What is your doctor's EXACT PROTOCOL for getting you BDNF?
If your doctor doesn't know of all these
BDNF stroke research articles there is a good reason! PURE INCOMPETENCE!
BDNF (170 posts to April 2011)
Salidroside directly activates HSC70, revealing a new role for HSC70 in BDNF signalling and neurogenesis after cerebral ischemia
Abstract
Salidroside, a principal bioactive component of Rhodiola crenulata,
is neuroprotective across a wide time window in stroke models. We
investigated whether salidroside induced neurogenesis after cerebral
ischemia and aimed to identify its primary molecular targets. Rats,
subjected to transient 2 h of middle cerebral artery occlusion (MCAO),
received intraperitoneal vehicle or salidroside ±
intracerebroventricular HSC70 inhibitor VER155008 or TrkB inhibitor
ANA-12 for up to 7 days. MRI, behavioural tests, immunofluorescent
staining and western blotting measured effects of salidroside. Reverse
virtual docking and enzymatic assays assessed interaction of salidroside
with purified recombinant HSC70. Salidroside dose-dependently decreased
cerebral infarct volumes and neurological deficits, with maximal
effects by 50 mg/kg/day. This dose also improved performance in beam
balance and Morris water maze tests. Salidroside significantly increased
BrdU+/nestin+, BrdU+/DCX+, BrdU+/NeuN+, BrdU−/NeuN+ and BDNF+
cells in the peri-infarct cortex, with less effect in striatum and no
significant effect in the subventricular zone. Salidroside was predicted
to bind with HSC70. Salidroside dose-dependently increased HSC70 ATPase
and HSC70-dependent luciferase activities, but it did not activate
HSP70. HSC70 immunoreactivity concentrated in the peri-infarct cortex
and was unchanged by salidroside. However, VER155008 prevented
salidroside-dependent increases of neurogenesis, BrdU−/NeuN+ cells and BDNF+
cells in peri-infarct cortex. Salidroside also increased BDNF protein
and p-TrkB/TrkB ratio in ischemic brain, changes prevented by VER155008
and ANA-12, respectively. Additionally, ANA-12 blocked
salidroside-dependent neurogenesis and increased BrdU−/NeuN+
cells in the peri-infarct cortex. Salidroside directly activates HSC70,
thereby stimulating neurogenesis and neuroprotection(Never use the word neuroprotection, it doesn't signify urgency; whereas the neuronal cascade of death suggests extreme urgency)
via BDNF/TrkB signalling after MCAO. Salidroside and similar activators of HSC70 might provide clinical therapies for ischemic stroke.
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