View Single Post
Old 09-02-2007, 11:13 PM
lou_lou's Avatar
lou_lou lou_lou is offline
In Remembrance
 
Join Date: Sep 2006
Location: about 45 minutes to anywhere!
Posts: 3,086
15 yr Member
lou_lou lou_lou is offline
In Remembrance
lou_lou's Avatar
 
Join Date: Sep 2006
Location: about 45 minutes to anywhere!
Posts: 3,086
15 yr Member
Lightbulb continued ~Dr. Russell Blaylock

This is important because with aging,
oxidized DNA begins to accumulate, resulting in dwindling
cell energy supplies.15 Cellular low energy causes reduced
function of the neurons and increased sensitivity to excitotoxicity.
The susceptibility of mitochondrial DNA to free radical
oxidation increases with age, being 15X more active
after age 70. As this process accelerates, a special autodestructive
gene, called the p53 gene, is activated.16 Its purpose
is to kill the neuron when the cell is so badly damaged that it
cannot be restored to health by the cell’s reparative enzymes.
Much of the destructive change seen in neurodegenerative
disorders, at least in the earlier stages, does not entail
neuron death. Several studies have shown that in the case of
Alzheimer’s disease, most of the damage is directed at the
neuron processes, such as the dendrites and synapses.17
While we do not completely understand the role played by
ß-amyloid peptides, we do know that much of their destructive
potential comes from the free-radical-generating molecule
hydrogen peroxide.18 Amyloid has also been shown to
enhance excitotoxicity.19
Another pathological characteristic of Alzheimer’s disease
is the presence of microscopic neurofibrillary tangles
composed of over-phosphorylated tau protein. Recent evidence
has demonstrated that the lipid peroxidation product
4-hydroxynonenal interacts with the tau protein to accelerate
this process, and prevents the tau proteins from dephosphorylating.
20 Several of the transition metals such as aluminum
and mercury, and exposure to MSG can precipitate
the same event experimentally.21
Finally, the entire process involves an overreacting
immune system apparently triggered by excitotoxicity and
free radical injury.22 The microglial cell, the cellular basis
of central nervous system immunity, is activated by any
event that increases the free radical-excitotoxicity cascade.
23 As we shall see, CNS immune activation plays a
major role in neurodegeneration.
This entire process appears to be the same for numerous
conditions including autoimmune diseases, viral
encephalitis, Lyme disease, AIDS dementia syndrome,
brain injury, strokes, heavy metal toxicity, spongioform
encephalitis (Mad Cow disease), and most of the degenerative
brain disorders, such as Alzheimer’s dementia,
Parkinson’s disease, Huntington’s disease, and ALS.
IRON AND NEURODEGENERATION
It is known that as we age our brain accumulates more
free iron.24 In the past it was assumed that only free iron
was harmful; recent evidence indicates that even iron combined
to ferritin can damage neurons.25 Excessive iron
accumulation is seen in many neurodegenerative disorders,
including Alzheimer’s dementia, Parkinson’s disease, and
ALS. In biological systems, iron is known as one of the
most powerful free radical generators.
__________________
with much love,
lou_lou


.


.
by
.
, on Flickr
pd documentary - part 2 and 3

.


.


Resolve to be tender with the young, compassionate with the aged, sympathetic with the striving, and tolerant with the weak and the wrong. Sometime in your life you will have been all of these.
lou_lou is offline   Reply With QuoteReply With Quote