scholarly journals Peripheral Treatment with Enoxaparin, a Low Molecular Weight Heparin, Reduces Plaques and  -Amyloid Accumulation in a Mouse Model of Alzheimer's Disease

2004 ◽  
Vol 24 (17) ◽  
pp. 4181-4186 ◽  
Author(s):  
L. Bergamaschini
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Weight ◽  
Mouse Model ◽  
Low Molecular Weight Heparin ◽  
Low Molecular Weight ◽  
Model Of Alzheimer’S Disease ◽  
Amyloid Accumulation

Inhibiting TLR2 activation attenuates amyloid accumulation and glial activation in a mouse model of Alzheimer’s disease

2016 ◽  
Vol 58 ◽  
pp. 191-200 ◽  
Author(s):  
Claire L. McDonald ◽  
Edel Hennessy ◽  
Ana Rubio-Araiz ◽  
Brian Keogh ◽  
William McCormack ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Glial Activation ◽  
Model Of Alzheimer’S Disease ◽  
Amyloid Accumulation ◽  
Tlr2 Activation

scholarly journals Presenilin-2 Mutation Causes Early Amyloid Accumulation and Memory Impairment in a Transgenic Mouse Model of Alzheimer's Disease

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Toshihiko Toda ◽  
Yoshihiro Noda ◽  
Genzo Ito ◽  
Masahiro Maeda ◽  
Takahiko Shimizu
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Memory Impairment ◽  
Amyloid Β Protein ◽  
Model Of Alzheimer’S Disease ◽  
Amyloid Accumulation ◽  
Presenilin 2 ◽  
Tg2576 Mice

In order to clarify the pathophysiological role of presenilin-2 (PS2) carrying the Volga German Kindred mutation (N141I) in a conventional mouse model of Alzheimer's disease (AD) expressing amyloid precursor protein (APP) with the Swedish mutation (Tg2576 line), we generated a double transgenic mouse (PS2Tg2576) by crossbreeding the PS2 mutant with Tg2576 mice. Here, we demonstrate that the PS2 mutation induced the early deposition of amyloid β-protein (Aβ) at 2-3 months of age and progressive accumulation at 4-5 months of age in the brains of the mutant mice. The PS2 mutation also accelerated learning and memory impairment associated with Aβ accumulation at 4-5 months of age in Tg2576 mice. These results suggest that the PS2 mutation causes early cerebral amyloid accumulation and memory dysfunction. PS2Tg2576 mice are a suitable mouse model for studying amyloid-lowering therapies.

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