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 This is longer with a greater bent to fold and self-assemble. By ‘self-assemble’, it means that the helically structured monomers of Abeta42 misfold and interact with themselves to assemble without any external direction. Although the process may seem organized, the situation is rather uncontrollable and the final result is an ‘insoluble product’ with a totally different folded structure (pleated) and a stubborn nature, which is stressful to neurons. Therefore, a tendency to unnecessary fold is the basic reason why the protein becomes a villain, giving rise to the belief that ‘a protein when misfolded produces a disorder’, which is known as the ‘amyloid hypothesis’. Our faith in such a hypothesis drove many clinical trials in different parts of the globe for nearly a quarter of a century without any light of success. The truth is that ever since the discovery of the disorder by Alois Alzheimer’s in 1906, we have been dealing with only unsuccessful translation of successful pre-clinical trials
conducted on animal model systems. Alzheimer’s disease is, therefore, a disorder for which modern medicine has not found any cure.
As far as we know,
Alzheimer’s disease is a state
in aged people, where there
is a progressive degeneration
of the nervous system,
causing memory decline and
behavioural problems. In
India, approximately 4 million
cases of Alzheimer’s disease
exist that gives our country
the 3rd highest load of clinical
cases after China and the
USA. To control some behavioural problems and reduce other symptoms associated with Alzheimer’s disease, patients diagnosed with the disease are supported using ‘enzyme blockers’ that slow down the progression of the
Dr Viji Vijayan || 61
disease. Nonetheless, this has hardly brought any relief. Some people, for no known reason, age into Alzheimer’s disease because of the lack of an effective medical support, creating a socio-economic burden that is unimaginable. I have witnessed my great grandmother, grandmother and grandaunts forget their last few years in the suffering.
What is my research?
I joined Molecular Science Lab, National Institute of Immunology, New Delhi, headed by Prof. Avadhesha Surolia and Dr. Sarika Gupta in 2010. Although I was primarily involved in bone biology projects, I was fascinated with some of the lab’s neurobiology projects. In one of the winter months of 2010, I accompanied a PhD scholar to an animal house for the sacrifice of a mouse model of Parkinson’s disease. I was surprised to find that these mice possessed tibial bones that chipped
easily. I was not sure why this brittleness occurred in a model with neurodegeneration. Therefore, I did a literature search on this matter and found that the patients diagnosed with Alzheimer’s disease suffered bone loss, but the mechanisms were unknown.
In 2012, after obtaining the ethical clearance for the use of amyloid overexpressing transgenic mice, herein FAD (F for familial and AD for Alzheimer’s disease) mice I performed pilot experiments to find out whether the bone function deficit occurred in
mice with Alzheimer’s disease. I assessed differences in the transcriptional status in the bones of diseased mice and compared the data with age-matched wild-type disease-free mice. Transcription is a process wherein the
   As far as we know, Alzheimer’s disease is a state in aged people, where there is a progressive degeneration of the nervous system, causing memory decline and behavioural problems. In India, approximately 4 million cases of Alzheimer’s disease exist that gives our country the 3rd highest load of clinical cases after China and the USA.
  











































































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