Modafinil is a synthetic drug with fewer adverse effects than traditional psychostimulants such as amphetamine and methylphenidate. It has also been shown to enhance cognitive performance without disrupting normal sleep rhythms.
Studies suggest that the vigilance-promoting effects of modafinil are mediated by central catecholamine systems. Unlike amphetamine, modafinil does not bind to the catecholamine transporter (CAT) or have any specific binding site on nerve membrane ion channels.
How does modafinil affect the brain?
The drug Modafinil Australia was developed to treat narcolepsy but is widely used off-license as a ‘smart drug’ to promote cognitive enhancement in people who are not sleep-deprived. Studies in healthy subjects have shown that a single dose of modafinil can improve performance on tasks that require high levels of cognitive control, such as the WCST and Hayling sentence completion test. However, evidence from more detailed investigations of the effects of modafinil on specific neurotransmitter systems is scarcer.
One study found that modafinil increased extracellular levels of noradrenaline and dopamine in the rat locus coeruleus. It also enhanced the activity of the thalamocortical system in the brainstem and inferior olivary region by increasing gap junction coupling between cortical interneurons (Fig 1B). This effect was not blocked by the inhibition of calcium-calmodulin protein kinase II and was independent of adenylyl cyclase and dopamine transporter function.
Another study, using dual whole-cell recordings of neurons in the rat cortex, showed that the drug enhances the responses of individual neurons to stimulation by increasing intercellular coupling between these cells. This was accompanied by a reduction in the amplitude of the voltage response to stimulation in cell A and an increase in the response in cell B, resulting in an overall enhanced thalamocortical response.
Other research has suggested that the arousal and activity-promoting effects of modafinil are mediated by catecholamine systems, with elevations in extracellular dopamine levels, as well as noradrenaline and dopamine autoreceptor functions, in the accumbens. Modafinil also increases the activity of -adrenergic receptors and the activation of choline acetyltransferase in the brain.
Can modafinil prevent cognitive decline?
Modafinil, a drug prescribed for sleep-related conditions like narcolepsy, may improve cognitive function without serious side effects. A recent study shows that people who take the medication perform better on tests of planning and decision-making. But the research is still very early, and many scientists are skeptical about the benefits of cognitive-enhancing drugs.
In some animal studies, modafinil has been shown to enhance learning processes. In one experiment, researchers recorded the electrical activity of pyramidal cells and interneurons in deep cortical layers of the brain of a rat. They found that the drug had a strong effect on the amplitude of responses to paired stimulation from the ventrobasal thalamic nucleus. Modafinil also increased the input conductance of the neurons, allowing them to respond more quickly.
Several clinical trials have also found that Modalert Tablet can boost cognition in healthy individuals. In one randomized trial, participants who took a single dose of the drug performed better on tests of spatial planning and digit span than those who received placebo. The study’s authors suggest that the improvements seen in this study may be a result of modafinil’s ability to improve working memory.
Other clinical trials have found that modafinil can reduce errors on the Wisconsin Card Sort Test and interference in the Stroop task. It has also been shown to increase oculomotor delayed response and arithmetic performance in a controlled study. Using drugs such as modafinil to promote alertness can be dangerous and could cause serious side effects.
Can modafinil protect the brain from Alzheimer’s disease?
Modafinil improves performance on several cognitive tasks in healthy individuals, as well as in people with various sleep disorders. This suggests that modafinil has general cognitive enhancement effects, which could also extend to neurodegeneration prevention. However, more research is needed to understand the mechanisms underlying these effects.
A recent study in rats showed that the phenethylamine derivative CE-123, which is closely related to modafinil, improved motivation and resulted in superior performance in a new-to-learn operant discrimination task, and in a cooperation assay of social cognition, but had no effect on attention, spatial or motor learning.
Moreover, the compound enhanced behavioral inhibition and reduced impulsivity but slightly increased premature responses in the 5-CSRTT, an index of impulsive responding to short stimuli. This finding resembles findings of other studies of the drug’s congener modafinil, which increased impulsive responding to shorter stimulus durations29.
Using seed-based functional connectivity analysis, the authors found that modafinil treatment induced increased functional correlations with the BA17 region in comparison to placebo. The peak voxel coordinates of the clusters showing significant increases in r2 were found in the left and right cerebellar Crus I and II, the left cingulate and VIIIa lobules, and the right inferior frontal sulcus (Figure 3).
These results suggest that the enhancement of cognitive performance by modafinil is associated with increased functional connections between the V1 visual cortex and prefrontal cortices. This functional characterization of modafinil’s enhancement of cognition supports previous findings that the drug enhances V1 activity during a delayed-response task and correlates with performance in the Pauli test.
Can modafinil protect the brain from dementia?
Modafinil is a wakefulness-promoting agent that improves cognitive function in both healthy and sleep-deprived humans. Its effect on cognition appears to be related to alterations in frontal cortex activity, which may account for its efficacy against several neuropsychiatric disorders, such as narcolepsy and ADD/ADHD.
Although modafinil can increase your reaction speed, it should not be used to drive or operate machinery. It can also make you dizzy. You should avoid alcoholic beverages and marijuana (cannabis) while taking this medication.
In Australia, Modafinil is available only with a prescription from a doctor. Importing, attempting to import, or possessing modafinil without a prescription is illegal in the country. Those caught face a maximum penalty of $222,000 under the Customs Act 1901(Cth). The Australian Border Force is able to detect such imports and intercept them until buyers can prove they have a valid prescription. This law prioritizes health and legal compliance. In addition, this medication should not be taken by pregnant women as it can cause birth defects.
The exact mechanism by which modafinil improves cognitive function is not known, but it is thought to influence several neurotransmitters, including serotonin and glutamate, as well as histamine systems. Modafinil has been shown to increase the availability of histamine in the brain, which is believed to enhance attention and executive functioning. It also increases the release of acetylcholine in the brain, which is an inhibitory neurotransmitter.
In one randomized placebo-controlled study of 60 adults, modafinil improved performance on several measures of vigilance and cognition, including digit span, letter-number span, spatial planning, and SSRT. However, it did not affect arithmetic memory or visual recognition memory, suggesting that the improvement was due to increased working memory capacity rather than a speed-accuracy tradeoff.
Another study of scalp somatosensory evoked potentials found that modafinil 100 mg single doses produced significant effects on the short-latency component, with a wide scalp distribution and uniform polarity, which was associated with dipole modeling suggesting subcortical origination from monoamine nuclei. This finding supports the hypothesis that modafinil affects somatosensory input processing in brainstem centers, which is in line with its effect on the CPT-IP and other EEG phenomena. Read More Blog…