Using methamphetamine may have long-lasting consequences on brain chemistry, impairing memory function even after the habit is kicked, according to a new report from scientists at the Hopkins School of Medicine.
The findings, published last week in Synapse, provide the first clear evidence of a link between meth use, altered brain chemistry and, ultimately, cognitive deficits.
Meth works primarily at the synapse, the junction between two neurons where messages are sent and received.
Most neurons don't actually make physical contact with their neighbors. Instead, signals are sent between them in the form of chemicals, called neurotransmitters. These are released into a very small gap that separates the two neurons.
Chemical synapses, as these are called, permit neurons to send a range of messages using the same neurotransmitter by allowing them to modulate how much neurotransmitter is released, or how fast, or at what time.
Likewise the neuron on the signal's receiving end will respond very differently depending on how much neurotransmitter is floating around in the synaptic cleft at any given time. Large amounts of free neurotransmitter outside the cell will cause dramatic responses.
An important part of a well-tuned synapse is the timely removal of old neurotransmitter. Otherwise, instead of getting an isolated, one-time message the receiving neuron will read the same signal over and over again.
This is analogous to keeping your hands under an automatic hand dryer for longer than it takes to dry them: The air will keep blasting until either your hands are scorched or the fuse blows.
Neurotransmitter-specific pumps that suck extra neurotransmitter out of the synaptic cleft are found on every neuron. Meth acts by interfering with one - the dopamine transporter (DAT) - in particular.
Dopamine is used in the brain's reward system, which reinforces certain behaviors (sex and eating, for example) by causing pleasurable feelings. Unsurprisingly, many other drugs in addition to meth act on this system.
Drugs hijack these normal reinforcement pathways, producing abnormal dependence and seeking behaviors. In the case of meth, lots of extra dopamine floating around the brain's 2.5 quadrillion synapses makes for some good vibrations.
But short-term euphoria goes hand-in-hand with long-term damage. Prolonged meth use drastically lowers the abundance of dopamine in the brain, since neurons don't produce more if their synapses are already clogged.
What's more, meth causes any DAT at the synapse to be pulled back far into the neuron's body, rendering it useless.
Damage on the cellular level often leads to cognitive impairments. Meth users have been observed to have shortened attention spans, decreased visual speed as well as problems with decision-making.
This effect is thought to be semi-permanent, since even ex-users show some cognitive decline months or years after they kick their addiction.
Until the present study, however, no solid evidence existed linking a reduced presence of DAT at the synapse and long-lasting cognitive impairments.
A previous study from 2006 even found no significant cognitive decline in ex-users.
The Hopkins team's results, however, showed a clear association. The team, led by George Ricaurte of the Department of Neurology, recruited 22 ex-meth users and 17 controls.
After undergoing a battery of cognitive tests, the subjects' brains were scanned using positron emission tomography (PET) - a 3-D imaging technique - to quantify exactly how much DAT was present at their synapses.
Not surprisingly, ex-users performed more poorly on the cognitive tests than controls, especially in the area of memory. What's more, the ex-users had significantly less DAT than did controls.
The biggest finding, though, was that both declines (cognitive and chemical) were still evident in the ex-users even after an average of six meth-free years. Today's abuse, it seems, has abiding consequences.
