ReviewProgress in neurobiology2011
Biomarkers in frontotemporal lobar degenerations--progress and challenges.
Review in Progress in neurobiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- TDP-43 as a possible biomarker for frontotemporal lobar degeneration: a systematic review of existing antibodies.Acta neuropathologica communications · 2015Pooled it
- Operationalizing postmortem pathology-MRI association studies in Alzheimer's disease and related disorders with MRI-guided histology sampling.Acta neuropathologica communications · 2025Article
- Production and characterization of novel monoclonal antibodies against pathological human TDP-43 proteins.Journal of neuropathology and experimental neurology · 2024Article
- Tau Immunotherapies for Alzheimer's Disease and Related Tauopathies: Status of Trials and Insights from Preclinical Studies.Journal of Alzheimer's disease : JAD · 2024Review
- Tau-targeting therapies for Alzheimer disease: current status and future directions.Nature reviews. Neurology · 2023Review
- Targeting tau only extracellularly is likely to be less efficacious than targeting it both intra- and extracellularly.Seminars in cell & developmental biology · 2022Review
- Immunotherapy for Alzheimer's disease: targeting β-amyloid and beyond.Translational neurodegeneration · 2022Review
- Blood-based biomarkers of inflammation in amyotrophic lateral sclerosis.Molecular neurodegeneration · 2022Review
- Tau-targeting therapies for Alzheimer disease.Nature reviews. Neurology · 2018Review
- A platform for discovery: The University of Pennsylvania Integrated Neurodegenerative Disease Biobank.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2014Article
- Adaptation to Early-Stage Nonfluent/Agrammatic Variant Primary Progressive Aphasia: A First-Person Account.American journal of Alzheimer's disease and other dementias · 2014Article
- Novel monoclonal antibodies to normal and pathologically altered human TDP-43 proteins.Acta neuropathologica communications · 2014Article
- Randomized controlled trials in frontotemporal dementia: cognitive and behavioral outcomes.Translational neurodegeneration · 2014Review
- Therapeutic and diagnostic challenges for frontotemporal dementia.Frontiers in aging neuroscience · 2014Review
- GWAS of cerebrospinal fluid tau levels identifies risk variants for Alzheimer's disease.Neuron · 2013Article
- Cerebrospinal fluid biomarkers for differentiation of frontotemporal lobar degeneration from Alzheimer's disease.Frontiers in aging neuroscience · 2013Article
- Entorhinal cortical neurons are the primary targets of FUS mislocalization and ubiquitin aggregation in FUS transgenic rats.Human molecular genetics · 2012Article
- Advances in understanding the molecular basis of frontotemporal dementia.Nature reviews. Neurology · 2012Review
- Comparison of cerebrospinal fluid levels of tau and Aβ 1-42 in Alzheimer disease and frontotemporal degeneration using 2 analytical platforms.Archives of neurology · 2012Article
- CSF biomarkers cutoffs: the importance of coincident neuropathological diseases.Acta neuropathologica · 2012Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Neuronal and glial changes associated with tau, TAR DNA binding protein of ∼43 kDa (TDP-43), and fused in sarcoma (FUS) together constitute the pathologic spectrum of frontotemporal lobar degeneration (FTLD). Most patients with FTLD present with prominent behavior or language changes, sometimes accompanied by extrapyramidal symptoms or motor neuron disease. Identification of FTLD patients with mutations in genes for tau, TDP-43, and FUS lends strong support for their pathogenic roles in FTLD, and elucidation of their dysfunction will pave the way for development of substrate specific therapy. However, there remains no reliable biomarker for early detection of FTLD or prediction of underlying FTLD pathologic change. Clinical syndromes usually reflects the earliest affected brain regions where atrophy can be visualized on structural MRI, but neither clinical nor structural imaging-based biomarkers has been accurately correlated with underlying pathology on the individual patient level. Biochemical markers in the cerebrospinal fluid (CSF) have also been investigated in FTLD and related disorders, including amyotrophic lateral sclerosis (ALS) and progressive supranuclear palsy (PSP). However, their accuracy and pathologic significance need to be confirmed in future multi-center studies. Here we review the progress made in FTLD biomarkers, including clinical phenotype/feature characterization, neuropsychological analysis, CSF and plasma analytes, and patterns of brain atrophy and network dysfunction detectable on brain imaging. Given the pathologic overlap of FTLD with ALS and PSP, collaboration with specialists in those fields will be essential in the translation of promising FTLD biomarkers into clinical practice.
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