Document Detail


Cyanobacterial neurotoxin BMAA in ALS and Alzheimer's disease.
MedLine Citation:
PMID:  19254284     Owner:  NLM     Status:  In-Process    
Abstract/OtherAbstract:
OBJECTIVE: The aim of this study was to screen for and quantify the neurotoxic amino acid beta-N-methylamino-L-alanine (BMAA) in a cohort of autopsy specimens taken from Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), and non-neurological controls. BMAA is produced by cyanobacteria found in a variety of freshwater, marine, and terrestrial habitats. The possibility of geographically broad human exposure to BMAA had been suggested by the discovery of BMAA in brain tissues of Chamorro patients with ALS/Parkinsonism dementia complex from Guam and more recently in AD patients from North America. These observations warranted an independent study of possible BMAA exposures outside of the Guam ecosystem. METHODS: Postmortem brain specimens were taken from neuropathologically confirmed cases of 13 ALS, 12 AD, 8 HD patients, and 12 age-matched non-neurological controls. BMAA was quantified using a validated fluorescent HPLC method previously used to detect BMAA in patients from Guam. Tandem mass spectrometric (MS) analysis was carried out to confirm the identification of BMAA in neurological specimens. RESULTS: We detected and quantified BMAA in neuroproteins from postmortem brain tissue of patients from the United States who died with sporadic AD and ALS but not HD. Incidental detections observed in two out of the 24 regions were analyzed from the controls. The concentrations of BMAA were below what had been reported previously in Chamarro ALS/ Parkinsonism dementia complex patients, but demonstrated a twofold range across disease and regional brain area comparisons. The presence of BMAA in these patients was confirmed by triple quadrupole liquid chromatography/mass spectrometry/mass spectrometry. CONCLUSIONS: The occurrence of BMAA in North American ALS and AD patients suggests the possibility of a gene/environment interaction, with BMAA triggering neurodegeneration in vulnerable individuals.
Authors:
J Pablo; S A Banack; P A Cox; T E Johnson; S Papapetropoulos; W G Bradley; A Buck; D C Mash
Related Documents :
6721714 - Language disturbance. an initial symptom of cortical degenerations and dementia.
10804074 - The relationship between donepezil and behavioral disturbances in patients with alzheim...
7753344 - Postoperative cognitive and single photon emission computed tomography assessment of pa...
8889914 - Cognitive effects of flumazenil in patients with alzheimer's disease.
16887374 - Exploring the relationship between essential tremor and parkinson's disease.
11177694 - Should patients with chronic hepatitis c who have normal alt levels be treated?
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-02-26
Journal Detail:
Title:  Acta neurologica Scandinavica     Volume:  120     ISSN:  1600-0404     ISO Abbreviation:  Acta Neurol. Scand.     Publication Date:  2009 Oct 
Date Detail:
Created Date:  2009-09-22     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0370336     Medline TA:  Acta Neurol Scand     Country:  Denmark    
Other Details:
Languages:  eng     Pagination:  216-25     Citation Subset:  IM    
Copyright Information:
(c) 2009 The Authors Journal compilation (c) 2009 Blackwell Munksgaard.
Affiliation:
Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Translating pathology in multiple sclerosis: the combination of postmortem imaging, histopathology a...
Next Document:  Ageing influences myonuclear domain size differently in fast and slow skeletal muscle of rats.