Abstract
Alzheimer’s disease (AD) has been linked to the degeneration of central cholinergic and glutamatergic transmission, which correlates with progressive memory loss and the accumulation of amyloid-β (Aβ). It has been claimed that aged garlic extract (AGE) has a beneficial effect in preventing neurodegeneration in AD. Therefore, the objective of this study was to investigate the effects of AGE on Aβ-induced cognitive dysfunction with a biochemical basis in the cholinergic, glutamatergic, and GABAergic systems in rats. Adult male Wistar rats were orally administered three doses of AGE (125, 250, and 500 mg/kg) daily for 65 days. At day 56, they were injected with 1 μL of aggregated Aβ (1–42) into each lateral ventricle, bilaterally. After six days of Aβ injection, the rats’ working and reference memory was tested using a radial arm maze. The rats were then euthanized to investigate any changes to the cholinergic neurons, vesicular glutamate transporter 1 and 2 proteins (VGLUT1 and VGLUT2), and glutamate decarboxylase (GAD) in the hippocampus. The results showed that AGE significantly improved the working memory and tended to improve the reference memory in cognitively-impaired rats. In addition, AGE significantly ameliorated the loss of cholinergic neurons and increased the VGLUT1 and GAD levels in the hippocampus of rat brains with Aβ-induced toxicity. In contrast, the VGLUT2 protein levels did not change in any of the treated groups. We concluded that AGE was able to attenuate the impairment of working memory via the modification of cholinergic neurons, VGLUT1, and GAD in the hippocampus of Aβ-induced rats.
Highlights
Memory formation is a complex process that is associated with various neurotransmitter systems.Three major systems, including the cholinergic, glutamatergic, and GABAergic, are commonly involved and have predominate roles in the process [1,2,3,4]
Ach is synthesised by the Choline acetyltransferase (ChAT) enzyme which is found in high concentrations in cholinergic neurons as visualized by choline acetyltransferase (ChAT)
When compared to the vehicle plus Aβ groups, the mean number of errors in groups that received aged garlic extract (AGE) at any dose indicated that AGE significantly prevented working memory loss (One way ANOVA test, F4, 35 = 17.23, p < 0.05 and p < 0.01)
Summary
Memory formation is a complex process that is associated with various neurotransmitter systems. Three major systems, including the cholinergic, glutamatergic, and GABAergic, are commonly involved and have predominate roles in the process [1,2,3,4]. Acetylcholine (ACh), a neurotransmitter of the cholinergic system, released within the hippocampal circuits is important for learning and memory. It is a powerful presynaptic modulator of both glutamatergic and GABAergic synaptic transmission [1]. Ach is synthesised by the Choline acetyltransferase (ChAT) enzyme which is found in high concentrations in cholinergic neurons as visualized by choline acetyltransferase (ChAT). In the modulation of network activity, Ach-activated muscarinic
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