Metaplasticity mechanisms restore plasticity and associativity in an animal model of Alzheimer’s disease

• DOI: 10.1073/pnas.1613700114
• Publication Date: 2017-05-09T01:00:30Z
• Authors: Qin Li; Sheeja Navakkode; Martin Rothkegel; Tuck Wah Soong; Sreedharan Sajikumar; Martin Korte
• Keywords: 0301 basic medicine; 0303 health sciences; Neuronal Plasticity; Amyloidogenic Proteins; Mice, Transgenic; Ryanodine Receptor Calcium Release Channel; 3. Good health; Disease Models, Animal; Mice; 03 medical and health sciences; Alzheimer Disease; Presenilin-1; Animals; Humans; Protein Kinase C

Significance Under physiological conditions, metaplasticity is ideally suited to prepare neuronal networks for encoding specific information, thereby ensuring subsequent learning and long-lasting memory storage. Our capacity lies at the heart of all cognitive function, correct scaling synaptic plasticity vital normal brain function. Here we present data from amyloid precursor protein (APP)/presenilin-1 (PS1) mice, a mouse model Alzheimer’s disease, indicating that failure neurons scale predisposition undergo after earlier events (i.e., metaplasticity) might be determinant disease onset progression. findings indicate induction by ryanodine receptor activation contributes reestablishment associativity in hippocampal APP/PS1 mice potential therapeutic target.