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[P1–063]: SUVN‐G3031, A SELECTIVE H3 RECEPTOR INVERSE AGONIST: ASSESSMENT OF SAFETY, TOLERABILITY AND PHARMACOKINETICS IN HEALTHY HUMAN VOLUNTEERS
Author(s) -
MuddageswaraRao,
Bhyrapuneni Gopinadh,
Mudigonda Koteshwara,
Jayarajan Pradeep,
Abraham Renny,
Subramanian Ramkumar,
Goyal Vinod Kumar,
Pandey Santosh Kumar,
Boggavarapu Rajesh Kumar,
Ajjala Devender Reddy,
Shinde Anil K.,
Nirogi Ramakrishna
Publication year - 2017
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2017.06.130
Subject(s) - tolerability , pharmacokinetics , medicine , pharmacology , agonist , inverse agonist , adverse effect , receptor
treatment detected blood Ab1-42and p tau 181 levels, and comparison with normal old subjects. Results:Data from 20 AD patients were analyzed in this study. The ADAS-cog score in the treatment group was significantly improved compared to the sham group (ADAS-cog(P1⁄40.003), MMSE (p1⁄40.014), ACE—III (p1⁄40.004)), ADL (P1⁄40.014. Resting-state functional MRI shows brain functional connections related to cognition changing, including the connection between left prefrontal cortex and left inferior frontal gyrus, the right prefrontal cortex and the right cerebellum; but there is no link to other regions in the left temporal lobe. Blood tests found that in experimental group Ab1-42 was lower than those of normal aging control (P 1⁄4 0.04), before and after treatment Ab1-42(P 1⁄4 0.15), group treatment has a rising trend; P tau 181 content was higher than normal aging (p 1⁄4 0.06), treatment has a declining trend, but without statistical significance. Conclusions:The present results suggest that high-frequency rTMS represents a useful adjuvant therapy with AD, which can improve cognitive function and its possible mechanism of magnetic stimulation improving brain function in the left prefrontal cortex is associated with other cognitive function connection area. In addition, rTMS may also affect the patients with pathological markers Ab1-42 / p tau 181, which may also be one of its therapeutic mechanism.