Illusory afterimages
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© 2001 Macmillan Magazines Ltd HIGHLIGHTS NATURE REVIEWS | NEUROSCIENCE VOLUME 2 | OCTOBER 2001 | 679 A key question in the pathogenesis of Alzheimer’s disease is the relation between the accumulation of β-amyloid (Aβ) and the formation of neurofibrillary tangles. Are the two processes entwined or are they independent manifestations of the disease? Two recent papers provide convincing evidence that the two archetypal neuropathological changes seen in Alzheimer’s disease are linked. Both papers converge on the idea that the formation of Aβ deposits acts to promote the appearance of tangles. Lewis et al. generated a long-awaited transgenic animal — a mouse carrying mutant forms of both the amyloid precursor protein (APP) and tau, the main component of neurofibrillary tangles. Mice bearing either one of the two mutant genes fail to recapitulate all of the neuropathological changes found in Alzheimer’s disease. It was therefore hoped that the double- transgenic mice would constitute a better model of the pathology. Indeed, these mice showed both amyloid plaques and tangles but, more importantly, the number of tangles in the double mutant was higher than in mice expressing only tau, indicating that the accumulation of Aβ might stimulate the formation of tangles. But is Aβ responsible for the observed phenotype or is it APP itself? In an independent study, Götz et al. used transgenic mice expressing tau but, instead of generating a double mutant, they injected Aβ directly into the cortex and hippocampus of these animals. They found that this treatment also increased the number of tangles, providing evidence that Aβ is indeed the molecule that stimulates tangle formation. An intriguing aspect of both studies is that Aβ and tau were spatially segregated. Lewis et al. found that, in contrast to what is found in Alzheimer’s disease, amyloid plaques were not surrounded by tau-positive neurites in the double mutants, and Götz et al. found that tangle formation was stimulated in brain regions far from the Aβ injection sites. So, it seems that these models also fail to reproduce every aspect of Alzheimer’s disease, although the two of them provide better tools to test more rigorously the benefit of new treatments for this pathology. Juan Carlos López References and links ORIGINAL RESEARCH PAPERS Lewis, J. et al. Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP. Science 293, 1487–1491 (2001) | Götz, J. et al. Formation of neurofibrillary tangles in P301L tau transgenic mice induced by Aβ42 fibrils. Science 293, 1487–1491 (2001) FURTHER READING Duff, K. & Rao, M. V. Progress in the modeling of neurodegenerative diseases in transgenic mice. Curr. Opin. Neurol. 14, 441–447 (2001) We are all familiar with afterimages. If you look at a bright light for a couple of seconds, then close your eyes, you will see a dark spot; similarly, gazing at a coloured shape can induce an after- image in the complementary colour — for example, a red square will pro- duce a green afterimage. This is usual- ly attributed to bleaching of the pig- ments in the retinal photoreceptors or to neural adaptation in the retina. But Shimojo et al. have found evidence that some afterimages can result from adaptation at a cortical level. They used a type of visual stimu- lus that is designed to cause ‘filling-in’, where the visual system draws on ele- ments in a visual scene to ‘complete’ a shape that is not actually there. In the Varin configuration, for example, four circles like those depicted in the figure are arrayed in a square layout. In each circle, the quadrant (or wedge) nearest the centre of the square is coloured differently from the rest of the circles, so that the four coloured quadrants appear to form the corners of a smaller, coloured square seen through the circles or superimposed on them. Our visual system fills in the missing lines so that we perceive a complete square. Looking at this stimulus for a while leads to the perception of an afterimage of a square, the colour of which is complementary to the per- ceived square’s colour, as well as after- images of the incomplete circles and the wedges. There are two possible mechanisms for the ‘global afterim- age’ of the square. It could arise from the perceived afterimages of the circles and wedges (the ‘local afterimages’), just as the original perception arises from the perception of the