Pseudo-Synesthesia through Reading Books with Colored Letters

Background Synesthesia is a phenomenon where a stimulus produces consistent extraordinary subjective experiences. A relatively common type of synesthesia involves perception of color when viewing letters (e.g. the letter ‘a’ always appears as light blue). In this study, we examine whether traits typically regarded as markers of synesthesia can be acquired by simply reading in color. Methodology/Principal Findings Non-synesthetes were given specially prepared colored books to read. A modified Stroop task was administered before and after reading. A perceptual crowding task was administered after reading. Reading one book (>49,000 words) was sufficient to induce effects regarded as behavioral markers for synesthesia. The results of the Stroop tasks indicate that it is possible to learn letter-color associations through reading in color (F(1, 14) = 5.85, p = .030). Furthermore, Stroop effects correlated with subjective reports about experiencing letters in color (r(13) = 0.51, p = .05). The frequency of viewing letters is related to the level of association as seen by the difference in the Stroop effect size between upper- and lower-case letters (t(14) = 2.79, p = .014) and in a subgroup of participants whose Stroop effects increased as they continued to read in color. Readers did not show significant performance advantages on the crowding task compared to controls. Acknowledging the many differences between trainees and synesthetes, results suggest that it may be possible to acquire a subset of synesthetic behavioral traits in adulthood through training. Conclusion/Significance To our knowledge, this is the first evidence of acquiring letter-color associations through reading in color. Reading in color appears to be a promising avenue in which we may explore the differences and similarities between synesthetes and non-synesthetes. Additionally, reading in color is a plausible method for a long-term ‘synesthetic’ training program

A Novel Neurotrophic Drug for Cognitive Enhancement and Alzheimer's Disease

Currently, the major drug discovery paradigm for neurodegenerative diseases is based upon high affinity ligands for single disease-specific targets. For Alzheimer's disease (AD), the focus is the amyloid beta peptide (Aß) that mediates familial Alzheimer's disease pathology. However, given that age is the greatest risk factor for AD, we explored an alternative drug discovery scheme that is based upon efficacy in multiple cell culture models of age-associated pathologies rather than exclusively amyloid metabolism. Using this approach, we identified an exceptionally potent, orally active, neurotrophic molecule that facilitates memory in normal rodents, and prevents the loss of synaptic proteins and cognitive decline in a transgenic AD mouse model

What have we learned from the streptozotocin-induced animal model of sporadic Alzheimer's disease, about the therapeutic strategies in Alzheimer's research

Experimental models that faithfully mimic the developmental pathology of sporadic Alzheimer's disease (sAD) in humans are important for testing the novel therapeutic approaches in sAD treatment. Widely used transgenic mice AD models have provided valuable insights into the molecular mechanisms underlying the memory decline but, due to the particular β-amyloid-related gene manipulation, they resemble the familial but not the sporadic AD form, and are, therefore, inappropriate for this purpose. In line with the recent findings of sAD being recognised as an insulin resistant brains state (IRBS), a new, non-transgenic, animal model has been proposed as a representative model of sAD, developed by intracerebroventricular application of the betacytotoxic drug streptozotocin (STZ-icv). The STZ-icv-treated animals (mostly rats and mice) develop IRBS associated with memory impairment and progressive cholinergic deficits, glucose hypometabolism, oxidative stress and neurodegeneration that share many features in common with sAD in humans. The therapeutic strategies (acetylcholinesterase inhibitors, antioxidants and many other drugs) that have been tested until now on the STZ-icv animal model have been reviewed and the comparability of the drugs' efficacy in this non-transgenic sAD model and the results from clinical trials on sAD patients, evaluated

Synaesthetic colour in the brain: Beyond colour areas: A functional magnetic resonance imaging study of synaesthetes and matched controls

Contains fulltext : 126917.pdf (publisher's version ) (Open Access)Background: In synaesthesia, sensations in a particular modality cause additional experiences in a second, unstimulated modality (e. g., letters elicit colour). Understanding how synaesthesia is mediated in the brain can help to understand normal processes of perceptual awareness and multisensory integration. In several neuroimaging studies, enhanced brain activity for grapheme-colour synaesthesia has been found in ventral-occipital areas that are also involved in real colour processing. Our question was whether the neural correlates of synaesthetically induced colour and real colour experience are truly shared. Methodology/Principal Findings: First, in a free viewing functional magnetic resonance imaging (fMRI) experiment, we located main effects of synaesthesia in left superior parietal lobule and in colour related areas. In the left superior parietal lobe, individual differences between synaesthetes (projector-associator distinction) also influenced brain activity, confirming the importance of the left superior parietal lobe for synaesthesia. Next, we applied a repetition suppression paradigm in fMRI, in which a decrease in the BOLD (blood-oxygenated-level-dependent) response is generally observed for repeated stimuli. We hypothesized that synaesthetically induced colours would lead to a reduction in BOLD response for subsequently presented real colours, if the neural correlates were overlapping. We did find BOLD suppression effects induced by synaesthesia, but not within the colour areas. Conclusions/Significance: Because synaesthetically induced colours were not able to suppress BOLD effects for real colour, we conclude that the neural correlates of synaesthetic colour experience and real colour experience are not fully shared. We propose that synaesthetic colour experiences are mediated by higher-order visual pathways that lie beyond the scope of classical, ventral-occipital visual areas. Feedback from these areas, in which the left parietal cortex is likely to play an important role, may induce V4 activation and the percept of synaesthetic colour.12 p

Anomalous perception in synaesthesia: A cognitive neuroscience perspective

An enduring question in cognitive neuroscience is how the physical properties of the world are represented in the brain to yield conscious perception. In most people, a particular physical stimulus gives rise to a unitary, unimodal perceptual experience. So, light energy leads to the sensation of seeing, whereas sound waves produce the experience of hearing. However, for individuals with the rare phenomenon of synaesthesia, specific physical stimuli consistently induce more than one perceptual experience. For example, hearing particular sounds might induce vivid experiences of colour, taste or odour, as might the sight of visual symbols, such as letters or digits. Here we review the latest findings on synaesthesia, and consider its possible genetic, neural and cognitive bases. We also propose a neurocognitive framework for understanding such anomalous perceptual experiences