Laminar degeneration of frontal and temporal cortex in Parkinson disease dementia

Neurol Sci. 2017 Apr;38(4):667-671. doi: 10.1007/s10072-017-2828-6. Epub 2017 Feb 8.


To investigate cortical laminar degeneration in Parkinson's disease (PD) with dementia (PDD). Changes in density of α-synuclein-immunoreactive Lewy bodies (LB), Lewy neurites (LN), and Lewy grains (LG) together with surviving neurons, abnormally enlarged neurons (EN), vacuoles, and glial cell nuclei were measured across cortical laminae of frontal and temporal cortex in fifteen cases of PDD using quantitative methods and polynomial curve-fitting. Most frequently, LB and LN were distributed across all laminae, while LG were distributed in upper cortical laminae. Low densities of EN were present in most cases distributed across all cortical laminae. Densities of vacuoles and glia were greatest in upper and lower cortical laminae, respectively. In most gyri, there were no spatial correlations between the densities of LB, LN, and LG. Cortical degeneration of frontal and temporal lobes in PDD affects all cortical laminae. Laminar distributions may result from the spread of α-synuclein pathology from subcortical regions and subsequent spread via the cortico-cortical pathways. This spread may be a major factor in the development of dementia in PD.

Keywords: Cortical degeneration; Laminar distribution; Lewy body (LB); Parkinson’s disease dementia (PDD); Polynomial curve fitting; Synucleinopathy.

MeSH terms

  • Aged
  • Aged, 80 and over
  • Female
  • Frontal Lobe / metabolism
  • Frontal Lobe / pathology*
  • Humans
  • Immunohistochemistry
  • Male
  • Neuroglia / metabolism
  • Neuroglia / pathology
  • Neurons / metabolism
  • Neurons / pathology
  • Parkinson Disease / metabolism
  • Parkinson Disease / pathology*
  • Temporal Lobe / metabolism
  • Temporal Lobe / pathology*
  • alpha-Synuclein / metabolism


  • SNCA protein, human
  • alpha-Synuclein