The main symptom resulting from<unk>  is a decrease in visuospatial and visuoperceptual capabilities, since the area of<unk>  involves the occipital lobe responsible for visual processing. The<unk>  is progressive; early symptoms include difficulty reading, blurred vision, light sensitivity, issues with depth perception, and trouble navigating through space. Additional symptoms include apraxia, a disorder of movement planning, alexia, an impaired ability to read, and visual agnosia, an object recognition disorder. In the two-streams hypothesis damage to the ventral, or “what” stream, of the visual system, located in the temporal lobe, leads to the symptoms related to general vision and object recognition deficits; damage to the dorsal, or “where/how” stream, located in the parietal lobe, leads to<unk>  symptoms related to impaired movements in response to visual stimuli, such as navigation and apraxia. dorsal stream (green) runs through the parietal lobe, and the ventral stream (purple) runs through the temporal lobe. Both streams originate in the occipital lobe (blue) located<unk> ly. As neurodegeneration spreads, more severe symptoms emerge, including the inability to recognize familiar people and objects, trouble navigating familiar places, and sometimes visual hallucinations. In addition, difficulty may be experienced in making guiding movements towards objects, and a decline in literacy skills including reading, writing, and spelling may develop. Furthermore, if neural death spreads into other anterior<unk>  regions, symptoms similar to Alzheimer's disease, such as memory loss, may result. In<unk>  where there is significant<unk>  in one hemisphere of the brain hemispatial neglect may result – the inability to see stimuli on one half of the visual field. Anxiety and depression are also common symptoms. Connection to Alzheimer's disease Studies have shown that<unk>  may be a variant of Alzheimer's disease (AD), with an emphasis on visual deficits. Although in primarily different, but sometimes overlapping, brain regions, both involve progressive neural degeneration, as shown by the loss of neurons and synapses, and the presence of neurofibrillary tangles and senile plaques in affected brain regions; this eventually leads to dementia in both diseases. In<unk>  there is more<unk>  damage and gray matter (cell body) loss in<unk>  regions, especially in the occipital, parietal, and temporal lobes, whereas in Alzheimer’s there is typically more damage in the prefrontal cortex and hippocampus.<unk>  tends to impair working memory and anterograde memory, while leaving episodic memory intact, whereas in AD there is typically impaired episodic memory, suggesting some differences still lie in the primary areas of<unk>  damage. Over time, however,<unk>  in<unk>  may spread to regions that are commonly damaged in AD, leading to shared AD symptoms such as deficits in memory, language, learning, and cognition. Although<unk>  has an earlier onset, a diagnosis with Alzheimer’s is often made, suggesting that the degeneration has simply migrated anteriorly to other<unk>  brain regions. There is no standard definition of<unk>  and no established diagnostic criteria, so it is not possible to know how many people have the condition. Some studies have found that about 5 percent of people diagnosed with Alzheimer’s disease have<unk> . However, because<unk>  often goes unrecognized, the true percentage may be as high as 15 percent. Researchers and physicians are working to establish a standard definition and diagnostic criteria for<unk> .<unk>  may also be correlated with Lewy body disease, Creutzfeldt–Jakob disease, Bálint's syndrome, and Gerstmann syndrome. In addition,<unk>  may result in part from mutations in the presenilin 1 gene (PSEN1).
Posterior cortical atrophy
Geographic atrophy
Pellucid marginal degeneration
Hippocampal sclerosis
Polymicrogyria
Cerebral atrophy
Central chromatolysis
Neurofibrillary tangle