Replies to post #6741 on Cerebain Biotech Corp (fka CBBT) (CBBT)

[mick]

$CBBT/thank you, i am going with trump's wording --- THE RIGHT TO TRY

'Cerebain Biotech Corp. (CBBT)'

Alzheimer's disease, IS AH DEATH ISSUE ALSO.

[mick]

#1/READING, 'Cerebain Biotech Corp. (CBBT)'Surg Neurol Int. 2017; 8: 133.
Published online 2017 Jul 7. doi: 10.4103/sni.sni_116_17
PMCID: PMC5523480
PMID: 28781910



[-chart]www.ncbi.nlm.nih.gov/corehtml/pmc/pmcgifs/logo-sni.png[/chart]

The greatest gift one can give a patient with AD is the possibility
that their cognitive condition can be improved. This is the hope for anyone with AD.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5523480/

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Alzheimer's disease can be treated: Why the delay?
Harry S. Goldsmith*
Author information Article notes Copyright and License information Disclaimer
This article has been cited by other articles in PMC.
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INTRODUCTION
Thousands of published papers have continued to report that
amyloid deposition in the brain of Alzheimer disease (AD) patients
is the basis for the disease. Two observations deserve attention.

It has been found at autopsy that the percentage of amyloid plaques within the brains of nondemented, age-adjusted individuals can be
the same percentage of amyloid plaques found at autopsy within the brains of AD patients.

[3] Another study found no relationship between the number of
amyloid plaques located in the brains of AD patients and their
degree of dementia severity.

[36] These findings clearly challenge the presumption that the
presence of amyloid in the AD brain is the basis for the disease.

There is an increasing consideration that a decrease in cerebral
blood flow (CBF) may be the cause of dementia in AD.

The decrease in CBF typically found in AD has long been believed
to be due to the death of critical neurons which, because of their nonviability, no longer required a sustainable CBF.

An alternative explanation to this idea is that it is not dead or
dying neurons that cause the decrease in CBF,

but it is the actual decrease in CBF over a prolonged period
that results in the death of critical neurons in AD.

Spin-labeled magnetic resonance studies have confirmed the
marked decline in CBF in AD as compared to age-matched controls.

[1] Further magnetic resonance imaging (MRI) studies measured the
total volume of CBF that flowed to the brain of AD patients through
the internal carotid and basilar arteries.

A significant decrease in the volume of blood flow through these arteries was noted in AD patients who exhibited a mean blood flow

of 442 mL/min as compared to a mean blood flow of 551 mL/min in nondemented, age-matched particpipants (p < 0.001).