The name is absent

neurons, demands that in the longer time period cannot be satisfied. As a result toxic prod-
ucts should accumulate and neurons should die creating senile plaques.

Synaptic runaway may arise due to excessive memory overload, reduced synaptic de-
cay or a low level of cortical inhibition. If external strength is large enough or if internal
inhibition is sufficiently strong synaptic runaway may be prevented, but beyond critical
storage capacity it is unavoidable. This model explains some intriguing experimental facts
in AD:

• Enthorinal regions (involved in recognition memory) suffer greater degradation
than cortical areas. These regions lack internal inhibition present in cortical
modules.

• Cholinergic innervation in dentate gyrus in AD patients is sprouting.

Acetylcholine is a neurotransmitter that has complex functions. In dentate gyrus it
does not influence external afferent synaptic transmission but it selectively suppresses the
internal excitatory transmission, effectively increasing internal inhibition (experiments that
proved this were inspired by theoretical considerations of Hasselmo [9]). Thus sprouting of
cholinergic innervation may reflect the brain’s attempts to stop the synaptic runaway by in-
creasing internal inhibition.

Both these neural models complement rather than compete with each other. There may
be at least two routes to development of Alzheimer Disease: synaptic loss and insufficient
compensation should lead to AD cases with little structural damage of the brain, while syn-
aptic runaway should eventually lead to death of the hyperactive neurons and significant
structural damage. Both type of AD cases are indeed known.

5. TherapeutiC SuGGeStiOn fOr the early AD

Can we draw any therapeutic suggestions from these theoretical considerations? If
synaptic runaway processes and failure of proper compensation are the cause of rapid mem-
ory impairment several suggestions can be made. These suggestions may be tested experi-
mentally, although in view of high variability of the AD symptoms evaluation of efficiency
of any new therapy is always difficult.

• Minimize new memory load.

Minimization of new memory load may involve a simple and regular daily routine and
minimization of the number of new facts or items that should be remembered. Heavy mem-
ory load may contribute to the rapid progress of synaptic deletion. Patients should not be

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