By Amruth Chinnappa
A functioning mind is an individual’s greatest asset. Its storehouse of memories and thoughts is the source of ecstasy and misery, sensation and numbness. Alzheimer’s disease rids a person of these memories, incapacitating the normal course of life. It is characterised by reduced memory and comprehension power, leaving an individual unable to comprehend even the presence of affliction. Researchers from The Indian Institute of Science, Bengaluru have made progress in determining the onset of this dreaded affliction.
Explaining this debilitating syndrome
Alzheimer’s is a type of dementia, which is a degenerative brain condition affecting about 50 million people globally. The type of dementia depends on the part of the brain affected, and a vast majority of cases involves degeneration of the hippocampus which leads to Alzheimer’s. The hippocampus is a part of the Central Nervous System and is responsible for memory, which explains the loss of it in the case of Alzheimer’s. The syndrome does not have a concrete treatment and there is a lack of understanding about it, despite being under researchers’ magnifying glasses for centuries.
Presence of toxic proteins
Although there remains an unfortunate absence of a cure, scientists have made rapid progress in the last 20 years in finding out the syndrome’s mechanism and its signs on the body. Alzheimer’s occurs with the build-up of a protein named amyloid beta in the nerve cells of the body. A non-invasive blood test has been developed to check the presence of the toxic protein in the brain and the findings have been published in ‘Nature’ magazine. The test was performed on a control group of 121 Japanese and 252 Australians at varying levels of health and was found to be correct 90% of the time.
“This test is at least as good as current brain scan techniques and far surpasses existing blood tests,” said Colin Masters, professor of dementia research at Melbourne’s Florey Institute of Neuroscience and Mental Health. While the test determines the onset of Alzheimer’s, the associated symptoms could take up to 30 years to materialise in the individual. The researchers also mentioned a word of caution that the presence of amyloids would not necessitate the presence of Alzheimer’s and vice versa.
Biomarkers that can aid recovery
The scientists at IISC, Bengaluru have observed a biomarker in the human body and believe in a recovery from the syndrome, provided its early diagnosis. It has been previously known that the loss of dendritic spines of a nerve cell is an early indicator of Alzheimer’s. Dendrites are the arms of a nerve cell and are used to communicate amongst each other. The underlying mechanism behind its loss has now been understood through the efforts of a team led by Vijayalakshmi Ravindranath from the Centre for Neuroscience at IISC.
The study, which was published in the ‘Journal of Neuroscience’, implies a direct correlation between a loss in memory and dendritic shrinkage. Filamentous Actin (F-Actin) is a cytoskeletal protein which provides the structure for the dendritic spines. It is formed by the polymerisation of monomers called Globular Actin (G-Actin). Polymerisation is a process where single units called monomers join together to form chains called polymers. Depolymerisation of F-Actin leads to the formation of G-Actin and a subsequent decrease in the number of spines on the nerve cell.
Experimentation and results
The study was conducted on lab mice with two control groups chosen, with and without the Alzheimer’s gene present in them. The mice, genetically altered to have Alzheimer’s, showed a decrease in F-Actin levels after one month and presented the associated symptoms after two months. This was a marked difference from those which developed the amyloid proteins naturally at around 8 months. The mice were then subjected to behavioural tests where an electric shock was used to develop contextual fear conditioning. Unlike regular mice which froze, those afflicted with the syndrome did not associate the shocks with the context and continued with the experiment. This response changed when they were dosed with F-Actin and the mice froze in the context. This result was validated when regular mice which were subjected to a chemical to lower F-Actin levels behaved like the Alzheimer’s afflicted mice.
These two experiments conclusively proved that loss in F-actin level leads to early behavioural changes that would eventually lead to Alzheimers disease, says Dr Kommaddi, of the project. The team further noticed lower levels of F-Actin in brain samples of people who had the syndrome which correlated the results between mice and humans.
Common symptoms
Different studies have been carried out to determine a potential cure for the syndrome. A study by Oxford University and NIHR Southampton Biomedical Research Centre demonstrated that drugs used to treat rheumatoid arthritis could have the risk of contracting dementia. 3,876 people who took anti-rheumatoid drugs were compared against 1,938 people who did not. The results showed that those who did take the anti-rheumatoid drugs showed half the risk of getting Alzheimer’s and other forms of dementia. Rheumatoid arthritis occurs when the immune system attacks the cells lining the joints and other parts. The researchers believe that the drugs could work against the syndrome because of the common inflammation symptoms existing between dementia and arthritis.
There has always been an interest in this area since early reports of a lower incidence of dementia in people with rheumatoid arthritis and the possible role for example of nonsteroidal anti-inflammatory drugs, says Prof. Peter Passmore, Professor of Ageing and Geriatric Medicine, Queens University, Belfast.
Precautionary measures against Alzheimer’s
The condition is a bane to millions and as of now, is mired in uncertainty about the future. There are, however, multiple methods to reduce the chances of contracting dementia. These include maintaining an active lifestyle free from obesity, diabetes, and high blood sugar. The road to cure this syndrome seems to be long but the end is worth the wait for millions across the world.
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