Authored by Mario D Garrett
Psychologically it is easy to see how attractive it is to define
old age as a disease [1,2]. We can then explain Alzheimer’s disease,
the fifth killer in the U.S. as simply accelerated aging. A faulty
switch that starts a cascade of misfolded proteins that congeal in
the brain forming plaques and tangles [3] that ultimate lead to
Alzheimer’s disease [4]. But this scenario only holds true in our
mind. Observations contradict these assumptions. Aging is not
just a switch that accelerates diminished capacities, and plaques
and tangles do not solely cause Alzheimer’s disease. Unlike with
younger people, older adults have complex neurological problems.
Singling out Alzheimer’s disease and trying to show neurological
correlates are doomed to failure with older adults since they have
so many other pathologies [5]. That is why the most recent U.S.
National Institute on Aging directive-to define Alzheimer’s purely
on biological indicators of the plaques and tangles-is doomed to
failure with older people [6]. The correlation of these biomarkers
with Alzheimer’s disease declines as people get older [7]. There
are many other neuropathologists interfering with the brain at
older age [8,9]. Although we cannot explain Alzheimer’s disease as
caused by simple malfunction of two misfolded protein, we can also
not assign the cause to old age, even though both are correlates of
the disease. As Sherwin Nuland portrayed, diseases in older age are
choreographed disorder that climaxes in death [10].
In 2011 Heido Braak [11] autopsied more than two thousand
brains from 1 to 100 years of age. They found that nearly all had
both plaques and tangles. But what was interesting was that they
found that these misfolded proteins first show up in the brainstem
at much earlier age [12]. The seeds of what we call aging have a
lifetime of gestation. We are programmed to age as part of planned
obsolescence. When Alzheimer’s disease hits early, we notice
it because it is not anticipated that early. This is the observation
also made by Alois Alzheimer. He only noticed it because it was too
early ‘Senile dementia was never considered because of the onset
at the age of 54 [13], otherwise it was the same as senile (old age)
dementia there are cases of senile dementia which do not differ
from these presenile cases with respect to the severity of disease
process.’ [14].
Planned obsolescence is not a disease it is our natural state.
This explains why among older people we never see Alzheimer’s
disease in isolation, and we see it together with other dementias
Creutzfeldt Jakob disease [15]; Lewy Body dementia [16] and
another neuropathologist Jentoft et al., Sonnen et al. At the end
all the engineering in planned obsolescence converge so that only
0.01 percent of older patients have a diagnosis of dementia with
no co-morbid conditions [17]. Planned obsolescence differs from
a disease. With planned obsolescence you have to address the
engineering of nature rather than its mishap as in a disease [18].
Perhaps that is the barrier for moving ahead in studying Alzheimer’s
disease, it is easier to blame nature rather than to understand it.
None.
No conflict of interest.
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