Caffeine is known to cause dementia by interrupting the
normal cycle of apoptosis and neurogenesis in
hippocampus, by enhancing apoptosis and inhibiting
neurogenesis. Prolonged use will cause hippocampal atrophy.

As the altered A-N cycle causes deteriation of
functions dependant of the normal cycle, this affects
memory and spatial learning functions, and as the cell
damage advances, so do the symptoms.

The data in this study has been interpreted as if the
biotransformation and cns-based sensitivity to caffeine
would be homogenous in the entire population. If this
was the case, the study would, without a doubt, be a
very strong evidence, supporting the conclusions of the
research team.

When taking in consideration known medical scientific
knowledge about the pharmacological effects of
caffeine, and their proven connection to dementia, the
raw data of this study leaves only one possible
explanation.

Processes causing dementia may be triggered by various
reactions between endogenic and exogenic factors.

Individuals whose body is well protected against
caffeine induced dementia, are also protected against
other exogenic triggers, while individuals with an
endogenous sensitivity to caffeine, may also be
sensitive to other exogenous triggers.

This is the only way to get the data of the study to
match with proved medical scientific knowledge.