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H E A L H A N D S O C I E Y
R E S E A R C H @ H K U S
The Partner State Key Laboratory (PSKL) of Molecular Neuroscience,
established in 2010 by the Ministry of Science and Technology of China,
is the first laboratory focused on molecular neuroscience research in
Hong Kong. The core focus of the PSKL is to develop frontier research in
neuroscience and address fundamental questions related to function of
the nervous system and neurological diseases.
The PSKL has forged a long-term partnership with the State Key
Laboratory of Neuroscience in Shanghai, and established a research
team at the HKUST Shenzhen Research Institute to broaden the platform
for innovative basic research as well as drive initiatives in translational
research through collaborations with industrial partners.
Partner State Key Laboratory:
Focus on Molecular Neuroscience Research
Opening ceremony for Partner State Key Laboratory of Molecular Neuroscience.
Overall, IL-33
restores neuronal
communication and
memory in the mouse
model of Alzheimer’s
disease and alleviates
Alzheimer’s disease
pathology by reducing
inflammation and
amyloid toxicity.
Normal
Pathological condition
pathology and identified the IL-33 protein
as a potential treatment for Alzheimer’s.
IL-33 is a protein found in a wide
variety of cell types in humans, and
modulates immune functions. The team
discovered that IL-33 function is compro-
mised in individuals with mild cognitive
impairment, those who are at high risk
of developing Alzheimer’s disease. To
elucidate its role in disease pathology,
the protein was injected into AD model
mice, with astonishing results. The mice
rapidly recovered their neuronal commu-
nication and memory. Additionally, IL-33
injection for only two consecutive days
was sufficient to reduce the levels of
beta-amyloid (A
β
) protein and, in turn,
decrease the deposits of amyloid plaque,
a major pathological hallmark of the
disease, in the mice brains.
The team further demonstrated that
IL-33 mobilized microglia, the immune
cells of the brain, to the amyloid plaques to
promote the clearance of the A
β
protein.
It has been hypothesized that defects in
the mechanism underlying A
β
clearance
is one of the leading causes of Alzheimer’s
disease. With additional investigation,
IL-33 was found to trigger changes in the
microglia, which in turn reduced overall
inflammation in the brain. This is a critical
finding since inflammation contributes to
and drives the pathology of the disease.
The study was published in
PNAS
in April 2016. The team aims to build
upon its findings to further understand
the mechanisms underlying Alzheimer’s
disease as well as evaluate the viability
of using IL-33 as a clinical treatment in
human. The research has been supported
by the Hong Kong Research Grants
Council’s Collaborative Research Fund.
Search for Early Diagnosis
While the interdisciplinary team contin-
ues to investigate the complex signaling
mechanisms between brain cells and oth-
er potential triggers for malfunction, the
hunt is now on for biomarkers for early
Alzheimer’s disease and mild cognitive
impairment.
Toward this goal, Prof Ip has initiated
a critical project with clinicians in Hong
Kong, Mainland China, and globally to
identify biomarkers associated with early
Alzheimer’s and mild cognitive impair-
ment. Success in this area could potential-
ly lead to diagnostic tools and tests that
simply and effectively identify individuals
with these conditions, prior to manifesta-
tion of symptoms.
Furthermore, the question of why
some patients with mild cognitive impair-
ment develop Alzheimer’s disease, while
others do not is also being investigated.
The genetic make-up of an individual,
combined with inflammatory and envi-
ronmental factors, are among the poten-
tial factors. To unravel these mysteries,
Prof Ip is investigating inflammation in
the brain to understand the interplay
between the immune and nervous systems.
Control
IL-33
A
β
Iba1
The immune system
contributes to the
pathogenesis of
Alzheimer’s disease,
but the basis is
unclear. Prof Ip
demonstrated that
injection with IL-33
recruits immune cells
to the amyloid plaques,
which then triggers
amyloid clearance.
