[1][2][3] The disease causes atrophy of the posterior part of the cerebral cortex, resulting in the progressive disruption of complex visual processing.

[8] The atrophy is progressive; early symptoms include difficulty reading, blurred vision, light sensitivity, issues with depth perception, and trouble navigating through space.

[11] 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 PCA symptoms related to impaired movements in response to visual stimuli, such as navigation and apraxia.

[8][9] 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.

[9][12][13] Furthermore, if neural death spreads into other anterior cortical regions, symptoms similar to Alzheimer's disease, such as memory loss, may result.

[9][12] In PCA where there is significant atrophy in one hemisphere of the brain hemispatial neglect may result – the inability to see stimuli on one half of the visual field.

[11][12][15][16] Although PCA has an earlier onset, a diagnosis with Alzheimer's is often made, suggesting that the degeneration has simply migrated anteriorly to other cortical brain regions.

It has been suggested that depression or anxiety may result from the symptoms of decreased visual function, and the progressive nature of the disease.

[10][23] A key aspect found through brain imaging of PCA patients is a loss of grey matter (collections of neuronal cell bodies) in the posterior and occipital temporal cortices within the right hemisphere.

[10][25] At times people with PCA are treated with AD treatments, such as cholinesterase inhibitors: donepezil, rivastigmine, galantamine, and also memantine.