Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Monday, January 2, 2017

Current Opinion on the Role of Neurogenesis in the Therapeutic Strategies for Alzheimer Disease, Parkinson Disease, and Ischemic Stroke; Considering Neuronal Voiding Function

What the fuck are the appropriate stimulation and various approaches to neurogenesis? Demand your doctor find them and put them in layperson terms.
This article has been cited by other articles in ScienceCentral.


Neurological diseases such as Alzheimer, Parkinson, and ischemic stroke have increased in occurrence and become important health issues throughout the world. There is currently no effective therapeutic strategy for addressing neurological deficits after the development of these major neurological disorders. In recent years, it has become accepted that adult neural stem cells located in the subventricular and subgranular zones have the ability to proliferate and differentiate in order to replace lost or damaged neural cells. There have been many limitations in the clinical application of both endogenous and exogenous neurogenesis for neurological disorders. However, many studies have investigated novel mechanisms in neurogenesis and have shown that these limitations can potentially be overcome with appropriate stimulation and various approaches. We will review concepts related to possible therapeutic strategies focused on the perspective of neurogenesis for the treatment of patients diagnosed with Alzheimer disease, Parkinson disease, and ischemic stroke based on current reports.
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As the aging population increases, common neurological disorders including Alzheimer disease (AD), Parkinson disease (PD), and ischemic stroke (IS) have increased and become important health issues with increasing socioeconomic burdens throughout the world [1].
The clinical characteristics of AD are related to progressive memory loss and cognitive deterioration. The neuropathological traits of AD are massive neuronal death with senile plaques, which are formed by the aggregation of amyloid-β (Aβ) peptides, and neurofibrillary tangles, which form from abnormal hyperphosphorylation of cytoskeletal tau protein [2,3]. These pathological changes in the brains of AD patients represent important targets for diagnosis and treatment [3].
The motor symptoms and mechanisms of PD are well known, including age-dependent uncontrollable tremors, postural imbalance, and slowness of movement and rigidity which are caused by the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc) located in the midbrain [4]. The neuropathological hallmarks of PD are eosinophilic intracellular inclusion bodies termed Lewy-bodies, and argyrophilic processes (Lewy neurites) [5].
The pathophysiology of IS is provoked by a reduction or complete blockage in blood supply to the brain, leading to dysfunction in the ischemic area [6]. The main causes of ischemia are thrombosis, embolism, systemic hypoperfusion, or lacunar infarction from small vessel disease. Various neurologic deficits remain after IS attacks.
There is currently no effective therapeutic strategy for addressing the neurological deficits after the development of these major neurological disorders. However, adult neurogenesis has become a topic of interest, since it was reported that the brain has the capability to generate new neurons from self-renewing and multipotent adult neural stem cells (NSCs) placed in the subventricular zone (SVZ) and subgranular zone (SGZ) of the dentate gyrus [7-11]. Therefore, the objective of this review is to evaluate possible therapeutic neurogenesis strategies for the treatment of neurological deficits in patients diagnosed with AD, PD, and IS.

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