So you have identified a problem, useless with NO SOLUTION. Your mentors and senior researchers need re-education on the whole point of stroke research. 100% recovery for all.
Brain zinc and glial cells in ischemic stroke
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Abstract
Zinc, an essential trace element, plays an important role in a large
number of biological functions. In mammalian brain, whereas the majority
of brain zinc is bound to proteins including metallothionein, about
5-15% is stored in presynaptic vesicles of glutamatergic neurons
throughout the forebrain, especially in the hippocampus, in a relatively
free state. Thus, free zinc (Zn2+) concentration in the brain is
considered to be regulated in order to maintain normal brain functions
such as learning and memory. On the other hand, brain Zn2+
dyshomeostasis has been recognized as a mechanism for neuronal injury in
brain disorders including Alzheimer's disease and brain ischemia. In
particular, after transient brain ischemia, Zn2+ accumulates in
hippocampal neurons via a zinc transport system, or via release from
cytosolic zinc-binding proteins, which results in neuronal cell death.
Recently, it has been demonstrated that Zn2+ dyshomeostasis also occurs
in glial cells such as microglia, astrocytes and oligodendrocytes after
brain ischemia. In oligodendrocytes, ischemic insult triggers
intracellular Zn2+ accumulation, resulting in cell death via
mitochondrial dysfunction. Increased extracellular Zn2+ inhibits
astrocytic glutamate uptake. In addition, extracellular Zn2+ massively
released from ischemic neurons primes microglia to enhance production of
pro-inflammatory cytokines in response to stimuli that trigger M1
activation. This review aims to describe the impact of brain Zn2+
dyshomeostasis on alterations in glial cell survival and functions in
post-ischemic brains.
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