Previous thought about learning has tended to treat the neural structure as neutral; not having a direct role in learning except as the means to reflect function. There has been little work that has seen the structure of the brain as an equal partner with function. There has been recognition that the brain changes by function such as training but littler thought that the active structure can influence the function. Lately there has been an interest in learning as the brain is put in motion.
Danielle S. Bassett, a MacArthur Award Fellow and a physicist at University of Penn, analyzed neuron interactions in the brain as people perform various tasks. She found that different parts of the brain communicate in distinct patterns and communication changes with learning or in the aftermath of a brain injury or disease. This research is developing the analytic tools to probe the hard-wired pathways and transient communication patterns inside of the brain in an effort to identify organizational principles which can lead to novel diagnoses and a design for personalized therapeutics for rehabilitation and treatment of neurological diseases. Bassett collected brain imaging data from people performing a motor task, pushing a series of buttons, similar to a sequence of notes on a piano keyboard, as fast as possible. The functional MRI images were separated into 112 different regions and analyzed how the different areas connected while they performed the task. They found that If you are very flexible, then you will end up learning better on the second day, and if you are not very flexible, then you learn less.
The conclusion from this work is that individuals differ in structural relation to functional tasks and that some structural patterns relate to different learning. The following question is if this functional-structural relationship can be modified by modifying structure. Burbaumer and Nitssche used Transcranial direct-current stimulation (tDCS), an experimental technique for delivering extremely low dose of electrical stimulation to the brain that uses less than 1% of the electrical energy necessary for electroconvulsive therapy, powered by an ordinary nine-volt battery. Side effects appear limited to a mild tingling at the site of the electrode, sometimes a slight reddening of the skin, very rarely a headache and certainly no seizures or memory loss. Administering tDCS can improve the speed or accuracy with which people perform attention-switching tasks. Other work has found it to improve everything from working memory to long-term memory, math calculations, reading ability, solving difficult problems, complex verbal thought, planning, visual memory, the ability to categorize, the capacity for insight, post-stroke paralysis and aphasia, chronic pain and even depression. Effects have been shown to last for weeks or months.
Hansen, N . et al., (2012) measured action mechanisms of transcranial direct current stimulation in Alzheimer’s disease and memory loss, and reported that tDCS is an easy to perform and non-invasive alternative therapeutic tool for neurodegenerative diseases such as AD. Its effects comprise the enhancement of cognitive functions in explicit and implicit memory. The mechanisms of tDCS are based on changes in membrane polarization, cerebral blood flow, functional connectivity, and brain oscillatory activity that may be altered in AD and other dementia disorders.
Several studies address the physiological effects of tDCS in working memory as a part of declarative memory playing a pivotal role in long-term memory, language, and executive function. tDCS has demonstrated efficacy in improving recognition memory in AD (Boggio et al., 2009, 2011) and that it is a useful tool in cognitive neuro=rehabilitation.
The effect of anodal tDCS (tDCS) over the left temporal cortex (TC) and dorsolateral pre frontal cortex (DLPFC) was investigated on recognition and working memory (WM) in 10 AD patients (Boggio, et al.,2009), and revealed enhancement in a visual recognition memory task after a tDCS of the DLPFC and left TC (Boggio etal., 2009). In another study, an improvement in word-recognition memory in 10 patients with probable AD was proven after a tDCS of the temporoparietal areas (Ferrucci etal., 2008). In contrast, cathodal tDCS (ctDCS) led to decreased word-recognition memory. The effect of a tDCS persisted up to 30 min after stimulation, indicating along-lasting increase in brain excitability (Ferrucci et al., 2008a). Long-term enhancement of visual recognition memory for up to 4 weeks after therapy was found after a tDCS in15 AD patients (Boggio etal., 2011). tDCS over the temporoparietal cortex in 20 elderly healthy subjects resulted in improved retention of object-location learning for up to 1week after learning (Flöel et al., 2011).
In a systematic review, itching, tingling, headache, burning sensation, and discomfort were the most often reported adverse side effects of active tDCS vs. sham tDCS (Brunoni et al., 2011). Skin irritation and skin burning can occur after tDCS application due to the electrochemical products’ skin contact generated by the direct current.
