1. ¹Clinica Neurologica, Dipartimento di Neuroscienze, Università di Roma 'Tor Vergata', Roma, Italy
2. ²IRCCS S. Lucia, Ospedale di Neuroriabilitazione, Via Ardeatina, Roma, Italy

Correspondence: Dr A Martorana, Clinica Neurologica, Dipartimento di Neuroscienze, Università di Roma 'Tor Vergata', via Montpellier, 1- 00133, Rome, Italy. Tel.: +0039 06 72596020; Fax: +0039 06 72596022; E-mail: martorana@med.uniroma2.it

Received 17 February 2009; Revised 5 May 2009; Accepted 8 May 2009; Published online 10 June 2009.

Abstract

In Alzheimer's disease (AD) patients dysfunction of cholinergic neurons is considered a typical hallmark, leading to a rationale for the pharmacological treatment in use based on drugs that enhance acetylcholine neurotransmission. However, besides altered acetylcholine transmission, other neurotransmitter systems are involved in cognitive dysfunction leading to dementia. Among others, dopamine seems to be particularly involved in the regulation of cognitive processes, also having functional relationship with acetylcholine. To test whether cholinergic dysfunction can be modified by dopamine, we used short latency afferent inhibition (SLAI) as a neurophysiological tool. First, we tested the function of the cholinergic system in AD patients and in healthy subjects. Then, we tested whether a single L-dopa challenge was able to interfere with this system in both groups. We observed that SLAI was reduced in AD patients, and preserved in normal subjects. L-dopa administration was able to restore SLAI modification only in AD, having no effect in healthy subjects. We conclude that dopamine can modify SLAI in AD, thus confirming the relationship between acetylcholine and dopamine systems. Moreover, it is suggested that together with cholinergic, dopaminergic system alteration is likely to occur in AD, also. These alterations might be responsible, at least in part, for the progressive cognitive decline observed in AD patients.