Animal models of Alzheimer's disease and frontotemporal dementia

By J. Götz, L. Ittner. Nature Reviews Neuroscience, 2008

709 citations recorded by the source corpus.

Subfields: Computational Theory and Mathematics, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/3001a2c4a156c34623702a97230e9f6aabaa4b4b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Computational Theory and Mathematics

1. E. Mandelkow
2. J. Götz
3. L. Ittner
4. Rudolph E. Tanzi
5. Fred H. Gage

In Molecular Biology

1. E. Nestler
2. L. Ittner
3. J. Götz
4. S. Hyman
5. E. Mandelkow
6. Fred H. Gage
7. E. Thies
8. Rudolph E. Tanzi

In Physiology

1. E. Mandelkow
2. S. Hyman
3. L. Ittner
4. J. Götz
5. E. Thies
6. Thomas Wisniewski
7. Rudolph E. Tanzi
8. H. Zempel

Citations in the corpus

• Mitochondrial dysfunction - the beginning of the end in Alzheimer's disease? Separate and synergistic modes of tau and amyloid-β toxicity (2011, background): “Although the hallmark lesions of the disease were already described by Alois Alzheimer in 1906 - amyloid-β (Aβ)containing plaques and microtubule-associated protein tau-containing neurofi brillary tangles (NFTs) - the underlying molecular mechanisms that cause the formation of these end-stage lesion”
• Animal Models of Neuropsychiatric Disorders (2010, background): “For familial Alzheimer's disease, insertion of disease-causing alleles has produced useful rodent model”
• Induced Adult Neurogenesis plus BDNF Mimicks the Effects of Exercise on Cognition in an Alzheimer’s Mouse Model (2018, methodology): “We used the RAM and Y-maze, which are routine methods to assess memory function in AD mice (18), to explore whether increasing AHN also ameliorates AD-associated cognitive impairment in 5×FAD mice.”
• Dendritic function of tau mediates amyloid-beta toxicity in Alzheimer's disease mouse models. (2010, positive): “…phosphorylation, in the absence of deposition and NFT formation, has been reproduced in several transgenic mouse lines that express human APP together with pathogenic mutations identified in familial AD (Go¨tz and Ittner, 2008; Hsiao et al., 1996; Mucke et al., 2000; Sturchler-Pierrat et al., 1997).”
• Aβ Oligomers Cause Localized Ca2+ Elevation, Missorting of Endogenous Tau into Dendrites, Tau Phosphorylation, and Destruction of Microtubules and Spines (2010, background): “Examples of local effects are the early loss of synapses and the appearance of Tau in somata and dendrites (Götz and Ittner, 2008).”
• Amyloid-β and tau — a toxic pas de deux in Alzheimer's disease (2011, background): “The identification of these pathogenic mutations in people with Alzheimer's disease and FTD has assisted in the generation of a plethora of transgenic animal models (reviewed in Ref”
• Alzheimer’s disease: experimental models and reality (2017, background): “In contrast, NFTs readily form in transgenic mice that express human tau containing mutations associated with FTLD; the most commonly used models being those that express 4R tau with P301L or P301S mutations [49, 91, 92, 135, 177].”