Parkinson's disease is caused by excessive loss of cells in the small population of dopamine-generating neurons. This is an exaggerated version of a loss that we all suffer due to the wear and tear of aging: many age-related conditions are of this nature, aggravated or more rapidly occuring versions of the same damage that everyone suffers. So all people lose some of the cells that generate the neurotransmitter dopamine, just not enough for that loss to become a named and known medical condition. But even this more modest loss of dopamine neurons causes functional decline in the brain, as researchers here demonstrate - with the intent to show that drugs that deliver dopamine to the brain could at least partially compensate for this decline:
Activation of the hippocampus is required to encode memories for new events (or episodes). Observations from animal studies suggest that, for these memories to persist beyond 4-6 hours, a release of dopamine generated by strong hippocampal activation is needed. This predicts that dopaminergic enhancement should improve human episodic memory persistence also for events encoded with weak hippocampal activation.
Here, using pharmacological functional MRI (fMRI) in an elderly population in which there is a loss of dopamine neurons as part of normal aging, we show this very effect. The dopamine precursor levodopa led to a dose-dependent (inverted U-shape) persistent episodic memory benefit for images of scenes when tested after 6 hours, independent of whether encoding-related hippocampal fMRI activity was weak or strong (U-shaped dose-response relationship). This lasting improvement even for weakly encoded events supports a role for dopamine in human episodic memory consolidation, albeit operating within a narrow dose range.