Research paper for PSY 506 Fall 2004 (Return to classweb page)
A venerable body of literature has been amassed researchingAlzheimer's disease and related disorders. Alzheimer's disease (AD)is classified as a dementia disorder, which is "characterized by thedevelopment of multiple cognitive deficits (including memoryimpairment) that are due to the direct physiological effects of ageneral medical condition, to the persisting effects of a substance,or to multiple etiologies (e.g., the combined effects ofcerebrovascular disease and Alzheimer's disease)" (AmericanPsychiatric Association, 2000, p.147). Alzheimer's disease is themost commonly observed form of dementia (Small et al., 1997).
Alzheimer's disease is a neurodegenerative disorder. Investigationof the etiology of causal factors of AD has revealed evidence thatpathological change in cortical structures is associated with amyloidplaques and neurofibrillary tangles that affect the visual processingstreams and other areas. Amyloid plaques are abnormal structures thatemanate from a protein compound know as amyloid protein precursors orAPP. APP has no known function within cortical structures but isknown to be normally broken down into soluble fragments. Enzymes helpto create beta-amyloid peptides from the APP, which form amyloidfibers. These fibers combine to form plaques (senile plaques) thatare found in the post-mortem brains of AD patients (Robner,2004).
Alzheimer's disease has no confirmatory laboratory test exceptpost-mortem examination. Thus, psychological and neurologicalexaminations become a diagnosis of exclusion, based upon the symptomspresented by the patient. AD patient symptomology involves change inmultiple cognitive areas. AD is often first observed as a loss ofshort-term memory function (Jarvik, Lavretsky, & Neshkes, 1992;Kramer & Miller, 2000; Small et al., 1997) but is alsocharacterized by cognitive impairments such as aphasia andvisuocognitive disturbances.
Visual deficits are often observed despite the negative finding ofimpaired visual acuity or ocular disease (Sadun, Borchert, DeVita,Hinton, & Bassi, 1987). However, pathological changes have beenfound in the pre-cortical visual structures. Post-mortem evidencefrom AD patients has been found to show a reduction in optic nervefibers (Hinton, Sadun, Blanks, & Miller, 1986). More recentresearch has revealed that AD does not affect retinal ganglion cellswithin the retina or optic nerve axon structure (Curcio &Drucker, 1993; Davies, McCoubrie, McDonald, & Jobst, 1995). In amore recent study, Kergoat et al., 2001, demonstrated that opticnerve atrophy or retinal ganglion cell degeneration was notconsistent with AD.
The fact that AD may lead to visuocognitive impairment has nowbeen well documented (Cronin-Golomb, 2001; Cronin-Golomb, &Amick, 2001; Cronin-Golomb, Corkin, & Rosen, 1993; Cronin-Golomb;Mendez, Mendez, Martin, Smyth, & Whitehouse, 1990). The growingbody of evidence establishing the effects of AD on visual impairmentsuggests that the visual disturbances observed in AD may result fromneuropathology within the cortical regions associated with vision(Fujimori, et al., 2000). There is evidence of the existence of twomain neuronal streams that subserve the visual cognition in primates(Ungerleider & Mishkin, 1982) and in humans (Haxby, et al., 1991;Haxby et al., 1994). Ungerleider and Mishkin described the twoneuronal streams as the dorsal and ventral pathways. The dorsalpathway converges on the parietal lobe from the primary visualreceiving area (occipital lobe) and the ventral pathway converges onthe temporal lobe from the primary visual receiving area of theoccipital lobe. Each one of these pathways has been found to havespecialized functions in visual processing. The ventral pathway,called by Ungerleider and Mishkin as the "what" pathway is associatedwith object recognition and the dorsal pathway, described as the"where" pathway, is associated with spatial localization.
These visual processing pathways extend from the retina to thevisual association cortex, each serving a separate, but integralfunction. The ventral pathway extends from the retina with theP-ganglion cells through the parvocelluar layers of the lateralgeniculate nucleus (LGN) reaching the inferotemporal cortex (IT).This "P-pathway" is associated with our ability to discriminate colorand contrast sensitivity. The dorsal pathway extends from the retinawith the M-ganglion cells through the magnocellular layers of the LGNreaching the middle temporal cortex (MT). This M-pathway isassociated with our ability of motion detection.
Visual processing dysfunction in AD has also been shown to beassociated with neurological change and pathology within the ventraland dorsal pathways (Haxby, et al., 1991, 1994). Senile plaques foundin the post-mortem parvocellular areas of the LGN of AD patients havebeen found to be associated with P-pathway dysfunction (Leuba &Saini, 1995). Butter, Trobe, Foster, and Berent (1996) furtherdemonstrated that object recognition is more impaired than spatiallocalization in AD, with Arnold, Hyman, Flory, Damasio, & VanHoesen (1991) finding a magnified density of senile plaque in the ITregions. These studies indicate that many normal visual processesinvolve the P- or M- pathways and that senile plaque of AD patientbrains create abnormalities and dysfunctions within these corticalregions. Observable changes due to the widespread effects of senileplaques within the M-pathway have been found to affect contrastsensitivity in AD patients (Mendola, Cronin-Golumb, Corkin, &Growdon, 1995). A more recent study demonstrated that impairment ofcontrast sensitivity is not a primary result of general cognitivedecline but an actual perceptual dysfunction (Cronin-Golomb &Gilmore, 2003).
