Showing posts with label alpha-synuclein. Show all posts
Showing posts with label alpha-synuclein. Show all posts

Thursday, November 6, 2014

Neuroinflammation in Parkinson's disease: role in neurodegeneration and tissue repair.

reposted from

Neuroinflammation in Parkinson's disease: role in neurodegeneration and tissue repair.

Int J Neurosci. 2014 Nov 3:1-17. [Epub ahead of print]
Vivekanantham SShah SDewji RDewji AKhatri COlogunde R.

Abstract

Neuroinflammation in Parkinson's disease [PD] is a process that occurs alongside the loss of dopaminergic neurones, and is associated with alterations to many cell types, most notably microglia. This review examines the key evidence contributing to our understanding of the role of inflammation-mediated degeneration of the dopaminergic (DA) nigrostriatal pathway in PD. It will consider the potential role inflammation plays in tissue repair within the brain, inflammation linked gene products that are associated with sporadic parkinsonian phenotypes (alpha-synuclein, parkin and Nurr 1), and developing anti-inflammatory drug treatments in PD. With growing evidence supporting the key role of neuroinflammation in PD pathogenesis, new molecular targets are being found that could potentially prevent or delay nigrostriatal DA neurone loss. Hence, this creates the opportunity for disease modifying treatment, to currently what is an incurable disease.

Thursday, April 24, 2014

Gut feelings about smoking and coffee in Parkinson's disease.

reposted from

Gut feelings about smoking and coffee in Parkinson's disease.
Mov Disord. 2014 Apr 21. doi: 10.1002/mds.25882. [Epub ahead of print]

Derkinderen P, Shannon KM, Brundin P.

Abstract

Strong epidemiologic evidence suggests that smokers and coffee drinkers have a lower risk of Parkinson's disease (PD). The explanation for this finding is still unknown, and the discussion has focused on two main hypotheses. The first suggests that PD patients have premorbid personality traits associated with dislike for coffee-drinking and smoking. The second posits that caffeine and nicotine are neuroprotective. We propose an alternative third hypothesis, in which both cigarette and coffee consumption change the composition of the microbiota in the gut in a way that mitigates intestinal inflammation. This, in turn, would lead to less misfolding of the protein alpha-synuclein in enteric nerves, reducing the risk of PD by minimizing propagation of the protein aggregates to the central nervous system, where they otherwise can induce neurodegeneration.

Thursday, April 10, 2014

Alpha-synuclein in peripheral tissues and body fluids as a biomarker for Parkinson's disease - a systematic review.

Alpha-synuclein in peripheral tissues and body fluids as a biomarker for Parkinson's disease - a systematic review.

Nice up to date review of the field...

Acta Neurol Scand. 2014 Apr 5. doi: 10.1111/ane.12247. [Epub ahead of print]
Malek N, Swallow D, Grosset KA, Anichtchik O, Spillantini M, Grosset DG.

Abstract

Parkinson's disease (PD) is neuropathologically characterized as an alpha-synucleinopathy. Alpha-synuclein-containing inclusions are stained as Lewy bodies and Lewy neurites in the brain, which are the pathological hallmark of PD. However, alpha-synuclein-containing inclusions in PD are not restricted to the central nervous system, but are also found in peripheral tissues. Alpha-synuclein levels can also be measured in body fluids. The aim of this study was to conduct a systematic review of available evidence to determine the utility of alpha-synuclein as a peripheral biomarker of PD. We searched PubMed (1948 to 26 May 2013), Embase (1974 to 26 May 2013), the Cochrane Library (up to 26 May 2013), LILACS (up to 26 May 2013) and CINAHL (up to 26 May 2013) for the studies of alpha-synuclein in peripheral tissues or body fluids in PD. A total of 49 studies fulfilled the search criteria. Peripheral tissues such as colonic mucosa showed a sensitivity of 42-90% and a specificity of 100%; submandibular salivary glands showed sensitivity and specificity of 100%; skin biopsy showed 19% sensitivity and 80% specificity in detecting alpha-synuclein pathology. CSF alpha-synuclein had 71-94% sensitivity and 25-53% specificity for distinguishing PD from controls. Plasma alpha-synuclein had 48-53% sensitivity and 69-85% specificity. Neither plasma nor CSF alpha-synuclein is presently a reliable marker of PD. This differs from alpha-synuclein in solid tissue samples of the enteric and autonomic nervous system, which offer some potential as a surrogate marker of brain synucleinopathy.