Finding treatment for Alzheimer’s disease

Alzheimer’s disease (AD) was discovered and named after a German psychiatrist and pathologist, Alois Alzheimer in 1906. It is a neurodegenerative disease which causes memory loss, mood swings and lack of self-care to the extent that the patient can’t recognise anyone and loss of body functions leads to death. It is more common in the developed countries and that is why there’s a lot of research on it.

AD starts with accumulation of amyloid plaques around the neurons in the brain. Our body is constantly producing and breaking down substances which can be harmful to us. However, in this case the amyloid fragments tend to harden around the nerve cells, thereby preventing nerve impulses and nutrients to pass through the nervous system which in turn degenerates the brain.

As AD is caused by abnormal proteins, the cause is traced to the gene producing that protein. Recently, researchers from the Massachusetts Institute of Technology (MIT) have mapped out the altered genes allowing them to study the different cellular pathways and their effects on the brain.

The Human Genome Project which was published in 2004, showed the complete set of the gene sequences. Following this, many diseases have been further studied by investigating the altered gene and this is no exception. Each gene in our DNA has a specific nucleic acid sequence which produces normal proteins. However, if the sequence is even slightly changed, the resulting protein changes and thus, isn’t able to perform its function. Instead of being useful, it can cause genetic diseases.

Manolis Kellis, a professor from the MIT said “This study provides, in my view, the very first map for going after all of the molecular processes that are altered in Alzheimer’s disease in every single cell type that we can now reliably characterize. It opens up a completely new era for understanding Alzheimer’s.”

The researchers compared gene sequences of post-mortem brain samples from 24 patients who had AD and 24 people of similar age who didn’t have AD.

Li-Huei Tsai, one of the researchers explained “We wanted to know if we could distinguish whether each cell type has different gene expression patterns between healthy and diseased brain tissues. This is the power of single-cell-level analysis. You have the resolution to really see the differences among all the different cell types in the brain.”

It was noted that in the later stages of the disease, many cells followed similar patterns of gene expression change which gradually reduces gene function such as those for stress response and programmed cell death. It was found that there’s noticeable difference in the brain structures of males and females.

“That’s when we realized there’s something very interesting going on. We were just shocked” said Tsai.

While it’s unclear why these differences occur, it was also found that the females had much more white matter damage than the males.

“There is mounting clinical and preclinical evidence of a sexual dimorphism in Alzheimer’s predisposition, but no underlying mechanisms are known. Our work points to differential cellular processes involving non-neuronal myelinating cells as potentially having a role. It will be key to figure out whether these discrepancies protect or damage the brain cells only in one of the sexes – and how to balance the response in the desired direction on the other,” said Davila-Velderrain, one of the lead authors of the paper.

After this discovery, there’s plan for more research on the different cellular pathways and how this method can be used to study other brain dysfunctions such as bipolar disorder and psychosis.

Garima Nabh is the founder of New Age Magazine.

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