Valproic acid inhibits Ab production, neuritic plaque formation, and behavioral deficits in Alzheimer's disease mouse models

2008 ◽  
Vol 183 (3) ◽  
pp. i8-i8
Author(s):  
Hong Qing ◽  
Guiqiong He ◽  
Philip T.T. Ly ◽  
Christopher J. Fox ◽  
Matthias Staufenbiel ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Valproic Acid ◽  
Mouse Models ◽  
Plaque Formation ◽  
Neuritic Plaque ◽  
Behavioral Deficits

scholarly journals Valproic acid inhibits Aβ production, neuritic plaque formation, and behavioral deficits in Alzheimer's disease mouse models

2008 ◽  
Vol 205 (12) ◽  
pp. 2781-2789 ◽  
Author(s):  
Hong Qing ◽  
Guiqiong He ◽  
Philip T. T. Ly ◽  
Christopher J. Fox ◽  
Matthias Staufenbiel ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Valproic Acid ◽  
Amyloid Β ◽  
Memory Deficits ◽  
Plaque Formation ◽  
Neuritic Plaque ◽  
Amyloid Β Protein ◽  
Neuritic Plaques ◽  
Aβ Production

Neuritic plaques in the brains are one of the pathological hallmarks of Alzheimer's disease (AD). Amyloid β-protein (Aβ), the central component of neuritic plaques, is derived from β-amyloid precursor protein (APP) after β- and γ-secretase cleavage. The molecular mechanism underlying the pathogenesis of AD is not yet well defined, and there has been no effective treatment for AD. Valproic acid (VPA) is one of the most widely used anticonvulsant and mood-stabilizing agents for treating epilepsy and bipolar disorder. We found that VPA decreased Aβ production by inhibiting GSK-3β–mediated γ-secretase cleavage of APP both in vitro and in vivo. VPA treatment significantly reduced neuritic plaque formation and improved memory deficits in transgenic AD model mice. We also found that early application of VPA was important for alleviating memory deficits of AD model mice. Our study suggests that VPA may be beneficial in the prevention and treatment of AD.

Dihydromyricetin Ameliorates Behavioral Deficits and Reverses Neuropathology of Transgenic Mouse Models of Alzheimer’s Disease

2014 ◽  
Vol 39 (6) ◽  
pp. 1171-1181 ◽  
Author(s):  
Jing Liang ◽  
A. Kerstin Lindemeyer ◽  
Yi Shen ◽  
Héctor E. López-Valdés ◽  
Hilda Martínez-Coria ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mouse ◽  
Mouse Models ◽  
Transgenic Mouse Models ◽  
Behavioral Deficits

scholarly journals Amyloid β 1-42 deposits do not lead to Alzheimer's neuritic plaques in aged dogs

1996 ◽  
Vol 313 (2) ◽  
pp. 575-580 ◽  
Author(s):  
Thomas WISNIEWSKI ◽  
Maciej LALOWSKI ◽  
Marketta BOBIK ◽  
Michael RUSSELL ◽  
Joanna STROSZNAJDER ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Senile Plaques ◽  
Amyloid Β ◽  
Plaque Formation ◽  
Neuritic Plaque ◽  
Amyloid Angiopathy ◽  
Neuritic Plaques ◽  
Cerebral Vessel ◽  
Aβ Peptides

In Alzheimer's disease, amyloid β (Aβ) is deposited in senile plaques and amyloid angiopathy. Longer Aβ peptides, which extend to residue 42 (Aβ42), have been suggested to be critical for the seeding of amyloid. Aged dogs develop cerebral vessel amyloid and parenchymal preamyloid lesions. Preamyloid in humans is related to senile plaques, whereas in dogs such progression is rare. We evaluated the composition of aged canine vessel amyloid and preamyloid both biochemically and immunohistochemically. The vessel amyloid extended mainly to residue 40 (Aβ40), while preamyloid contained a mixture of Aβ17-42 and Aβ42, with minimal Aβ40. Our results suggest other factors besides Aβ42 are important for neuritic plaque formation.

scholarly journals CXCR3 promotes plaque formation and behavioral deficits in an Alzheimer’s disease model

2014 ◽  
Vol 125 (1) ◽  
pp. 365-378 ◽  
Author(s):  
Marius Krauthausen ◽  
Markus P. Kummer ◽  
Julian Zimmermann ◽  
Elisabet Reyes-Irisarri ◽  
Dick Terwel ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Model ◽  
Plaque Formation ◽  
Behavioral Deficits

scholarly journals Erratum to: Dihydromyricetin Ameliorates Behavioral Deficits and Reverses Neuropathology of Transgenic Mouse Models of Alzheimer’s Disease

2014 ◽  
Vol 39 (7) ◽  
pp. 1403-1403 ◽  
Author(s):  
Jing Liang ◽  
Héctor E. López-Valdés ◽  
Hilda Martínez-Coria ◽  
A. Kerstin Lindemeyer ◽  
Yi Shen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mouse ◽  
Mouse Models ◽  
Transgenic Mouse Models ◽  
Behavioral Deficits
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