Article

Dementia in 2013: Frontotemporal lobar degeneration-building on breakthroughs.

Nature Reviews Neurology (Impact Factor: 14.1). 01/2014; DOI: 10.1038/nrneurol.2013.270
Source: PubMed
Download full-text

Full-text

Available from: Christine Van Broeckhoven, Jan 11, 2014
4 Followers
 · 
130 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Frontotemporal lobar degeneration (FTLD) is one of the leading causes of dementia after Alzheimer’s disease. A high-ranking candidate to become a diagnostic marker for a major pathological subtype of FTLD is the transactive response DNA binding protein of 43 kDa (TDP-43). The main objective is to elucidate which antibodies are specific for pathological TDP-43, with special interest in its modified isoforms. Indeed, TDP-43 has been shown to be hyperphosphorylated and truncated in disease. A secondary objective is to review existing immunoassays that quantify TDP-43 in biofluids. A systematic review of literature was performed by searching PubMed and Web of Science using predefined keywords. Of considered research papers the methods section was reviewed to select publications that enabled us to answer our learning objective. After quality assessment, antibody characteristics and related outcomes were extracted. We identified a series of well-characterized antibodies based on a scoring system that assessed the ability of each antibody to detect TDP-43 pathology. A selection of 29 unique antibodies was made comprising 10 high-ranking antibodies which were reported multiple times to detect TDP-43 pathology in both immunostaining and immunoblotting experiments and 19 additional antibodies which detected TDP-43 pathology but were only scored once. This systematic review provides an overview of antibodies that are reported to detect pathological TDP-43. These antibodies can be used in future studies of TDP-43 proteinopathies. Additionally, selected antibodies hold the potential to be used in the development of novel immunoassays for the quantification of TDP-43 in biofluids, as a possible biomarker for FTLD-TDP.
    12/2015; 3(15). DOI:10.1186/s40478-015-0195-1
  • Source
    The Lancet Neurology 02/2015; 64(3). DOI:10.1016/S1474-4422(15)70019-0 · 21.82 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Hereditary frontotemporal dementia (FTD) associated with mutations in the Microtubule Associated Protein Tau gene (MAPT) is a protean disorder. Three neuropathologic subtypes can be recognized, based on the presence of inclusions made of tau isoforms with 3 and 4 repeats, predominantly 3 repeats and mostly 4 repeats. This is relevant for establishing a correlation between structural magnetic resonance imaging and positron emission tomography using tracers specific for aggregated tau. Longitudinal studies will be essential to determine the evolution of anatomical alterations from the asymptomatic stage to the various phases of disease following the onset of symptoms.
    Neuropathology and Applied Neurobiology 12/2014; 41(1). DOI:10.1111/nan.12213 · 4.97 Impact Factor