circles themselves; or it could be due to adap- tation of cortical neural circuits that represent the filled-in square surface (the ‘surface-adaptation hypothesis’). Shimojo and colleagues set out to discover which of these hypotheses was true. They used varying stimuli designed to induce different degrees of filling-in and different strengths of local afterimage, and asked people to rate the intensity and duration of the global afterimage. The results showed that the strength of the global after- image did not depend on the strength of the local afterimages, but rather on the degree of filling-in that had been induced by the stimulus. This result was predicted by the surface-adapta- tion hypothesis, but would not have been expected if the global afterimage arose from the local afterimages. Another unexpected finding was that the local and global afterimages appeared to rival each other, with most subjects reporting that they were seen separately but not together. This argues against even a compromise explanation, in which both proposed mechanisms contribute to the global afterimage. But the authors also report that some peripheral adaptation seems to be necessary for the global afterim- age to be perceived — when only one eye was adapted, for example, the global afterimage was not seen by the unadapted eye. Undoubtedly, there are still ques- tions to be answered before we will fully understand the mechanisms of adaptation. But studies such as these will also help us to understand how the visual system represents surfaces, whether real or illusory. Rachel Jones References and links ORIGINAL RESEARCH PAPER Shimojo, S. et al. Afterimage of perceptually filled-in surface. Science 293, 1677–1680 (2001) FURTHER READING Pessoa, L. et al. Finding out about filling-in: a guide to perceptual comple- tion for visual science and the philosophy of per- ception. Behav. Brain Sci. 21, 723–748 (1998) | Wilson, H. R. A neural model of foveal light adap- tation and afterimage formation. Vis. Neurosci. 14, 403–423 (1997) WEB SITE Shimojo’s lab: http://neuro.caltech.edu/ Aβ, τ and the fAβricaτion of τangles NEURODEGENERATIVE DISORDERS Illusory afterimages VISUAL PSYCHOPHYSICS
Transcript of Illusory afterimages
© 2001 Macmillan Magazines Ltd
H I G H L I G H T S
NATURE REVIEWS | NEUROSCIENCE VOLUME 2 | OCTOBER 2001 | 679
A key question in the pathogenesis of Alzheimer’s disease is therelation between the accumulation of β-amyloid (Aβ) and theformation of neurofibrillary tangles. Are the two processesentwined or are they independent manifestations of the disease?Two recent papers provide convincing evidence that the twoarchetypal neuropathological changes seen in Alzheimer’s diseaseare linked. Both papers converge on the idea that the formation ofAβ deposits acts to promote the appearance of tangles.
Lewis et al. generated a long-awaited transgenic animal — amouse carrying mutant forms of both the amyloid precursorprotein (APP) and tau, the main component of neurofibrillarytangles. Mice bearing either one of the two mutant genes fail torecapitulate all of the neuropathological changes found inAlzheimer’s disease. It was therefore hoped that the double-transgenic mice would constitute a better model of the pathology.Indeed, these mice showed both amyloid plaques and tangles but,more importantly, the number of tangles in the double mutantwas higher than in mice expressing only tau, indicating that theaccumulation of Aβ might stimulate the formation of tangles.
But is Aβ responsible for the observed phenotype or is it APPitself? In an independent study, Götz et al. used transgenic miceexpressing tau but, instead of generating a double mutant, theyinjected Aβ directly into the cortex and hippocampus of theseanimals. They found that this treatment also increased thenumber of tangles, providing evidence that Aβ is indeed themolecule that stimulates tangle formation.
An intriguing aspect of both studies is that Aβ and tau werespatially segregated. Lewis et al. found that, in contrast to what isfound in Alzheimer’s disease, amyloid plaques were notsurrounded by tau-positive neurites in the double mutants, andGötz et al. found that tangle formation was stimulated in brainregions far from the Aβ injection sites. So, it seems that thesemodels also fail to reproduce every aspect of Alzheimer’s disease,although the two of them provide better tools to test morerigorously the benefit of new treatments for this pathology.
