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Inhibition of long term memory and induction of biochemical deficits in rats following protofibrillar Aβ 1-42 injection

B. Nehru, S. Sharma (Chandigarh, India)

Meeting: 2017 International Congress

Abstract Number: 615

Keywords: Cognitive dysfunction

Session Information

Date: Tuesday, June 6, 2017

Session Title: Pathophysiology (Other Movement Disorders)

Session Time: 1:45pm-3:15pm

Location: Exhibit Hall C

Objective: The present study was undertaken to study the effects of single intracerebroventricular (i.c.v.) injection of protofibrillar Aβ 1-42 on the long term memory

Background: Amyloid-beta (Aβ) peptide deposition into insoluble plaques is a pathological hallmark of Alzheimer’s disease (AD) but the soluble oligomeric Aβ has been hypothesized to directly impair the learning and memory in AD. Evidences from some clinical studies indicated that Aβ protofibril formation is induced by the Arctic mutation (E22G) and is the major cause for early AD onset. However, the biochemical mechanism involved in the protofibril-induced toxicity is not very well addressed. 

Methods: Rats were divided into two groups (n = 5 per group): (1) sham control group and (2) Aβ 1-42 injected group. A single dose of protofibrillar Aβ 1-42 (5 ul) through i.c.v. injection was bilaterally administered to 2nd group animals while sham control animals were administered with 5 ul of vehicle

Results: The results demonstrated that protofibrillar Aβ significantly induced reactive oxygen species (ROS) production, acetylcholinesterase activity, nitrite levels and lipid peroxidation in hippocampus, cortex and striatum regions after six weeks. Also, the behavioral studies have shown an increase in the anxiety levels and inhibition of long term memory after protofibrillar Aβ injection. The activity of antioxidant enzymes was also significantly reduced after protofibrillar Aβ injection in hippocampus, cortex and striatum regions. Thioflavin-T staining confirmed the presence of amyloid deposits and Nissl’s staining have shown the neuronal loss after six weeks of protofibrillar Aβ injection

Conclusions: The present study indicated that protofibrillar Aβ 1-42 injection inhibits the long term memory and also leads to various biochemical alterations. 

To cite this abstract in AMA style:

B. Nehru, S. Sharma. Inhibition of long term memory and induction of biochemical deficits in rats following protofibrillar Aβ 1-42 injection [abstract]. Mov Disord. 2017; 32 (suppl 2). https://www.mdsabstracts.org/abstract/inhibition-of-long-term-memory-and-induction-of-biochemical-deficits-in-rats-following-protofibrillar-a%ce%b2-1-42-injection/. Accessed June 15, 2025.
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