Other studies have revealed the effect of senile plaques in thediscrimination of faces. Damage to the IT region of the brain canresult in a condition known as prosopagnosia. Victims of thiscondition have demonstrated dysfunction in the facial recognition offamiliar people. As often experienced by caregivers and family, ADpatients may not be able to recognize the faces of family members,long-time friends, or even their own reflection in mirror. An areaidentified as the fusiform face area (FFA) located within thefusiform gyrus of the temporal lobe has been associated through fMRIstudies as being activated during facial recognition tasks (Clark etal., 1996). Other studies have isolated the function of facialrecognition within the ventral temporal and middle inferotemporalareas (Haxby et al., 1994). More recently, Van Rhijin et al. (2004)found impairment of unfamiliar face matching with reduced cerebralactivation in the middle inferotemporal cortex in AD patients.Cronin-Golomb & Gilmore (2003) also have studied the effect ofcontrast sensitivity impairment on face discrimination in AD. Withinthe AD population low spatial frequency ranges are the most prominentfactors associated with contrast sensitivity impairment(Cronin-Golomb & Gilmore, 2003). In a similar study Costen,Parker, & Craw (1994) found that the peak contrast sensitivityresponse for AD patients was found to be between 3 and 6 cycles perdegree for effective face recognition.
Van Rhijin et al. (2004) has posited the argument that assessmentand understanding of basic visual functions of AD patients mayprovide information on how to make adjustments within their livingenvironments that would raise their quality of life. Their studyrevealed a significant correlation between performance ratings ondaily life activities and brain activity. Their results furtherdemonstrated that pathology observed in AD corresponds to dailyliving skills that incorporate visual perception tasks.
Cronin-Golomb & Gilmore (2003) have suggested thatinterventions based upon the knowledge of these perceptualdysfunctions can translate into real-time adjustments that may be ofbenefit to the quality of life of the AD patient. They have suggestedthat increasing light intensity and enhancing visual stimulation canhave an effect. Providing high contrast dishes, drinking glasses, andeating utensils along with enhanced lighting intensity can maximumvisual contrast during meals.
Using research evidence in regards to contrast sensitivity, Sakaiet al. (2002) found that an AD patient diagnosed with apperceptiveagnosia visually benefited from enhanced contrast sensitivity. Thecontrast threshold of the patient was significantly increased withthe use of yellow tinted lenses in specially fitted eyeglasses.
Cernin, Keller, & Stoner (2003) investigated the potentialeffect of color cues as an environmental enhancement in an ADpopulation. Their findings suggested that color cues can make adifference in short-term memory recall. Vivid color-coding withinlong-term care facilities, i.e., color coding of patient's doors, mayresult in an enhanced quality of life and the functional capabilitiesof AD patients.
Investigation of the visuocognitive dysfunctions in AD patientsneeds to continue in areas of environmental adjustments. Cernin etal. (2003) suggest that studies need to focus on assessing the effectof environmental color enhancements for the AD population. Van Rhijinet al. (2004) suggest that continued research be conducted to measurethe effects of AD pathology using PET or SPECT technologies toprovide information on the capabilities of AD patients. By assessingthe capabilities of patients, environmental adjustments may bedeveloped to enhance their quality of life.
American Psychiatric Association. (2000). Diagnostic andStatistical Manual of Mental
Disorders (text revision). Washington, DC: Author.
Arnold, S.E., Hyman, B.T., Flory, J., Damasio, A.R., & VanHoesen, G.W. (1991) The
topographical and neuroanatomical distribution ofneurofibrillary tangles and neuritic
plaques in the cerebral cortex of patients withAlzheimer's disease. Cerebral Cortex, 1,
Butter,C.M., Trobe, J.D., Foster, N.L., & Berent. S. (1996).Visual-spatial deficits explain visual
symptoms in Alzheimer's disease. American Journal ofOpthalmology, 122, 97-105.
Cernin, P.A., Keller, B.K., & Stoner, J.A. (2003). Colorvision in Alzheimer's patients: Can we
improve object recognition with color cues? Aging,Neuropsychology, & Cognition, 10(4),
Costen, N.P., Parker, D.M., & Craw, I. (1994). Spatial contentand spatial quantization effects in
face recognition. Perception, 23, 129-146.
Cronin-Golomb, A. (2001). Color vision, object recognition, andsptial localization in aging and
Alzheimer's disease. In P.R. Hof and C.V. Mobbs (Eds.),Functional Neurobiology of
Aging (pp. 517-529). San Diego: Academic Press.
Cronin-Golomb, A., & Amick, M. (2001). Spatial abilities inaging. Alzheimer's disease, and
Parkingson's disease. In F. Boller and S. Cappa (Eds.),Handbook of Neuropsychology,
2nd edition, Vol. 6 (pp.119-143).