Juan Carlos López
References and linksORIGINAL RESEARCH PAPERS Lewis, J. et al. Enhanced neurofibrillary degeneration intransgenic mice expressing mutant tau and APP. Science 293, 1487–1491 (2001) | Götz, J.et al. Formation of neurofibrillary tangles in P301L tau transgenic mice induced by Aβ42fibrils. Science 293, 1487–1491 (2001)FURTHER READING Duff, K. & Rao, M. V. Progress in the modeling of neurodegenerativediseases in transgenic mice. Curr. Opin. Neurol. 14, 441–447 (2001)
We are all familiar with afterimages. Ifyou look at a bright light for a coupleof seconds, then close your eyes, youwill see a dark spot; similarly, gazing ata coloured shape can induce an after-image in the complementary colour— for example, a red square will pro-duce a green afterimage. This is usual-ly attributed to bleaching of the pig-ments in the retinal photoreceptors orto neural adaptation in the retina. ButShimojo et al. have found evidencethat some afterimages can result fromadaptation at a cortical level.
They used a type of visual stimu-lus that is designed to cause ‘filling-in’,where the visual system draws on ele-ments in a visual scene to ‘complete’ ashape that is not actually there. In theVarin configuration, for example,four circles like those depicted in thefigure are arrayed in a square layout.In each circle, the quadrant (orwedge) nearest the centre of thesquare is coloured differently fromthe rest of the circles, so that the fourcoloured quadrants appear to formthe corners of a smaller, colouredsquare seen through the circles orsuperimposed on them. Our visualsystem fills in the missing lines so thatwe perceive a complete square.
Looking at this stimulus for awhile leads to the perception of anafterimage of a square, the colour ofwhich is complementary to the per-ceived square’s colour, as well as after-images of the incomplete circles andthe wedges. There are two possiblemechanisms for the ‘global afterim-age’ of the square. It could arise fromthe perceived afterimages of the circlesand wedges (the ‘local afterimages’),just as the original perception arisesfrom the perception of the circlesthemselves; or it could be due to adap-tation of cortical neural circuits thatrepresent the filled-in square surface(the ‘surface-adaptation hypothesis’).
Shimojo and colleagues set out todiscover which of these hypotheseswas true. They used varying stimulidesigned to induce different degreesof filling-in and different strengths oflocal afterimage, and asked people torate the intensity and duration of the
global afterimage. The results showedthat the strength of the global after-image did not depend on the strengthof the local afterimages, but rather onthe degree of filling-in that had beeninduced by the stimulus. This resultwas predicted by the surface-adapta-tion hypothesis, but would not havebeen expected if the global afterimagearose from the local afterimages.
Another unexpected finding wasthat the local and global afterimagesappeared to rival each other, with mostsubjects reporting that they were seenseparately but not together. Thisargues against even a compromiseexplanation, in which both proposedmechanisms contribute to the globalafterimage. But the authors also reportthat some peripheral adaptation seemsto be necessary for the global afterim-age to be perceived — when only oneeye was adapted, for example, theglobal afterimage was not seen by theunadapted eye.
Undoubtedly, there are still ques-tions to be answered before we willfully understand the mechanisms ofadaptation. But studies such as thesewill also help us to understand howthe visual system represents surfaces,whether real or illusory.
Rachel Jones
References and linksORIGINAL RESEARCH PAPER Shimojo, S. et al. Afterimage of perceptually filled-in surface.Science 293, 1677–1680 (2001)FURTHER READING Pessoa, L. et al. Findingout about filling-in: a guide to perceptual comple-tion for visual science and the philosophy of per-ception. Behav. Brain Sci. 21, 723–748 (1998) |Wilson, H. R. A neural model of foveal light adap-tation and afterimage formation. Vis. Neurosci.14, 403–423 (1997)WEB SITE Shimojo’s lab: http://neuro.caltech.edu/
Aβ, τ and the fAβricaτion of τangles
N E U R O D E G E N E R AT I V E D I S O R D E R S
Illusory afterimages
V I S U A L P S Y C H O P H Y S I C S
