Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 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:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. 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 lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Monday, April 6, 2020

Blood Flow Through the Brain & Alzheimer’s Disease

But what EXACTLY is the best way to get better blood flow? And wouldn't you immediately want better blood flow to your brain now to try to prevent Alzheimer's?

So ask your doctor for EXACT PROTOCOLS to increase blood flow.  These posts contain my writings and ideas on increasing blood flow.  DO NOT FOLLOW THEM, I'M NOT MEDICALLY TRAINED. Your doctor supposedly is, so ask him/her. 

 

Blood Flow Through the Brain & Alzheimer’s Disease

Alzheimer’s disease is characterized by the presence of beta-amyloid plaques and neurofibrillary tangles of tau, that together lead to the progressive neurodegeneration of neurons in the brain leading to the symptoms of dementia.
Alzheimers Disease
Image Credit:Atthapon Raksthaput
Recent research has revealed that patients and animal models of Alzheimer’s disease display significant disturbances to brain blood flow from early on in disease-course. This article will highlight the importance of brain blood flow to health and how Alzheimer’s disease is marked with severe reductions.
Given that many traditional therapeutic approaches have failed in the past, perhaps brain blood flow-related therapies may pave the way to more successful treatments in the future.

Blood Flow to the Brain

The brain accounts for just 2% of total body weight but receives 20% of all the blood flow in the body from the heart every minute.
Brain cells (neurons) require vast amounts of energy to function properly and to maintain the metabolic demands neuronal activity exerts, the brain has an intricate system called neurovascular coupling.
Neurovascular coupling ensures that active brain regions receive a proportionally matched blood supply by increasing local cerebral blood flow (CBF).
Neurovascular coupling is facilitated by various cell types within the brain including neurons, astrocytes, pericytes, endothelial cells, smooth muscle cells, interneurons, and others.
Signaling between neurons and these cells eventually leads to increased CBF at both the capillary level as well as at the surface arterial level. Damage to specific cell types or signaling pathways could be the cause of neurovascular decline in aging and dementia.

Cerebral Blood Flow in Alzheimer’s Disease

Cerebrovascular dysfunction is implicated in the development and onset of dementia, including Alzheimer’s disease and vascular dementia.
The biggest risk factors that may compromise vascular function in Alzheimer’s disease include atherosclerosis (hardening and narrowing of arteries), hypertension (high blood pressure), diabetes and obesity.
These risk factors are the same for the development of cardiovascular diseases and cerebrovascular diseases including stroke. Many of these diseases have similar mechanisms, including oxidative stress and inflammation.
In addition to the vascular risk factors for the development of Alzheimer’s disease, it is known that CBF can be reduced as much as 25% if not more in patients with Alzheimer’s disease, known as chronic hypoperfusion (long term reduced blood flow).
The mechanisms behind this are still largely not fully understood, though impairments to neurovascular coupling as well as to the prolonged constriction of brain blood vessels and density could also be important.
Chronic hypoperfusion over time can lead to reduced oxygen delivery to brain tissue, causing neurons to become stressed and eventually die. This is in parallel to the neurodegenerative decline in neuronal numbers in the cortex as initiated by amyloid-beta plaques and tau tangles.
Furthermore, amyloid-beta deposits can form around blood vessels in the brain in what is known as cerebral amyloid angiopathy (CAA) that can also affect vessel reactivity (ability to vessels to dilate) and to cause vasoconstriction (constricted blood vessels).
Also, as the brain clears away amyloid-beta by clearance pathways that operate with functional blood flow, impairments to blood flow can lead to reduced clearance of amyloid-beta, causing it to accumulate in the brain, further exacerbating the condition.

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