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Times Cited: 1
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TMS for staging and predicting functional decline in frontotemporal dementia.
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Mutation in the tau gene in familial multiple system tauopathy with presenile dementia.
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A harmonized classification system for FTLD-TDP pathology.
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An exploratory clinical study of p38α kinase inhibition in Alzheimer's disease.
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Diagnostic and prognostic value of serum NfL and p-Tau181 in frontotemporal lobar degeneration.
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Prefrontal cortex rTMS enhances action naming in progressive non-fluent aphasia.
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The impact of transcranial magnetic stimulation on diagnostic confidence in patients with Alzheimer disease.
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Poly(ADP-Ribose) Prevents Pathological Phase Separation of TDP-43 by Promoting Liquid Demixing and Stress Granule Localization.
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Nomenclature and nosology for neuropathologic subtypes of frontotemporal lobar degeneration: an update.
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Antisense reduction of tau in adult mice protects against seizures.
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A case study of Primary Progressive Aphasia: improvement on verbs after rTMS treatment.
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Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis.
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Genetic and clinical features of progranulin-associated frontotemporal lobar degeneration.
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Lysine-Directed Post-translational Modifications of Tau Protein in Alzheimer's Disease and Related Tauopathies.
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MK-8719, a Novel and Selective O-GlcNAcase Inhibitor That Reduces the Formation of Pathological Tau and Ameliorates Neurodegeneration in a Mouse Model of Tauopathy.
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FET proteins TAF15 and EWS are selective markers that distinguish FTLD with FUS pathology from amyotrophic lateral sclerosis with FUS mutations.
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Advances in understanding the molecular basis of frontotemporal dementia.
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Repetitive transcranial magnetic stimulation for the treatment of cognitive impairment in frontotemporal dementia: an open-label pilot study.
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Targeting nuclear protein TDP-43 by cell division cycle kinase 7 inhibitors: A new therapeutic approach for amyotrophic lateral sclerosis.
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TDP43 nuclear export and neurodegeneration in models of amyotrophic lateral sclerosis and frontotemporal dementia.
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Behavioral and Neurophysiological Effects of Transcranial Direct Current Stimulation (tDCS) in Fronto-Temporal Dementia.
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Physiological and pathological phosphorylation of tau by Cdk5.
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Metformin inhibits RAN translation through PKR pathway and mitigates disease in C9orf72 ALS/FTD mice.
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Reductions in GABA following a tDCS-language intervention for primary progressive aphasia.
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Variable clinical phenotype in TBK1 mutations: case report of a novel mutation causing primary progressive aphasia and review of the literature.
Imogen J Swift, Martina Bocchetta, Hanya Benotmane, Ione Oc Woollacott, Rachelle Shafei, Jonathan D Rohrer. Neurobiol Aging 2021
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Gain of Toxicity from ALS/FTD-Linked Repeat Expansions in C9ORF72 Is Alleviated by Antisense Oligonucleotides Targeting GGGGCC-Containing RNAs.
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Effects of transcranial direct current stimulation on language improvement and cortical activation in nonfluent variant primary progressive aphasia.
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Neurophysiological Correlates of Positive and Negative Symptoms in Frontotemporal Dementia.
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Increased 4R-Tau Induces Pathological Changes in a Human-Tau Mouse Model.
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Tau aggregation inhibitor therapy: an exploratory phase 2 study in mild or moderate Alzheimer's disease.
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Left Prefrontal Repetitive Transcranial Magnetic Stimulation in a Logopenic Variant of Primary Progressive Aphasia: A Case Report.
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Three VCP Mutations in Patients with Frontotemporal Dementia.
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Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS.
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Transcranial direct current stimulation for the treatment of primary progressive aphasia: An open-label pilot study.
Felix Gervits, Sharon Ash, H Branch Coslett, Katya Rascovsky, Murray Grossman, Roy Hamilton. Brain Lang 2016
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Retiring the term FTDP-17 as MAPT mutations are genetic forms of sporadic frontotemporal tauopathies.
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Diagnosis of Mild Cognitive Impairment Due to Alzheimer's Disease with Transcranial Magnetic Stimulation.
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100
Neuropathologic diagnostic and nosologic criteria for frontotemporal lobar degeneration: consensus of the Consortium for Frontotemporal Lobar Degeneration.
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Pathological phosphorylation of tau and TDP-43 by TTBK1 and TTBK2 drives neurodegeneration.
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Soluble forms of polyQ-expanded huntingtin rather than large aggregates cause endoplasmic reticulum stress.
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Phosphorylation of S409/410 of TDP-43 is a consistent feature in all sporadic and familial forms of TDP-43 proteinopathies.
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Clinicopathologic correlations in a family with a TBK1 mutation presenting as primary progressive aphasia and primary lateral sclerosis.
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Brain volumes as predictors of tDCS effects in primary progressive aphasia.
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Identification of casein kinase-1 phosphorylation sites on TDP-43.
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A phase 2 trial of the GSK-3 inhibitor tideglusib in progressive supranuclear palsy.
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100
Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.