Animal models for Alzheimer's disease and frontotemporal dementia: a perspective
| Autor: | Jürgen Götz, Naeman N. Götz |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2009 |
| Předmět: |
FTD
frontotemporal dementia Amyloid β SOD1 superoxide dismutase 1 Disease Review Bioinformatics frontotemporal dementia PSEN presenilin rat JIP1 c-Jun N-terminal kinase-interacting protein 1 tau GFP green fluorescent protein General Neuroscience amyloid TAR DNA-binding protein 43 (TDP-43) FAD familial AD MND motor neuron disease Alzheimer's disease S11 Fish Drosophila AD Alzheimer's disease Frontotemporal dementia Aβ amyloid β S1 Amyloid TH tyrosine hydroxylase Tau protein Biology S3 PIB Pittsburgh Compound-B PET positron emission tomography lcsh:RC321-571 APP amyloid precursor protein medicine Caenorhabditis elegans CaMKII Ca2+/calmodulin-dependent protein kinase II lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry mouse NFT neurofibrillary tangle transgenic Perspective (graphical) FTDP-17 familial FTD with parkinsonism linked to chromosome 17 medicine.disease zebrafish AGE advanced glycation end-product biology.protein BAC bacterial artificial chromosome Neurology (clinical) TDP-43 TAR DNA-binding protein 43 Neuroscience MRI magnetic resonance imaging Dementia research |
| Zdroj: | ASN NEURO ASN Neuro, Vol 1 (2009) |
| ISSN: | 1759-0914 |
| Popis: | In dementia research, animal models have become indispensable tools. They not only model aspects of the human condition, but also simulate processes that occur in humans and hence provide insight into how disease is initiated and propagated. The present review discusses two prominent human neurodegenerative disorders, Alzheimer's disease and frontotemporal dementia. It discusses what we would like to model in animals and highlights some of the more recent achievements using species as diverse as mice, fish, flies and worms. Advances in imaging and therapy are explored. We also discuss some anticipated new models and developments. These will reveal how key players in the pathogenesis of Alzheimer's disease and frontotemporal dementia, such as the peptide Aβ (amyloid β) and the protein tau, cause neuronal dysfunction and eventually, neuronal demise. Understanding these processes fully will lead to early diagnosis and therapy. |
| Databáze: | OpenAIRE |
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