Reversal of Memory Loss in Alzheimer's Model

Diseases of the brain often have a special kind of horror associated with them; our brains are who we are, and to have that compromised is a special kind of unjust. Perhaps the worst of these diseases are those that rob us of our memories, leaving us unable to recognise even close relatives. Alzheimer’s is such a disease, and with approximately 30 million people afflicted with it worldwide, Alzheimer’s disease is the most common of all fatal neurodegenerative disorders. Alarmingly, that number is growing as the age of our population increases, with the number of sufferers expected to double by 2030. Consequently, research into potential treatments is of great importance.

source: ilovehealthyandhappy.com

Though Alzheimer’s disease is a sporadic disease, there are genetic risk factors that can predispose individuals to the disease. The most significant is apoE4, carriers of which make up 15 % of the population, but account for 65 – 75 % of Alzheimer’s patients. The expression of apoE4 results in hyperactivity in the hippocampus, through impairment and loss of inhibitory neurons. Interestingly, the hippocampus has a role in memory, and is one of the first regions to become damaged in Alzheimer’s diseases. As excitatory-inhibitory balance of neural activity is known to be crucial for normal brain function, a group from Gladstone institutes investigated whether apoE4 predisposition to Alzheimer’s disease is dependent upon this loss of balance. To do this, the researchers implanted inhibitory neuron progenitors, into two widely used mouse models of Alzheimer’s disease. They also used aged mice, to better replicate the disease in humans.

Amazingly, the neuron progenitors integrated successfully into the mouse brains, and were able to restore learning and memory. This is particularly surprising, as they were integrating into an essentially toxic environment, as the mouse brains contained apoE4, and accumulation of amyloid-beta, a peptide which is thought to mediate neurotoxicity in Alzheimer’s disease. This suggests that the detrimental effects that occur to inhibitory neurons in Alzheimer’s disease are cell autonomous; good news for stem cell therapy, as cells may have a better than expected chance of integrating. Additionally, though stem cell therapy may still be a thing of the future, finding drugs that could enhance inhibitory neuronal function may be viable now. Important to note is the fact that this research is not just relevant to carriers of apoE4, as a loss of inhibitory neurons in the hippocampus also happens to sufferers of Alzheimer’s disease as amyloid-beta accumulates.

 

 

 

 

 

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A final year PhD student, studying the role of metal ions in Alzheimer's disease at Queen Mary University, London. If you enjoy my articles, you can follow me on twitter to stay updated (twitter.com/Chris_Matheou).

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