This work suggests that by introducing tDCS or similar structural changes to the current MTCA program we will find a greater effect of improvement in memory performance than with the sole training applied in the present. Ferrucci et al. (2008) evaluated the cognitive effect of transcranial direct current stimulation (tDCS) over the temporoparietal areas in patients with Alzheimer’s disease (AD) and found that it improved recognition memory performance in patients with Alzheimer’s disease.
Freitas, C., Mondragón-Llorca, H., & Pascual-Leone, A. (2011) found that transcranial magnetic stimulation (TMS), another potential therapeutic application, is a non-invasive technique for stimulation of the human brain and modulation of brain activity, while tDCS is a purely neuromodulatory intervention. TMS is based on electromagnetic induction and can be used to examine brain-behavior relations, map sensory, motor, and cognitive functions, and explore the excitability of different cortical regions. Repetitive TMS (rTMS) and tDCS have therapeutic potential in patients with neurologic and psychiatric disorders, as both can induce lasting modulation of brain activity in the targeted brain region and across brain networks through transcranial induction of electric currents in the brain. It is not, however, completely understood by which mechanisms of action TMS and tDCS induce these lasting effects on the brain. There is burgeoning evidence to suggest that the physiologic impact of both techniques involves synaptic plasticity, specifically long-term potentiation and long-term depression.
Short-latency afferent inhibition (SAI) is a consistent finding of altered motor cortical reactivity in AD regarded short-latency afferent inhibition. SAI refers to the suppression of the amplitude of a motor evoked potential (MEP) produced by a conditioning afferent electrical stimulus applied to the median nerve. The central cholinergic neural circuit has been shown to be reduced or abolished by the muscarinic antagonist scopolamine in healthy subjects. It has long been suggested that the pathogenesis of AD may involve deficits in the cholinergic circuits and agents that enhance cholinergic neurotransmission – e.g., acetylcholine-esterase inhibitors (AChEIs) – are associated with improvements in cognitive function and activities of daily living.
Gordon Dougal, Director of Virulite, a medical research company in England along with researchers at Durham University and the University of Sunderland, found that infrared light works to reverse memory loss in mice. Exposing middle-aged mice to infrared light improved their performance in a 3-D maze. Another infrared study measured whether problems with executive functioning (including attention, working memory, strategies of learning and remembering, planning, organizing, self-monitoring, inhibition, and flexible thinking) in humans can be effectively treated by repeated brief infrared light stimulation in order to increase cerebral blood flow, oxygenation, and facilitate removal of toxic proteins. More importantly, the method significantly altered the slope and course of dementia.
In conclusion, there are a number of techniques that modify structure either during learning or before, and find increases in function. The question is whether this can occur in AD as the individual is performing memory tasks and whether the procedure would magnify the training effect, and by how much.
1) Hansen, N. (2012). Action mechanisms of transcranial direct current stimulation in alzheimer’s disease and memory loss. Frontiers in Psychiatry, 3, 48
2) Boggio,P.S., Ferrucci,R., Mameli,F., Martins,D., Martins,O., Vergari,M., Tadini, L.,Scarpini, E., Fregni, F., and Priori, A. (2011). Prolonged visual memory enhancement after direct current stimulation in Alzheimer’s disease. Brain Stimul.
30 Boggio, P. S., Khoury, L. P., Martins, D.C., Martins, O. E.,de Macedo, E.C., and Fregni, F. (2009). Temporal cortex direct current stimulation enhances performance on a visual recognition memory task in Alzheimer disease. J. Neurol. Neurosurg. Psychiatr. 80, 444–447.
4) R. Ferrucci et al. Transcranial direct current stimulation improves recognition memory in Alzheimer disease. Neurology. 2008 Aug 12; 71 (7):493-8.
5) Flöel, A., Suttorp, W., Kohl, O., Kürten, J., Lohmann, H., Breitenstein, C., and Knecht, S.(2011).Non-invasive brain stimulation improves object- location learning in the elderly. Neurobiol. Aging
6) Freitas, C., Mondragón-Llorca, H., & Pascual-Leone, A. (2011). Noninvasive brain stimulation in Alzheimer’s disease: Systematic review and perspectives for the future. Experimental Gerontology, 46(8), 611.