Journal
REVIEWS IN THE NEUROSCIENCES
Volume 23, Issue 4, Pages 363-379Publisher
WALTER DE GRUYTER GMBH
DOI: 10.1515/revneuro-2012-0041
Keywords
Alzheimer's disease; epilepsy; motor coordination; myoclonus; paw-clasping; premature death
Categories
Funding
- National Institutes of Health [AG030399]
- Alzheimer's Association of America
Ask authors/readers for more resources
The discovery of gene mutations underlying autosomal dominant Alzheimer's disease has enabled researchers to reproduce several hallmarks of this disorder in transgenic mice, notably the formation of A beta plaques in brain and cognitive deficits. APP transgenic mutants have also been investigated with respect to survival rates, neurologic functions, and motor coordination, which are all susceptible to alteration in Alzheimer dementia. Several transgenic lines expressing human mutated or wild-type APP had higher mortality rates than non-transgenic controls with or without the presence of A beta plaques. Mortality rates were also elevated in APP transgenic mice with vascular amyloid accumulation, thereby implicating cerebrovascular factors in the precocious death observed in all APP transgenic models. In addition, myoclonic jumping has been described in APP mutants, together with seizure activity, abnormal limb-flexion and paw-clasping reflexes, and motor coordination deficits. The neurologic signs resemble the myoclonic movements, epileptic seizures, pathological reflexes, and gait problems observed in late-stage Alzheimer's disease.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available