Schnöder et al., 2020 - Google Patents
Neuronal deficiency of p38α‐MAPK ameliorates symptoms and pathology of APP or Tau‐transgenic Alzheimer's mouse modelsSchnöder et al., 2020
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- 9848864617033143340
- Author
- Schnöder L
- Gasparoni G
- Nordström K
- Schottek A
- Tomic I
- Christmann A
- Schäfer K
- Menger M
- Walter J
- Fassbender K
- Liu Y
- Publication year
- Publication venue
- The FASEB Journal
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Snippet
Alzheimer's disease (AD) is the leading cause of dementia with very limited therapeutic options. Amyloid β (Aβ) and phosphorylated Tau (p‐Tau) are key pathogenic molecules in AD. P38α‐MAPK is specifically activated in AD lesion sites. However, its effects on AD …
- 230000001537 neural 0 title abstract description 63
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- C12Q1/00—Measuring or testing processes involving enzymes, nucleic acids or micro-organisms; Compositions therefor; Processes of preparing such compositions
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- C12Q1/6876—Hybridisation probes
- C12Q1/6883—Hybridisation probes for diseases caused by alterations of genetic material
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- A61K31/00—Medicinal preparations containing organic active ingredients
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- A61K31/395—Heterocyclic compounds having nitrogen as a ring hetero atom, e.g. guanethidine, rifamycins
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- C12Q2600/00—Oligonucleotides characterized by their use
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- C12N15/09—Recombinant DNA-technology
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- 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 the preceding groups
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- G01N33/50—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing
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