The bite that kills can also provide a clue to a cure. A tiny fraction of Russell's viper venom, one of the most deadly toxins, has been shown to halt the memory loss associated with Alzheimer's disease in a new study by Indian scientists here.
Russell's viper is considered to be one of the most dangerous snakes in Southeast Asia.
Distributed throughout India, lurking even in highly populated areas, it is notorious for causing a significant number of snakebite incidents and deaths, courtesy its venom - a toxic concoction of proteins, peptides (short stretches of amino acids) and other molecules of specific biological function.
Consider this to get an idea of its lethality: at a dose of 0.03 mg per kg, the venom can wipe out 50 percent of test mice. Alzheimer's disease, dubbed a silent killer, is no less of a threat. It is the most common cause of dementia over the age of 65 that gets worse with time.
Its hallmarks are abnormally large clumps of sticky protein fragments called amyloid beta or Abeta peptide, normally present in the brain. These deposits, known as amyloid plaques, irreversibly disrupt memory and cognitive functions.
Exploring the therapeutic side to snake venoms, researchers at the Council of Scientific and Industrial Research's Indian Institute of Chemical Biology (CSIR-IICB) here have zeroed in on a component of the viper venom that shreds the Abeta peptides into its building blocks or monomeric form.
The fraction is called coagulation factor V activator or RVV-V.
"We investigated the protein aggregate cleaving activity of the venom of a type of Russell's viper found in eastern India (Daboiia russelli russelli) and found that small synthetic peptides derived from RVV-V as a template destabilized the Abeta peptide aggregates into monomers which are non-toxic," Debasish Bhattacharyya, chief scientist, division of structural biology and bioinformatics at CSIR-IICB, told IANS.
"If this is developed as a drug, then it can halt the progress of Alzheimer's at the stage at which it is administered. However, whatever neuronal damage is already there, that cannot be repaired," he pointed out, adding the experiments were carried out on human neuroblastoma cells in the laboratory (in vitro).
Through various in vitro studies, use of bioinformatics and microscopic evidence, Bhattacharyya and co-researcher Payel Bhattacharjee observed that a specific stretch of the synthetic peptide binds to a segment of the Abeta peptide and initiates the process. The study was published in the Journal of Biological Chemistry.
"The derived synthetic peptide has no relation to the venom and the peptides exhibited stability in the lab studies," Bhattacharjee clarified.
However, a major stumbling block needs to be overcome for successful drug development.
"An important criteria for drugs of neurological disorders is the ability to cross the highly selective blood-brain barrier that separates the circulating blood from the brain fluids. The synthetic peptides must be able to penetrate the barrier and also must remain stable in the body fluids," said Bhattacharjee.
The next step, said Bhattcharyya, is to test the potency of the peptides in animal studies.
Studies that provide new avenues to Alzheimer's cure is of paramount interest to experts dealing with the disease, said Amit Dias, coordinator of the medical and scientific advisory panel for dementia at the Alzheimer's and Related Disorders Society of India (ARDSI).
"This is an interesting find and its scope needs to be assessed. Additional research is needed to ensure the proposed component is non-toxic to the body," said Dias, a lecturer at the Goa Medical College.
(Sahana Ghosh can be contacted at email@example.com)