Serotonergic Function and Behavioural and Psychological Symptoms of Frontotemporal Dementia
Status:
Completed
Trial end date:
2009-09-01
Target enrollment:
Participant gender:
Summary
Frontotemporal lobar degeneration(FTLD) is a common cause of early-onset dementia. FTLD is
characterized multiple behavioral symptoms including mental rigidity, irritability, emotional
blunting, disinhibition, apathy, and aggression. These behavioural disturbances are
particularly important because they increase caregiver burden and may lead to earlier
institutionalization. While the causes of FTLD are largely unknown, there is a great deal of
evidence suggesting that a brain chemical called serotonin regulates many of the behaviours
that are disturbed in FTLD. Our objective is therefore to determine whether dysfunction in
the brain's serotonin system is responsible for behavioural problems among FTLD patients. We
hope to take the first steps towards a scientific understanding of the behavioural symptoms
of FTD, and use our findings to support a larger study optimizing the treatment of targeted
behavioural disturbances in FTLD using the antidepressant citalopram.
Citalopram increases transmission by serotonin; we plan to use this medication to determine
whether there are any differences in how the serotonin system functions in FTLD patients who
display different levels of behavioural disturbances. Patients will be given citalopram and
will have their blood drawn after 2 and 3 hours to determine plasma levels of the hormones
cortisol and prolactin at those times. These hormones are good indicators of serotonergic
functioning in the central nervous system.
We expect that patients with lower levels of serotonergic functioning will have more severe
behavioural disturbances and be less responsive to treatment with citalopram. Following their
first test day, we will provide patients with a 6-week supply of citalopram, and assess them
for any changes in behaviour at the end of this treatment.
This study aims to obtain a better understanding of how changes in the serotonin system
relate to behavioural symptoms in FTLD patients. Using the information from this pilot study,
we can plan a larger study to determine whether certain behaviours will respond to treatment
with citalopram, and if so, determine whether it is possible to predict which patients, based
on individual characteristics, are most likely to respond to this treatment. This methodology
will therefore not only provide a scientific rationale for treatment of FTLD, but also
provide guidance for ongoing, individualized therapy.