[Abstract Title]. - Society for Neuroscience

Program#/Poster#: 245.2/N8
Topic: C.01.h. Tau
Support: NIH Grant 5AG016570
Title: Fyn kinase is increased in synaptic terminals in Alzheimer‟s Disease
Authors: K. M. HENKINS 1 , S. SOKOLOW 2 , *B. TETER 5 , C. A. MILLER 6 , H. V. VINTERS 7 ,
G. M. COLE 8,3 , K. H. GYLYS 4 ;
2 Sch. of Nursing, 3 Sch. of Med. and Neurol., 4 Brain Res. Inst. and Sch. of Nursing, 1 UCLA, Los
Angeles, CA; 5 Geriatrics, UCLA-SFVP MC151, Sepulveda, CA; 6 Dept. of Pathology and
Neurol., Keck Sch. of Medicine, USC, Los Angeles, CA; 7 Pathology and Lab. Medicine,
Neurol., UCLA Sch. of Med., Los Angeles, CA; 8 VAMC GRECC, Sepulveda VA Med. Ctr.,
Sepulveda, CA
Abstract: Overexpression of Fyn, a tyrosine kinase in the Src family, and Aβ in double
transgenic animals (FYN/hAPP J-9) creates a phenotype with cognitive impairment that is very
similar to transgenic animals expressing much higher levels of Aβ (Palop et al. 2005) and
removing Fyn all together blocks some types of Aβ induced neurotoxicity (Lambert et al. 1998,
Chin et al. 2004). Fyn is relocated in AD brains from synapses to neuronal bodies where it was
found to co-localize with neurofibrillary tangles (Ho et al. 2005). Using flow cytometry analysis
of synaptosomes prepared from post-mortem AD cortex, we have previously demonstrated that
synaptic Aβ elevations are accompanied by pathologic changes and are co-localized with p-tau.
In the present experiments, synaptosomes from our cohort of AD cases and normal controls were
immunolabeled with an antibody directed against Fyn kinase (BD Transduction Laboratories,
Franklin Lakes, NJ), and immunolabeling was quantified by flow cytometry. AD cases (16.44%
positive ± 7.98, n =14) demonstrated elevated Fyn labeling compared to aged normal control
cases (7.12% positive ± 0.54, n = 4, p