TDP‐43 immunoreactivity in hippocampal sclerosis and Alzheimer's disease

By Catalina Amador-Ortiz, Wen‐lang Lin, Z. Ahmed, D. Personett, P. Davies, R. Duara, N. Graff-Radford, M. Hutton, Dennis W. Dickson. Annals of Neurology, 2007

887 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/4175439bd80808c0797af0c3d203747f0003704a

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Citations in the corpus

The neuropathological diagnosis of Alzheimer’s disease (2019, background): “TDP-43 protein deposition is often encountered in hippocampal sclerosis and AD [128] in addition to the fron-”
National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease (2012, neutral): “TDP-43– immunoreactive inclusions also are observed in a fraction of cases with AD neuropathologic change [86,89] or with LBD [90], among other neurodegenerative diseases.”
ALS mutations disrupt phase separation mediated by -helical structure in the TDP-43 low complexity C-terminal domain (2016, background): “The role of TDP-43 phase separation in neurodegenerative disease TDP-43 remains a primary target in neurodegenerative disease research because of its aggregate pathology and role in ALS, frontotemporal dementia(Neumann et al., 2006), and Alzheimer’s disease (Amador-Ortiz et al., 2007).”
Molecular Mechanisms of TDP-43 Misfolding and Pathology in Amyotrophic Lateral Sclerosis (2019, background): “Notably, immunoreactivity of TDP-43 has also been detected in the Alzheimer’s disease brain, in about 75% of the patients (Amador-Ortiz et al., 2007; Higashi et al., 2007; Uryu et al., 2008; King et al., 2010b; Josephs et al., 2014).”
Classification and basic pathology of Alzheimer disease (2009, background): “Medial temporal atrophy was more marked and the occurrence of hippocampal sclerosis more frequent [9, 175].”
Pathology of Neurodegenerative Diseases. (2017, background): “Cite this article as Cold Spring Harb Perspect Biol 2016;9:a028035 15 ronal loss affecting the CA1 sector of the hippocampus and is associated with an amnestic clinical syndrome (Amador-Ortiz et al. 2007).”
TDP-43 and FUS/TLS: emerging roles in RNA processing and neurodegeneration. (2010, background): “Other diseases Multiple system atrophy (MSA) No (7,49,98) No (83,85)”
TDP-43 Proteinopathy and Motor Neuron Disease in Chronic Traumatic Encephalopathy (2010, background): “Diseases with secondary TDP-43 pathology include AD and hippocampal sclerosis (63), Guam parkinsonism-dementia complex (PDC) (64), Pick disease, corticobasal degeneration, argyrophilic grain disease, and Lewy body disease (5, 28, 65).”
Neuropathologic diagnostic and nosologic criteria for frontotemporal lobar degeneration: consensus of the Consortium for Frontotemporal Lobar Degeneration (2007, background): “, hippocampus or corpus striatum) and the morphology of the lesions [2, 38].”
Phosphorylated TDP-43 in frontotemporal lobar degeneration and ALS (2008, result): “Furthermore, on immunoelectron microscopy, the phosphorylation-dependent antibodies label abnormal filaments in the motoneuronal inclusion of the ALS case, although these findings may not be the same as for other types of cytoplasmic and intranuclear inclusions.(26) Immunoblot analysis of sarkosyl-i”
National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach (2011, neutral): “6) [8, 28, 40, 64], about onehalf of cases with FTLD and ubiquitin inclusions with or without motor neuron disease, most sporadic cases of amyotrophic lateral sclerosis, and commonly in cases with AD neuropathologic change [8, 9] or with LBD [43], as well as other neurodegenerative diseases [48].”