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P4‐019: IDENTIFICATION OF SYNAPTIC TAU ANTIBODIES IN ALZHEIMER'S DISEASE AND RELATED TAUOPATHIES
Author(s) -
Tai Chin-Yin,
Ma Haou-Tzong,
Huang Sheng-Chieh,
Li Chung-Lin,
Wu Meng-Fang,
Wu Chia-Lin,
Serrano Geidy E.,
Beach Thomas G.,
Jang Ming-Kuei
Publication year - 2018
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.2018.06.2421
Subject(s) - neuroscience , synaptic vesicle , antibody , alzheimer's disease , synapse , cognitive decline , biology , chemistry , disease , biochemistry , pathology , dementia , medicine , immunology , vesicle , membrane
and biochemical assessments were conducted in plasma and spinal cord tissue. Results: MIA-induced OA resulted in hindpaw mechanical hypersensitivity (allodynia), initiating on day 3 (p < 0.001), in TASTPM and controls. However, from 14-28 days, TASTPM displayed partial reversal of allodynia. Naloxone, an opioid antagonist, re-established allodynia in TASTPM (p 1⁄4 0.029) as observed in WT controls. Morphine, an opioid agonist, induced heightened analgesia in AD-mice (p 1⁄4 0.041). TASTPM exhibited elevated plasma level of b-endorphin post MIA (p 1⁄4 0.038 vs. WT) which correlated with the impaired allodynia (R 1⁄4 0.589; p1⁄4 0.044). Finally, diminished spinal microglial response was observed in the TASTPM compared to controls. Conclusions: This study indicates disrupted opioidergic system in parallel with reduced excitation in the spinal cord of TASTPM as possible mechanisms underlying impaired chronic pain sensitivity in AD. This work provides basis for re-evaluation of opioid analgesic-use for management of pain in AD.