Memory deficits in APP23/Abca1+/− mice correlate with the level of Aβ oligomers

@inproceedings{Lefterov2009MemoryDI,
  title={Memory deficits in APP23/Abca1+/− mice correlate with the level of Aβ oligomers},
  author={Iliya Lefterov and Nicholas F. Fitz and Andrea A Cronican and Preslav I Lefterov and Matthias Staufenbiel and Radosveta Koldamova},
  booktitle={ASN neuro},
  year={2009}
}
ABCA1, a member of the ATP-binding cassette family of transporters, lipidates ApoE (apolipoprotein A) and is essential for the generation of HDL (high-density lipoprotein)-like particles in the CNS (central nervous system). Lack of Abca1 increases amyloid deposition in several AD (Alzheimer's disease) mouse models. We hypothesized that deletion of only one copy of Abca1 in APP23 (where APP is amyloid precursor protein) AD model mice will aggravate memory deficits in these mice. Using the Morris… CONTINUE READING

Citations

Publications citing this paper.
Showing 1-10 of 20 extracted citations

Deletion of Abca7 increases cerebral amyloid-β accumulation in the J20 mouse model of Alzheimer's disease.

The Journal of neuroscience : the official journal of the Society for Neuroscience • 2013
View 3 Excerpts
Highly Influenced

References

Publications referenced by this paper.
Showing 1-10 of 39 references

Liver X receptor signaling pathways in cardiovascular disease.

Molecular endocrinology • 2003
View 12 Excerpts
Highly Influenced

Similar Papers

Loading similar papers…