scholarly journals Genetic Ablation of Hematopoietic Cell Kinase Accelerates Alzheimer’s Disease–Like Neuropathology in Tg2576 Mice

2020 ◽  
Vol 57 (5) ◽  
pp. 2447-2460 ◽  
Author(s):  
Siok Lam Lim ◽  
Diana Nguyen Tran ◽  
Zanett Kieu ◽  
Christine Chen ◽  
Emmanuel Villanueva ◽  
...  
Glia ◽  
2018 ◽  
Vol 66 (12) ◽  
pp. 2700-2718 ◽  
Author(s):  
Siok Lam Lim ◽  
Diana Nguyen Tran ◽  
Joannee Zumkehr ◽  
Christine Chen ◽  
Sagar Ghiaar ◽  
...  

2011 ◽  
Vol 178 (3) ◽  
pp. 1298-1308 ◽  
Author(s):  
Yujie Cui ◽  
Mingwei Huang ◽  
Yingbo He ◽  
Shuyan Zhang ◽  
Yongzhang Luo

2010 ◽  
Author(s):  
Pu Chen ◽  
Xiaoling Shang ◽  
Zanchao Liu ◽  
Xiuqin Yao ◽  
Seong-Joon Baek ◽  
...  

2009 ◽  
Vol 18 (23) ◽  
pp. 4492-4500 ◽  
Author(s):  
J. C. Mitchell ◽  
B. B. Ariff ◽  
D. M. Yates ◽  
K.-F. Lau ◽  
M. S. Perkinton ◽  
...  

2011 ◽  
Vol 7 ◽  
pp. S666-S666
Author(s):  
David Singer ◽  
Monique Richter ◽  
Agneta Mewes ◽  
Manuela Fritsch ◽  
Corinna Höfling ◽  
...  

2007 ◽  
Vol 204 (6) ◽  
pp. 1273-1280 ◽  
Author(s):  
Kuen-Jer Tsai ◽  
Yueh-Chiao Tsai ◽  
Che-Kun James Shen

Most of the current clinical treatments for Alzheimer's disease (AD) are largely symptomatic and can have serious side effects. We have tested the feasibility of using the granulocyte colony-stimulating factor (G-CSF), which is known to mobilize hematopoietic stem cells (HSCs) from the bone marrow into the peripheral blood, as a therapeutic agent for AD. Subcutaneous administration of G-CSF into two different β-amyloid (Aβ)–induced AD mouse models substantially rescued their cognitive/memory functions. The rescue was accompanied by the accumulation of 5-bromo-2′deoxyuridine–positive HSCs, as well as local neurogenesis surrounding the Aβ aggregates. Furthermore, the level of acetylcholine in the brains of Tg2576 mice was considerably enhanced upon G-CSF treatment. We suggest that G-CSF, a drug already extensively used for treating chemotherapy-induced neutropenia, should be pursued as a novel, noninvasive therapeutic agent for the treatment of AD.


2013 ◽  
Vol 9 ◽  
pp. P329-P329
Author(s):  
Gururaj Joshi ◽  
Kok-Ann Gan ◽  
Joshua Everson ◽  
Jeffrey Johnson

Endocrinology ◽  
2015 ◽  
Vol 156 (12) ◽  
pp. 4592-4603 ◽  
Author(s):  
Karen Sooy ◽  
June Noble ◽  
Andrew McBride ◽  
Margaret Binnie ◽  
Joyce L. W. Yau ◽  
...  

Chronic exposure to elevated levels of glucocorticoids has been linked to age-related cognitive decline and may play a role in Alzheimer's disease. In the brain, 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) amplifies intracellular glucocorticoid levels. We show that short-term treatment of aged, cognitively impaired C57BL/6 mice with the potent and selective 11β-HSD1 inhibitor UE2316 improves memory, including after intracerebroventricular drug administration to the central nervous system alone. In the Tg2576 mouse model of Alzheimer's disease, UE2316 treatment of mice aged 14 months for 4 weeks also decreased the number of β-amyloid (Aβ) plaques in the cerebral cortex, associated with a selective increase in local insulin-degrading enzyme (involved in Aβ breakdown and known to be glucocorticoid regulated). Chronic treatment of young Tg2576 mice with UE2316 for up to 13 months prevented cognitive decline but did not prevent Aβ plaque formation. We conclude that reducing glucocorticoid regeneration in the brain improves cognition independently of reduced Aβ plaque pathology and that 11β-HSD1 inhibitors have potential as cognitive enhancers in age-associated memory impairment and Alzheimer's dementia.


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