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Schnöder et al., 2020 - Google Patents

Neuronal deficiency of p38α‐MAPK ameliorates symptoms and pathology of APP or Tau‐transgenic Alzheimer's mouse models

Schnöder et al., 2020

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Document ID
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 …
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    • C12Q1/00Measuring or testing processes involving enzymes, nucleic acids or micro-organisms; Compositions therefor; Processes of preparing such compositions
    • C12Q1/68Measuring or testing processes involving enzymes, nucleic acids or micro-organisms; Compositions therefor; Processes of preparing such compositions involving nucleic acids
    • C12Q1/6876Hybridisation probes
    • C12Q1/6883Hybridisation probes for diseases caused by alterations of genetic material
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    • A61KPREPARATIONS FOR MEDICAL, DENTAL, OR TOILET PURPOSES
    • A61K31/00Medicinal preparations containing organic active ingredients
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    • C12N15/00Mutation or genetic engineering; DNA or RNA concerning genetic engineering, vectors, e.g. plasmids, or their isolation, preparation or purification; Use of hosts therefor
    • C12N15/09Recombinant DNA-technology
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    • G01MEASURING; TESTING
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