Butyrylcholinesterase is associated with β-amyloid plaques in the transgenic APPSWE/PSEN1dE9 mouse model of Alzheimer disease.

نویسندگان

  • Sultan Darvesh
  • Meghan K Cash
  • George Andrew Reid
  • Earl Martin
  • Arnold Mitnitski
  • Changiz Geula
چکیده

Histochemical analysis of Alzheimer disease (AD) brain tissues indicates that butyrylcholinesterase (BuChE) is present in β-amyloid (Aβ) plaques. The role of BuChE in AD pathology is unknown, but an animal model developing similar BuChE-associated Aβ plaques could provide insights. The APPSWE/PSEN1dE9 transgenic mouse (ADTg), which develops Aβ plaques, was examined to determine if BuChE associates with these plaques, as in AD. We found that in mature ADTg mice, BuChE activity associated with Aβ plaques. The Aβ-, thioflavin-S- and BuChE-positive plaques mainly accumulated in the olfactory structures, cerebral cortex, hippocampal formation, amygdala, and cerebellum. No plaques were stained for acetylcholinesterase activity. The distribution and abundance of plaque staining in ADTg closely resembled many aspects of plaque staining in AD. Butyrylcholinesterase staining consistently showed fewer plaques than were detected with Aβ immunostaining but a greater number of plaques than were visualized with thioflavin-S. Double-labeling experiments demonstrated that all BuChE-positive plaques were Aβ positive, whereas only some BuChE-positive plaques were thioflavin-S positive. These observations suggest that BuChE is associated with a subpopulation of Aβ plaques and may play a role in AD plaque maturation. A further study of this animal model could clarify the role of BuChE in AD pathology.

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

Effect of Long-term Exposure to Extremely Low-frequency Electromagnetic Fields on β-amyloid Deposition and Microglia Cells in an Alzheimer Model in Rats

Background: Recently, researchers have considered extremely low-frequency electromagnetic fields (ELF-EMFs), as one of the non-invasive therapies, in the treatment of many severe neurological disorders, including Alzheimer Disease (AD). AD is a progressive neurodegenerative disease characterized by the deposition of amyloid plaques in the brain. However, the increase in microglial cells increas...

متن کامل

Combination treatment with leptin and pioglitazone in a mouse model of Alzheimer's disease

INTRODUCTION Combination therapy approaches may be necessary to address the many facets of pathologic change in the brain in Alzheimer's disease (AD). The drugs leptin and pioglitazone have previously been shown individually to have neuroprotective and anti-inflammatory actions, respectively, in animal models. METHODS We studied the impact of combined leptin and pioglitazone treatment in 6-mo...

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

Butyrylcholinesterase-knockout reduces brain deposition of fibrillar β-amyloid in an Alzheimer mouse model

In Alzheimer's disease (AD), numerous β-amyloid (Aβ) plaques are associated with butyrylcholinesterase (BChE) activity, the significance of which is unclear. A mouse model, containing five human familial AD genes (5XFAD), also develops Aβ plaques with BChE activity. Knock-out of BChE in this model showed diminished fibrillar Aβ plaque deposition, more so in males than females. This suggests tha...

متن کامل

Op-brai150131 2005..2019

Endophilin-B1, also known as Bax-interacting factor 1 (Bif-1, and encoded by SH3GLB1), is a multifunctional protein involved in apoptosis, autophagy and mitochondrial function. We recently described a unique neuroprotective role for neuron-specific alternatively spliced isoforms of endophilin-B1. To examine whether endophilin-B1-mediated neuroprotection could be a novel therapeutic target for A...

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:
  • Journal of neuropathology and experimental neurology

دوره 71 1  شماره 

صفحات  -

تاریخ انتشار 2012