Alzheimer’s disease is treatable by increased cerebral blood flow (CBF) from omentum to compensate for a decreased CBF in aging

Alzheimer's disease (AD) is one of the major problems that have confronted the medical community over the years.Millions of patients have suffered from this condition, and yet, despite decades of extensive research efforts, the origin and treatment of AD continue to remain uncertain.It has been suggested that amyloid within the brain might be the basis for the development of the condition, but more recently, a suggestion has been made that natural aging conditions cause AD. is statement is based on personal findings which have been reported. [3][4][5][6][7][8][9][10][11][12][13][14][15] In the presence of AD, there is a loss of energy in the intracerebral neurons, mitochondria, and adenosine triphosphate (ATP) due to a decreasing cerebral blood flow (CBF). [15]When the energy in these critical neurons decreases, a diminished cognitive state can result.ere is no evidence that a decrease in amyloid in an AD brain will increase the energy needed by the intracerebral neurons, mitochondria, and ATP, [2] which could lead to improved cognition.What is needed and has not been achieved is a supplemental increase in CBF to compensate for the loss of CBF that routinely occurs in an AD brain as a normal physiological occurrence with aging.e application of the omentum to an AD brain, however, has been shown to improve cognition in patients with AD because of its ability to supply an additional source of CBF to the AD brain. [11]e intracellular energy activity produced by ATP from mitochondria becomes the final energy source of all cells in the body, including the intracerebral neurons. [3]An increase in CBF to compensate for the decreased CBF, which occurs as a function of natural aging, becomes critical for the survival of the intracranial neurons, mitochondria, and ATP.For decades, a way has been sought to increase cognition in AD patients.is has been attempted by the insertion of various therapeutic agents into the body in the hope that a positive cognitive result could occur.Unfortunately, this goal was never achieved.It was earlier believed that the decreased CBF in an AD brain resulted from a slow deterioration in the energy of the intracerebral neurons, mitochondria, and ATP that no longer required their previous volume of CBF to the brain.But more recently, there has been increasing interest and information showing that it is not the deterioration of the energy of intracerebral neurons resulting in a decreased CBF, but it is actually the decrease in CBF itself that results in the diminished intraneuronal activity that leads to the loss of cognition found in AD.