Mental and Neurological Disorders 117
Alzheimer’s Disease
Before Rebecca developed Alzheimer’s she suffered from atherosclero-
sis. She said that the hardening of her arteries started when she was a
child. At the age of four she had severe pains in her feet; in her teens
the pain had crept up into her legs. Then in her early forties she devel-
oped chest pains. At the age of seventy, she was showing symptoms of
Alzheimer’s. I believe the same condition that caused the hardening of
Rebecca’s arteries when she was a child also hardened the protein
strands in her brain in older age.
Modern science views Alzheimer’s and cardiovascular disease as two
different pathologies presumably because calcifi ed plaques that trigger
the development of blood clots adhere to the arteries whereas the beta-
amyloid plaques that characterize Alzheimer’s fl oat in the watery
lymphlike fl uid surrounding the neurons in the brain.
However, before the onset of Alzheimer’s, the protein strands inside
the neurons that extend beyond the neurons’ cellular membranes per-
form the same function for the brain as arteries do for the rest of the
body: they transport materials to and from their destination. Further-
more, the protein strands in the brain harden (and are deposited in
amyloid plaques) just as arteries harden. It makes sense that both the
arteries in the circulatory system and the protein strands that grow
through the brain’s neurons are exposed to acidic wastes—the protein
strands from the acidic by-products of the metabolic processes that go
on inside the brain, and the arteries from the acidic waste by-products
the blood picks up from the various organ systems in the body.
The efforts of mainstream medicine to eliminate amyloid plaque in
the brains of Alzheimer’s patients, if successful, might very well interfere
with normal brain function. The protease enzymes that cut the protein
strands into segments so they can be deposited in amyloid plaques are
programmed to get rid of old protein strands. Amyloid plaques may
therefore act as waste deposit sites for protein strands that have outworn
their usefulness. The fact that these plaques are held together by a pro-
tective structure of metals and a waxy, cholesterol-like substance rein-
forces this possibility and makes the prevention of amyloid plaques
tantamount to interfering with the brain’s waste disposal system. The