12 January - 20 June 2016

Protective effect of black tea extract against aluminium chloride-induced Alzheimer's disease in rats

3 June 2015

Alzheimer’s disease (AD) in an age related neurodegenerative illness characterised by short term memory loss, leading to confusing, aggression, mood changes and long term memory loss. It is the most common cause of dementia, affecting 500,000 people in the UK. 

The cholinergic system of the brain especially the basal forebrain projections to the hippocampus and cortex, which is responsible for memory and learning.  Aluminium has been suggested to contribute to the pathogenesis and development of Alzheimer’s disease as it is a powerful cholinotoxin. Cholinotoxins cause apoptotic neuronal loss in the hippocampus and the degeneration of cortical areas.  Aluminium promotes the formation of amyloid-β plaques, which inhibit the function of nerve cells by blocking cell-to-cell signalling at synapses, and are a sign of Alzheimer’s disease.

Aluminium can gain entry into the body easily via many sources as it is a component of cooking utensils, medicine and drinking water.  Tea represents a major dietary source of aluminium, however previous research has found that bioavailability is low due to the action of polyphenols which bind aluminium preventing its absoprtion in the intestine. Research published in the Journal of Functional Foods by Manivasagam and colleagues, aimed to evaluate the neuroprotective effect of black tea extract (BTE).  

There were two phases to the study. In Phase I, rats were randomly divided into 6 groups.  Group I received saline and were considered as the control.  Rats in Group II were injected with AlCl3 (100mg/kg body weight) for 60 days to establish persistent aluminium toxicity to induce alzheimeric symptoms.  Group II, IV and V rats received BTE in drinking water orally (0.75, 1.5 and 3%) and were injected simultaneously with AlCl3.  Group VI rats received BTE (3%) only orally for 60 days.   At the end of the experimental period, a passive avoidance test was performed.  

In Phase II of the study, 48 rats were divided into four groups:  Control. AlCl3 (100 mg/kb bw), AlCl3 + BTE (1.5%) in drinking water and BTE for 60 days.  Neuroprotective effect of BTE against AlCl3-induced experimental model of AD was determined by executing Morris water maze test, estimating thiobarbituric acid reactive substances (TBARS), an indicator of lipid peroxidation processes, antioxidants and studying protein expressions of Aβ biosynthetic and apoptotic markers.

Researchers found that BTE treatment attenuated AlCl3 induced AD associated pathologies, including Ache activity, Aβ burden, oxidative stress and apoptosis, thereby exhibiting neuroprotective effect.  This possibly being due to the synergistic action of some active constituents.  Further study is therefore needed to understand the BT polyphenols metabolism, biotransformation, bioavailability and ability to cross the blood-brain barrier to further confirm its neuroprotective effect against AD.

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