. CSF amyloid {beta} 1-42 predicts cognitive decline in Parkinson disease. Neurology. 2010 Sep 21;75(12):1055-61. PubMed.

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  1. Amyloid-β is likely an intermediate in the development of dementia and neuronal cell death in Alzheimer disease and in some cases of Parkinson disease, whereas peroxynitrites may be the principal culprit. Through oxidation and nitration, peroxynitrites disrupt neurotransmissions and lead to a critical shortage of acetylcholine, which is involved in the retrieval of short-term memories. Polyphenols can be used to scavenge peroxynitrites and to partially reverse both peroxynitrite-mediated oxidation and nitration of proteins. The progression of certain types of dementia may thus not only be stopped, but partially reversed.

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    View all comments by Lane Simonian
  2. This interesting study strengthens the general association of β amyloid pathology with cognitive decline. The study is important since it both illustrates the importance of disturbed β amyloid metabolism in conditions other than Alzheimer disease (AD), and gives clues to the roots of cognitive decline in Parkinson disease (PD).

    Cognitive decline in PD was associated with low cerebrospinal fluid (CSF) Aβ1-42 at baseline, but not with total tau or phospho-tau levels. This suggests that brain amyloid pathology contributes to cognitive decline in PD. The findings may be viewed in relation to studies of brain amyloid pathology in normal aging. Brain amyloid accumulation is present in a high proportion of cognitive healthy elderly and in many elderly with stable mild cognitive impairment (1-5). Although this might represent cases of incipient AD, it also suggests individual differences in resistance to amyloid pathology. Concomitant PD pathology might aggravate the toxicity of amyloid, pushing patients over a critical threshold in the amyloid disease cascade. The mechanism behind this could be interactions between α-synuclein and amyloid, since these molecules promote each other’s respective accumulation and aggregation (6). In this regard, PD might be a force that drives age-associated subclinical amyloid pathology into clinical symptoms.

    To further understand these interesting associations, detailed studies are needed on interactions between α-synuclein and amyloid in vivo in humans. Follow-up investigations of the subjects in the current study would be valuable. Specifically, it would be interesting to know if amyloid pathology at baseline predicted biomarker measurements of neuronal degeneration at follow-up, such as CSF total tau or MRI findings of atrophy.

    References:

    . Neuropathology of older persons without cognitive impairment from two community-based studies. Neurology. 2006 Jun 27;66(12):1837-44. PubMed.

    . Diagnosis-independent Alzheimer disease biomarker signature in cognitively normal elderly people. Arch Neurol. 2010 Aug;67(8):949-56. PubMed.

    . Age, neuropathology, and dementia. N Engl J Med. 2009 May 28;360(22):2302-9. PubMed.

    . Cerebrospinal fluid biomarker signature in Alzheimer's disease neuroimaging initiative subjects. Ann Neurol. 2009 Apr;65(4):403-13. PubMed.

    . CSF biomarkers and incipient Alzheimer disease in patients with mild cognitive impairment. JAMA. 2009 Jul 22;302(4):385-93. PubMed.

    . Synergistic Interactions between Abeta, tau, and alpha-synuclein: acceleration of neuropathology and cognitive decline. J Neurosci. 2010 May 26;30(21):7281-9. PubMed.