AsianScientist (Apr. 27, 2016) – A research team led by scientists from the Hong Kong University of Science and Technology (HKUST) has discovered that a protein found in the human body could be potentially developed as an effective treatment for Alzheimer’s disease (AD).
AD is a progressive and highly debilitating brain disease which shows up as beta-amyloid (Aβ) plaques and neurofibrillary tangles in the brain. Globally, AD affects 46.8 million individuals, mainly over the age of 65, and the number of cases is projected to reach 131.5 million by 2050. Patients suffer from cognitive deficits such as impaired memory, reasoning, judgement and movement. It is currently irreversible and incurable.
The team, led by Professor Nancy Ip, dean of science at HKUST, has found that the protein interleukin-33 (IL-33) slows cognitive decline and reduce deposits of Aβ plaques in the brain. The results have been published in the Proceedings of the National Academy of Sciences.
IL-33 is a protein made by the human body that regulates immune function. The research team highlighted IL-33 due to its compromised function in individuals with mild cognitive impairment who are at high risk of developing AD.
They found that injections of IL-33 in mice genetically altered to exhibit AD symptoms resulted in remarkable and rapid recovery of cognitive functions. Within a week, the researchers observed a reversal of neuronal communication defects and memory loss in the mice. Significantly, the team found that IL-33 injections for two consecutive days was sufficient to reduce the levels of Aβ protein and, in turn, decrease the deposits of amyloid plaques in the brains of these mice.
Defects in the removal of Aβ protein in the brain are believed to be one of the major causes underlying AD. The researchers also showed that the presence of IL-33 mobilized the immune cells of the brain, the microglia, to the amyloid plaques and promoted the removal of Aβ protein.
IL-33 also triggered changes in the microglia to reduce overall inflammation, which contributes to and drives the pathology of the disease, in the brain.
“These exciting findings bring us one step closer to understanding the pathological process of this complex, multi-factorial disease and provide a new avenue for developing AD treatments,” said Ip.
“The next step will be to translate the findings from the mouse study into clinical treatments for humans.”
The article can be found at: Fu et al. (2016) IL-33 Ameliorates Alzheimer’s Disease-Like Pathology and Cognitive Decline.
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Source: Hong Kong University of Science and Technology.
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