Abstract
The present study aims to evaluate the effect of bone marrow mesenchymal stem cells (MSCs) grafts on cognition deficit in chemically and age-induced Alzheimer's models of rats. In the first experiments aged animals (30 months) were tested in Morris water maze (MWM) and divided into two groups: impaired memory and unimpaired memory. Impaired groups were divided into two groups and cannulated bilaterally at the CA1 of the hippocampus for delivery of mesenchymal stem cells (500 × 103/μL) and PBS (phosphate buffer saline). In the second experiment, Ibotenic acid (Ibo) was injected bilaterally into the nucleus basalis magnocellularis (NBM) of young rats (3 months) and animals were tested in MWM. Then, animals with memory impairment received the following treatments: MSCs (500 × 103/μL) and PBS. Two months after the treatments, cognitive recovery was assessed by MWM in relearning paradigm in both experiments. Results showed that MSCs treatment significantly increased learning ability and memory in both age- and Ibo-induced memory impairment. Adult bone marrow mesenchymal stem cells show promise in treating cognitive decline associated with aging and NBM lesions.
Highlights
Alzheimer’s disease (AD) has been called the disease of the century with significant clinical and socioeconomic impacts
The present study aims to evaluate the effect of bone marrow mesenchymal stem cells (MSCs) grafts on cognition deficit in chemically and age-induced Alzheimer’s models of rats
Total time spent in the target quadrant significantly increased in Ibotenic acid (Ibo) + MSCs compared with Ibo + PBS (28.6 ± 2.4 versus 12.8 ± 2.08 s, P < 0.0001)
Summary
Alzheimer’s disease (AD) has been called the disease of the century with significant clinical and socioeconomic impacts. One of the major pathological outcomes of both aging and Alzheimer’s disease is loss of neurons and function in the basal forebrain [5,6,7] especially NBM, the main cholinergic input to the neocortex [8,9,10]. As in humans, age-associated cognitive decline correlates with the degeneration of basal forebrain nuclei [1, 10]. Excitotoxic lesion of the NBM induces memory impairment in several tasks [11,12,13] and it is considered as a suitable approach to study cognitive deficit and dementia in animals [1, 12]
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