An 8-year-old, castrated male Shih-tzu dog (Case 1) showing ataxia and gait disorder was referred for neurological examination and magnetic resonance imaging. Through comprehensive examinations, the patient was tentatively diagnosed with meningoencephalitis of unknown origin (MUO) and treatment with prednisolone and cytosine arabinoside was started. The symptoms were improving with immunosuppressive treatment. However, severe bacterial cystitis occurred and we could not avoid tapering off prednisolone. Then, neurological signs recurred. Therefore, we added crisdesalazine, which allowed us to reduce the daily dosage of immunosuppressants easily. In another case, a 4-year-old, spayed female Yorkshire terrier dog (Case 2) was referred to our hospital showing a head tilt, circling, and loss of the menace reflex. The patient was tentatively diagnosed with MUO and treatment with some immunosuppressants was attempted. The clinical symptoms improved, but the alleviation was inadequate. Thus, we added crisdesalazine. The neurological signs then markedly improved. Moreover, the drugs could be tapered off more easily than before. Crisdesalazine is a novel drug that has antioxidant and anti-inflammatory action in brain disease and is used particularly for dementia. In this paper, we tried an off-label use of this drug in canine MUO patients, and found that it had, in these two patients, additional therapeutic effects on the MUO.

01 Dec 2020·Nature NeuroscienceQ1 · MEDICINE

Severe reactive astrocytes precipitate pathological hallmarks of Alzheimer’s disease via H2O2− production

Q1 · MEDICINE

Article

Author: Lee, Seung Eun ; Won, Woojin ; Ryu, Hoon ; Jo, Seonmi ; Park, Yongmin Mason ; Shin, Jin Hee ; Cho, Hansang ; Cho, Hyesun ; Lee, C Justin ; Kim, Yunha ; Ju, Yeonha ; Gwag, Byoung Joo ; Kang, You Jung ; Kim, Daesoo ; Seo, Jeong-Sun ; Kim, Doo Yeon ; Chun, Heejung ; Park, Ki Duk ; Kim, Young Soo ; Woo, Junsung ; Hwang, Yujin ; Im, Hyeonjoo ; Kaang, Bong-Kiun ; Kim, Sunpil ; Lim, Jiwoon ; Park, Jong-Hyun ; Lee, Jaekwang

Although the pathological contributions of reactive astrocytes have been implicated in Alzheimer's disease (AD), their in vivo functions remain elusive due to the lack of appropriate experimental models and precise molecular mechanisms. Here, we show the importance of astrocytic reactivity on the pathogenesis of AD using GiD, a newly developed animal model of reactive astrocytes, where the reactivity of astrocytes can be manipulated as mild (GiDm) or severe (GiDs). Mechanistically, excessive hydrogen peroxide (H₂O₂) originated from monoamine oxidase B in severe reactive astrocytes causes glial activation, tauopathy, neuronal death, brain atrophy, cognitive impairment and eventual death, which are significantly prevented by AAD-2004, a potent H₂O₂ scavenger. These H₂O₂^--induced pathological features of AD in GiDs are consistently recapitulated in a three-dimensional culture AD model, virus-infected APP/PS1 mice and the brains of patients with AD. Our study identifies H₂O₂ from severe but not mild reactive astrocytes as a key determinant of neurodegeneration in AD.

30 Mar 2013·Experimental NeurobiologyQ4 · MEDICINE

AAD-2004 Attenuates Progressive Neuronal Loss in the Brain of Tg-betaCTF99/B6 Mouse Model of Alzheimer Disease

Q4 · MEDICINE

Article

Author: Han, Pyung-Lim ; Baek, In-Sun ; Lee, Young Ae ; Gwag, Byoung Joo ; Seo, Ji-Seon ; Kim, Tae-Kyung ; Lee, Kang-Woo ; Cho, Jaeyoung

Alzheimer's disease (AD) is a neurodegenerative disease that proceeds with the age-dependent neuronal loss, an irreversible event which causes severe cognitive and psychiatric devastations. In the present study, we investigated whether the compound, AAD-2004 [2-hydroxy-5-[2-(4-trifluoromethylphenyl)-ethylaminobenzoic acid] which has anti-oxidant and anti-inflammatory properties, is beneficial for the brain of Tg-betaCTF99/B6 mice, a murine AD model that was recently developed to display age-dependent neuronal loss and neuritic atrophy in the brain. Administration of AAD-2004 in Tg-betaCTF99/B6 mice from 10 months to 18 months of age completely repressed the accumulation of lipid peroxidation in the brain. AAD-2004 markedly suppressed neuronal loss and neuritic atrophy, and partially reversed depleted expression of calbindin in the brain of Tg-beta-CTF99/B6. These results suggest that AAD-2004 affords neurodegeneration in the brain of AD mouse model.

100 Deals associated with Crisdesalazine

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Indication	Highest Phase	Country/Location	Organization	Date
Alzheimer Disease	Phase 1	-	GNT Pharma Co., Ltd.	-
Alzheimer Disease	Phase 1	-	Toyota Tsusho America, Inc.	-
Amyotrophic Lateral Sclerosis	Phase 1	-	GNT Pharma Co., Ltd.	-
Amyotrophic Lateral Sclerosis	Phase 1	-	Toyota Tsusho America, Inc.	-
Arthritis	Phase 1	-	Toyota Tsusho America, Inc.	-
Depressive Disorder	Phase 1	-	Toyota Tsusho America, Inc.	-
Diabetes Mellitus	Phase 1	-	Toyota Tsusho America, Inc.	-
Pancreatitis	Phase 1	-	Toyota Tsusho America, Inc.	-
Parkinson Disease	Phase 1	-	GNT Pharma Co., Ltd.	-
Parkinson Disease	Phase 1	-	Toyota Tsusho America, Inc.	-

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