Corrigendum (2019)

Article NavigationLATE to the PART-y Keith A Josephs, Ian Mackenzie, Matthew P Frosch, Eileen H Bigio, Manuela Neumann, Tetsuaki Arai, Brittany N Dugger, Bernardino Ghetti, Murray Grossman, Masato Hasegawa ... Show moreBrain, Volume 142, Issue 9, September 2019, Page e47, https://doi.org/10.1093/brain/awz224Published: 29 July 2019A correction has been published:Brain, Volume 142, Issue 12, December 2019, Page e73, https://doi.org/10.1093/brain/awz263pdfPDF Split ViewCitePermissions Icon Permissions Share Issue Section: Letters to the EditorSir,We wish to address the recent proposal of a disease entity newly titled ‘limbic-predominant age-related TDP-43 encephalopathy (LATE)’ (Nelson et al., 2019) which, to our reading, is itself a derivative of the 2016 proposed term cerebral age-related TDP-43 with sclerosis (CART) (Nelson et al., 2016). The transactive response DNA binding protein of ∼43 kD (TDP-43) was first reported in 2006 to be a main component of ubiquitinated inclusions in autopsy-confirmed cases of frontotemporal lobar degeneration (FTLD) negative for tau immunoreactivity (Arai et al., 2006; Neumann et al., 2006). Over a decade of research into FTLD-TDP (and FTLD-U before it) has highlighted important phenotypic variability in TDP-43-immunoreactive lesions resulting in the identification of five different types of FTLD-TDP (Mackenzie et al., 2006, 2011; Sampathu et al., 2006; Josephs et al., 2009; Lee et al., 2011, 2017). There have also been important advances in the molecular and biochemical characterization of TDP-immunoreactive in FTLD-TDP (Sampathu et al., 2006; Hasegawa et al., 2008; Igaz et al., 2008; Zhang et al., 2009; Bigio et al., 2013; Laferriere et al., 2019). Soon after the initial characterization of TDP-immunoreactive lesions in FTLD and amyotrophic lateral sclerosis, TDP-immunoreactive lesions were identified in 25–33% of cases with pathologically confirmed Alzheimer’s disease (Amador-Ortiz et al., 2007; Higashi et al., 2007). TDP-immunoreactive lesions related to Alzheimer’s disease were initially thought to appear first in the hippocampus (Amador-Ortiz et al., 2007), but more detailed morphological studies involving multiple anatomical regions revealed the amygdala to be the earliest affected region (Higashi et al., 2007; Hu et al., 2008; Arai et al., 2009) followed by the entorhinal cortex and hippocampus, occipitotemporal cortex, insular and inferior temporal cortex, brainstem, and frontal neocortex and basal ganglia (Josephs et al., 2014, 2016); a scheme that has been independently validated (Tan et al., 2015). TDP-immunoreactive lesions have also been described in cognitively normal individuals (Wilson et al., 2011; Arnold et al., 2013; Uchino et al., 2015; Wennberg et al., 2019) including those with asymptomatic definite primary age related tauopathy (PART) (Josephs et al., 2017; Zhang et al., 2019), as well being associated with other well-defined clinic-pathological entities (Fig. 1) including Lewy body disease (with or without co-existing Alzheimer’s disease) (Arai et al., 2009; McAleese et al., 2017), the amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam (Hasegawa et al., 2007; Geser et al., 2008), Pick’s disease (Freeman et al., 2008), progressive supranuclear palsy (Yokota et al., 2010; Koga et al., 2017), corticobasal degeneration (Uryu et al., 2008; Koga et al., 2018), polyglutamine diseases such as Huntington’s disease (Schwab et al., 2008), Machado-Joseph disease (Tan et al., 2009) and spinocerebellar ataxia type 2 (Toyoshima et al., 2011), Perry syndrome (Wider et al., 2009), and chronic traumatic encephalopathy (McKee et al., 2010).