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Alzheimer’s
disease (AD) is characterized by deficits
in cholinergic neurotransmission, a
mechanism involving a range of enzymes
and receptor ion channels. The family
of nicotinic acetylcholine receptors
(nAChR) which are activated by the endogenous
neurotransmitter acetylcholine is of
particular importance.
These receptors are expressed in many
regions of the central and peripheral
nervous system where homomeric or heteromeric
combination of 12 different subunits
(alpha2-alpha10, beta2-beta4) leads
to the formation of functional ion channels
with characteristic physiological and
pharmacological properties.
Recent studies have demonstrated that
amyloid-b (Ab) peptides can affect some
of these nonselective cation channels
and that agonists and positive modulators
have pro-cognitive effects in vivo.
Targeted modulation of nAChRs by small
molecules should thus lead to effective
treatments of cognitive deficits observed
in AD. |
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