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academies
March 14-16, 2019 | London, UK
12
th
International Conference on
8
th
International Conference on
Vascular Dementia and Dementia
Neurological Disorders and Stroke
Joint Event
&
Journal of Brain and Neurology | Volume 3
Dementia: Alzheimer as a run-away Auto-immune disease
Alain L Fymat
International Institute of Medicine and Science, USA
Dementia is a broad category of brain diseases that cause a
long-term and often gradual decrease in cognitive, emotional,
functional and behavioral ability, resulting ultimately in death.
The affected person’s consciousness is not impaired. The
most common type of dementia is Alzheimer disease (AD),
which makes up 50% to 70% of cases. Other common types
include vascular dementia (25%), Lewy body dementia (15%),
and frontotemporal dementia. Less common causes include
normal pressure hydrocephalus, Parkinson’s disease dementia,
syphilis, and Creutzfeldt–Jakob disease among others. More
than one type of dementia may exist in the same person. A
small proportion of cases run in families. I will concentrate on
AD which, once considered a rare disorder over the past few
decades, has emerged fromobscurity to become amajor public
health problem. Based on a lack of treatment, it has generally
been considered as an irreversible, progressive brain disease.
It is a chronic neurodegenerative disorder of poorly (or not)
understood cause(s). Based on identified risk factors, beyond
genetics, several theories (15 or more), have been propounded
for its cause(s). Such a wide array of hypotheses is by itself
indicative of our lack of true understanding and knowledge
of the disease notwithstanding the fact that the disease has
been identified since 1901 and has been the subject of a
considerable number of publications dealing with it (in excess
of 50,000, according to some authors). Despite claims by some
research clinicians, there are currently no known treatments if
only to stop or reverse its progression. Some of these alleged
”treatments”, including the advocated program (“DESS”:
Diet, Exercise, Stress, Sleep, and variations on this theme) are
palliative in nature, temporarily improving symptoms, while the
disease progresses unabated. One must keep in mind that risk
is not causation and risk management is not cure!
Research has rather focused on diagnosing the condition before
symptomsbegin. Thus, anumber of biochemical testshavebeen
developed to attempt earlier detection. Again, however helpful,
such tests are not curative. I will posit that the compromised
integrityof thebloodbrainbarrier is acomponent of theetiology
of the disease, not a consequence of it. I will further submit
that the root cause of the disease is the brain’s autoimmune
system having gone rogue (a sort of “run away” effect) in its
unsuccessful attempts to maintain brain homeostasis between
the antagonistic synaptoblastic and synaptoclastic pressures.
The cure would be to balance these pressures by regulating the
system rather than fiercely combating either the hyper-excited
synaptoblastic pressures or/and suppressing the synaptoclastic
ones. I will review and discuss the above factors and also offer
some potential curative approaches, including natural and
synthetic (chimeric antigen receptor CAR T-cells) cell-based
immunotherapies utilizing Treg-cells.
e:
alain.fymat@fiimas.org