Neurobiology of Disease Genetic Modulation of Soluble A Rescues Cognitive and Synaptic Impairment in a Mouse Model of Alzheimer’s Disease

نویسندگان

  • Stephanie W. Fowler
  • Angie C. A. Chiang
  • Ricky R. Savjani
  • Megan E. Larson
  • Mathew A. Sherman
  • Dorothy R. Schuler
  • John R. Cirrito
  • Sylvain E. Lesné
  • Joanna L. Jankowsky
چکیده

Stephanie W. Fowler,1* Angie C. A. Chiang,1* Ricky R. Savjani,1,3 Megan E. Larson,4 Mathew A. Sherman,4 Dorothy R. Schuler,5 John R. Cirrito,5 Sylvain E. Lesné,4 and Joanna L. Jankowsky1,2 1Departments of Neuroscience and 2Neurology and Neurosurgery, Huffington Center on Aging, Baylor College of Medicine, Houston, Texas 77030, 3Texas A&M Health Science Center, College Station, Texas 77843, 4Department of Neuroscience, N. Bud Grossman Center for Memory Research and Care, and Institute for Translational Neuroscience, University of Minnesota, Minneapolis, Minnesota 55454, and 5Department of Neurology, Washington University School of Medicine, St. Louis, Missouri 63110

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

The effects of chronic administration of pioglitazone on learning and memory in streptoztocin rat model of Alzheimer’s disease

Background: Alzheimer’s disease (AD) is a chronic neurodegenerative disease characterized by abnormal protein accumulation, synaptic dysfunction, and cognitive impairment. Peroxisome proliferator-activated gamma receptors (PPARγ) play a crucial role in regulating insulin sensitivity and may serve as potential therapeutic targets for AD. Pioglitazone (Piog) as a PPARγ   agonist reduce β-amyloid ...

متن کامل

Genetic modulation of soluble Aβ rescues cognitive and synaptic impairment in a mouse model of Alzheimer's disease.

An unresolved debate in Alzheimer's disease (AD) is whether amyloid plaques are pathogenic, causing overt physical disruption of neural circuits, or protective, sequestering soluble forms of amyloid-β (Aβ) that initiate synaptic damage and cognitive decline. Few animal models of AD have been capable of isolating the relative contribution made by soluble and insoluble forms of Aβ to the behavior...

متن کامل

The reversal effect of mefenamic acid in the sporadic model of Alzheimer's disease in rat: a behavioral analysis

Alzheimer’s disease (AD) is a chronic neurodegenerative disease causing progressive impairment of memory and cognitive function. Streptozotocin (STZ) injection into the brain is known to cause cognitive impairment in rats and is similar to sporadic AD in humans. Several lines of evidence have indicated that an inflammatory process contributes to the pathology of AD. On the basis of the results ...

متن کامل

The reversal effect of mefenamic acid in the sporadic model of Alzheimer's disease in rat: a behavioral analysis

Alzheimer’s disease (AD) is a chronic neurodegenerative disease causing progressive impairment of memory and cognitive function. Streptozotocin (STZ) injection into the brain is known to cause cognitive impairment in rats and is similar to sporadic AD in humans. Several lines of evidence have indicated that an inflammatory process contributes to the pathology of AD. On the basis of the results ...

متن کامل

Cholinergic neuropathology in a mouse model of Alzheimer's disease

Transgenic mice over-expressing mutant human amyloid precursor protein (PDAPP mouse) develop several Alzheimer’s disease (AD)-like lesions including an age-related accumulation of amyloid-?-containing neuritic plaques. Although aged, heterozygous PDAPP mice also exhibit synaptic and glial cell changes, that is characteristic of AD pathology, no evidence of neurodegeneration has been observed. T...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2014