | TRANSGENIC MAMMALLS MODIFIED IN BRI PROTEIN EXPRESSION - Provided are non-human mammals comprising a knock-in nucleic acid sequence capable of causing an alteration of expression of wild-type Bri2 in the mammal or a knockout of wild-type Bri2. Also provided are the non-human mammals as a model for Alzheimer's disease. | 05-23-2013 |
| 20130263298 | MODELS FOR DIAGNOSIS, PREVENTION AND TREATMENT OF ALZHEIMER'S DISEASE - A transgenic fly whose genome is modified to express enhanced levels of glutamate-cysteine ligase (GCL) gene is provided. The fly displays phenotypes associated with Alzheimer's disease (AD). Further, a method for diagnosing AD is provided, which includes assessing enzymatic activities in mitochondrial enzymes. Glutathione pathway are investigated by creating Alzheimer's model | 10-03-2013 |
| 20130291135 | TRANSGENIC MODEL OF ALZHEIMER'S DISEASE - Evidence indicates dysregulation. of the immunoregulatory molecule CD45 occurs in Alzheimer's disease (AD). Transgenic mice overproducing amyloid-β peptide (Aβ) and deficient in CD45 (PSAPP/CD45 | 10-31-2013 |
| 20140259192 | TRANSGENIC ANIMAL COMPRISING A DELETION OR FUNCTIONAL DELETION OF THE 3'UTR OF AN ENDOGENOUS GENE - The present invention relates to the fields of knockout (KO) animal production. The invention is directed to a transgenic KO animal comprising a heterozygous or homozygous deletion or functional deletion of the gene's native 3′ untranslated region (3′UTR) at least in one of its endogenous gene loci, wherein the disrupted endogenous gene is transcribed into an m RNA without its native 3′UTR. Instead, a 3′UTR of choice, knocked in by the experimenter, is transcribed into an m RNA. The 3′UTR KO animals provide a new approach to study gene function as they enable to overexpress the gene products what are negatively regulated via their 3′UTR-s exclusively in those cells that already transcribe the gene, thereby avoiding the misexpression problem present in the animals produced by conventional transgenesis methods. The invention is further directed to KO animals, in which the gene with deletion of 3′UTR is GDNF, NGF or BDNF. | 09-11-2014 |
| 20140304845 | ALZHEIMER'S DISEASE SIGNATURE MARKERS AND METHODS OF USE - Methods, biomarkers, and expression signatures are disclosed for assessing the disease progression of Alzheimer's disease (AD). In one embodiment, BioAge (biological age), NdStress (neurodegenerative stress), Alz (Alzheimer), and Inflame (inflammation) are used as biomarkers of AD progression. In another aspect, the invention comprises a gene signature for evaluating disease progression. In still another embodiment, methods for evaluating disease progression are provided. In yet another embodiment, the invention can be used to identify animal models for use in the development and evaluation of therapeutics for the treatment of AD. | 10-09-2014 |
| 20140331341 | AUTOMATED HIGH-CONTENT LIVE ANIMAL DRUG SCREENING USING C. ELEGANS - The present invention relates to methods and compositions for high content drug screening in | 11-06-2014 |
