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Alzheimer Disease

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The documentation of a severe form of dementia by Alois Alzheimer in 1907 began a massive investigation of the cause of this disorder. Some of the common symptoms of Alzheimer's Disease consist of memory loss, impaired language ability, impaired judgement, and learning (M. Wong, et al. , 1997). Alzheimer's Disease (AD) is mainly a disease of the cerebral cortex. Alzheimer's is marked structurally by the senile plaques, neurofibrillary tangles, and severe loss of neurons and synapses in the cerebral cortex. Alzheimer's is a neurodegenerative disorder ( Hof, Vogt, Bouras, and Morrison 1997). Recent attention has been focused on visual dysfunction in Alzheimer's Disease (K. U. Loffler, D. P. Edward, & M. O. M. Tso 1995).

Visual Problems

During the clinical evaluation of patients with mild to moderate dementia of the AD type, visual difficulties such as : topographic agnosia, visual agnosia, alexia without agraphia, and prosopagnosia are detected. AD patients have The problem of describing the individual components of a picture is consistent with the severity of cytochrome oxidase (C.O.) deficits in the association cortical areas. Other deficits experienced by AD patients were texture discrimination, blue-violet discrimination, and 4.72 deg/sec motion detection. When AD patients were compared to other age-matched controls, AD patients had shown specific deficits in contrast sensitivity. Deficits in color vision were only age-related (M. Wong-Riley, et al. , 1997).

Studies

Selective degeneration of large ganglion cell axons was observed in the optic nerves of AD patients, which suggested an impairment of broad-band channel visual function. Although studies show that the broad-band visual capabilities are not selectively impaired in AD. Dorsal LGN studies have shown that both the magno- and parvicellular neurons were greatly affected in AD patients.

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