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J Neurol Neurosurg Psychiatry doi:10.1136/jnnp-2012-304177
  • Editorial commentary

Motor deficits associated with changes in β-amyloid in Parkinson's disease

  1. Glenda M Halliday
  1. Correspondence to Professor Glenda M Halliday, Neuroscience Research Australia, Randwick, NSW 2031, Australia; g.halliday{at}neura.edu.au
  • Received 13 October 2012
  • Accepted 17 October 2012
  • Published Online First 9 November 2012

β-Amyloid (Aβ) deposition in the brain is one of the main pathological hallmarks of Alzheimer's disease (AD), with dominant gene mutations significantly increasing the amount of this protein in the brain and heralding an early onset of dementia.1 Deposition of Aβ in the brain identified by PET imaging is closely associated with decreased CSF levels of the protein, findings that are now used clinically to assist with the diagnosis of AD.

There is considerable ongoing debate regarding the contribution of AD pathology to Parkinson's disease (PD), but few studies have assessed the CSF levels of AD proteins for correlations with motor impairments in sporadic PD. The study by Alves and colleagues in this issue of the journal assessed 99 de novo PD patients with either tremor-dominant (PD-TD) or postural instability/gait disorder (PD-PIGD) disease for associations with CSF levels of Aβ proteins.2 It does not assess …

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