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Page 16 of 24 Neuroimmunol Neuroinflammation 2019;6:15 I http://dx.doi.org/10.20517/2347-8659.2019.019

by Morris water maze one day after isoflurane treatment. Our results show that the number of fragmented
Golgi and Cdk5 activity increased. Learning and memory ability were impaired in aged mice after
isoflurane exposure, while Cdk5 inhibitor roscovitine rescued the Golgi structure and improved learning
and memory performances. In addition, after isoflurane exposure, the levels of p25/p35 increased, while
Cdk5 levels unchanged. Our study reveals that the cleavage of p35 into p25 may contribute to aberrant
Cdk5 activation, and Cdk5 overactivation-induced Golgi fragmentation may mediate isoflurane-induced
cognitive decline in aged mice. Inhibition of aberrant Cdk5 activation alleviates Golgi fragmentation and
cognitive decline, which provides a potential therapeutic approach for isoflurane-induced cognitive decline.

22. A novel analytical method for detection of phosphorylated a-synuclein S129 in Parkinson’s
disease

1
1
2
1
Charles S. Y. Yang , Huei-Chun Liu , Chia-Shin Ho , Hsin-Hsien Chen , Wen-Ping Chen , Chin-
1
Hsien Lin , Ming-Jang Chiu 3
3
1 MagQu Co., Ltd., New Taipei City 231, Taiwan
2 MagQu LLC, Surprise, AZ, US
3 Department of Neurology, National Taiwan University Hospital, Taipei 100, Taiwan
Parkinson’s disease (PD) is characterized by the intraneuronal α-synuclein inclusions called Lewy bodies.
Increase of phosphorylation of a-synuclein in Serine 129 (pS129) has been correlated with the aggregation,
toxicity, protein interaction, and turnover of α-synuclein. Thus, pS129 can indicate the pathogenesis
of PD. Since the concentration of pS129 in the plasma (femtogram level) is far lower than the normal
detection range of ELISA, we developed an ultrasensitive immunomagnetic reduction assay to detect the
trace amount of pS129 in limited volume of human plasma (60 μL). The pS129 assay covered a range of
concentration (0.00048-144.78 pg/mL) with a limit of detection of 0.065 fg/mL. Furthermore, we analyzed
the pS129 level from healthy control (n = 10) and patients with PD (n = 23) and found a significant increase
of pS129 in plasma from PD (P < 0.0001). The cut-off value of pS129 for discriminating control from PD
was 0.505 fg/mL with corresponding clinical sensitivity and specificity of 95.65% and 100%, respectively.
In conclusion, we developed a novel plasma pS129 assay that is convenient, sensitive, sample saving, and
useful for identifying PD patients.

23. Linking autism to an imbalanced catabolism of synaptic monoamine

Dominique G. Béroule

LIMSI (Computer Sciences Laboratory for Mechanics and Engineering Sciences), CNRS, rue John Von
Neumann, Campus Universitaire d’Orsay - B.508, 91403 Orsay

An interdisciplinary study of autism led to implicate a relatively poor catabolism of one of the monoamines
released in the synapse, namely serotonin. This deficit would result from persistent epigenetic regulations
of two enzymes (i.e., MAOA- and COMT+) across neural differentiation, for counteracting an accidental
excess of MAOA in the early gestation. Epigenetic traits would outlast this temporary excess and be
inherited by generations of neurons, and possibly by next human generations. In addition, the late
occurrence of autistic symptoms may be consistent with the increase of the monoamine oxidase B (MAOB)