Cronin-Golomb, A., Corkin, S., & Rosen, T.J. (1993).Neuropsychological assessment of
dementia. In P.J. Whitehouse (ed.), Dementia,(pp.130-164). Philadelphia: F.A. Davis.
Cronin-Golomb, A., & Gilmore, G.C. (2003). Visual factors incognitive dysfunction and
enhancement in Alzheimer's disease. In S. Soraci, Jr.& K. Murata-Soraci (Eds.). Visual
Information Processing (pp. 3-34). Westport: PraegerPublishers.
Curcio, C.A., & Drucker, D.N. (1993). Retinal ganglion cellsin Alzheimer's disease and aging.
Annuals of Neurology, 33, 248-257.
Davies, D.C., McCourbie, P., McDonald, B., Jobst, K.A. (1995).Myelinated axon number in the
optic nerve is unaffected by Alzheimer's disease. BritishJournal of Opthalmology, 79, 596-
Fujimori,M., Imamura, T., Hirono, N., Ishii, K., Sasaki, M., & Mori, E. (2000). Disturbances of
spatial vision and object correlate differently withregional cerebral glucose metabolism in
Alzheimer's disease. Neuropsychogia, 38, 1356-1361.
Haxby, J.V., Grady, C.L., Horwitz, B., Ungerleider, L.G., Mishkin,M., Carson, R.E.,
Herscovitch, P., Schapiro, M.B., & Rapoport, S.I.(1991). Dissociation of object and
spatial visual processing pathways in human extrastriatecortex. Procedures of the National
Academy of Science, USA, 88, 1621-1652.
Haxby, J.V., Horwitz, B., Ungerleider, L.G., Maisog, J.M.,Pietrini, P., & Grady, C.L. (1994).
The functional organization of human extrastriate cortex:a PET-rCBF study of selective
attention to faces and locations. Journal ofNeuroscience, 14, 6336-1653.
Hinton, D.R., Sadun, A.A., Blanks, J.C., & Miller, C. (1986).Optic nerve degeneration in
Alzheimer's disease. New England Journal of Medicine,315, 485-487.
Jarvik, L.F., Lavretsky, E.P., & Neshkes, R.E. (1992).Dementia and delirium in old age. In J.C.
Brocklehurst, R.C. Tallis, & H.M. Fillit (Eds.).Textbook of geriatric medicine (pp. 326-
348). New York: Churchill Livingstone.
Kergoat,H., Kergoat, M-J., Justino, L., Robillard, A., Bergman,H., & Chertkow, H. (2001).
Normal nerve head topography in the early stages ofdementia of the Alzheimer's type.
Dementia and Geriatric Disorders, 12, 359-363.
Kramer, J.H., & Miller, B.L. (2000). Alzheimer's disease andits focal variants. Seminars in
Neurology, 20, 447-454.
Leuba, G., & Saini, K. (1995). Pathology of subcortical visualcentres in relation to cortical
degeneration in Alzheimer's disease. Neuropathology andApplied Neurobiology, 21, 410-
Mendez, M.F., Mendez, M.A., Martin, R., Smyth, K.A., & Whitehouse, P.J. (1990). Complex
visual disturbances in Alzheimer's disease. Neurology,40, 439-443.
Mendola, J.D., Cronin-Golomb, A., Corkin, S., & Growdon, J.H.(1995). Prevalence of visual
deficits in Alzheimer's disease. Optometry and VisionbScience, 72, 155-167.
Robner, S. (2004) New players in old amyloid precursorprotein-processing pathways.
International Journal of Developmental Neuroscience, 22,467-474.
Sadun, A.A., Borchert, M., DeVita, E., Hinton, D.R., & Bassi,C.J. (1987). Assessment of visual
impairment in patients with Alzheimer's disease.American Jopurnal of Opthalmology,
Sakai, S., Hirayama, K., Lwasaki, S., Fujii, T., Hashimoto, R.,& Yamadori, A. (2002). Yellow
glasses improve contrast sensitivity of a patient with avisual variant of Alzheimer's
disease. European Nerology, 48, 224-225.
Small, G.W., Rabins, P.V., Barry, P.P., Buckholtz, N.S., DeKosky,S.T., & Ferris, S.H. (1997).
Diagnosis and treatment of Alzheimer's disease andrelated disorders. Journal of the
American Medical Association, 278, 1363-1371
Ungerleider, L.G., & Mishkin, M.; (1982). Two cortical visualsystems. In D.J. Ingle, M.A.
Goodale, & R.J.W. Mansfield (Eds.). Analysis of visualbehavior (pp. 549-586). Cambridge.
MA: MIT Press.
Van Rhijin, S.J., Glosser, G., de Vries, J.J., Clark, C.M.,Newberg, A.B., & Alavi, A. (2004).
Visual processing impairments and decrements in regionalbrain activity in Alzheimer's
disease. Journal of Clinical and ExperimentalNeuropsychology, 26, 11-23.