ReviewJournal of neuropathology and experimental neurology2024
Limbic-predominant age-related TDP-43 encephalopathy (LATE-NC): Co-pathologies and genetic risk factors provide clues about pathogenesis.
Review in Journal of neuropathology and experimental neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed.
- Hormone replacement therapy and its association with LATE-NC in older adults.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Locus coeruleus TDP-43 pathology in a community-based cohort: Clinical and pathological correlates.Journal of neuropathology and experimental neurology · 2026Article
- Development and characterization of a novel TDP-43 positron emission tomography tracer: [Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Decreased amyloid-related structure-function coupling in preclinical Alzheimer's disease.Communications medicine · 2026Article
- AI-driven predictive modeling of sarcopenia progression in limbic-predominant age-related TDP-43 encephalopathy: a novel biomarker fusion approach.Annals of medicine and surgery (2012) · 2026Article
- Molecular signatures and biomarker development for limbic-predominant age-related TDP-43 encephalopathy (LATE).Acta neuropathologica · 2026Review
- Frequency of mixed neuropathologies in individuals with down syndrome with and without Alzheimer's dementia.Acta neuropathologica · 2026Article
- Chronic traumatic encephalopathy neuropathologic change is associated with highest stage limbic-predominant age-related TDP-43 encephalopathy.Journal of neuropathology and experimental neurology · 2026Article
- Amyloid-linked versus age-driven copathologies in Alzheimer's dementia: differential associations withResearch square · 2026Article
- Review
- The role of brain MR and FDG-PET in the diagnosis of neurodegenerative disease.European radiology · 2026Review
- Calcineurin depletion coincides with phosphorylated TDP-43 deposition in a mouse model of ALS/FTLD-TDP.Acta neuropathologica communications · 2026Article
- Genetic analysis of limbic-predominant age-related TDP-43 encephalopathy neuropathologic change in a population-based cohort of the oldest old.Brain communications · 2026Article
- The 2024 NIA-AA biological definition of Alzheimer's disease: linking biomarkers to clinical practice.Frontiers in dementia · 2026Review
- Genetic variation in TMEM106B alters microglial activation and cytokine responses in chronic traumatic encephalopathy.Acta neuropathologica · 2025Article
- Amygdalar and hippocampal volume loss in limbic-predominant age-related TDP-43 encephalopathy.Brain : a journal of neurology · 2025Article
- Cortical thickness subtypes in cognitively unimpaired individuals: Differential network and transcriptomic vulnerability to cortical thinning.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Alzheimer mimicry: LATE and PART.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Assessing Co-Localization of ITM2B With Alzheimer's Disease and Limbic-Predominant Age-Related TDP-43 Encephalopathy Neuropathologic Changes.Neuropathology : official journal of the Japanese Society of Neuropathology · 2025Article
- Increased Incidence of Epilepsy in a Brain Bank Alzheimer's Disease Cohort and Its Association With TDP-43 Pathology.Neuropathology and applied neurobiology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
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Abstract
Limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) is detectable at autopsy in more than one-third of people beyond age 85 years and is robustly associated with dementia independent of other pathologies. Although LATE-NC has a large impact on public health, there remain uncertainties about the underlying biologic mechanisms. Here, we review the literature from human studies that may shed light on pathogenetic mechanisms. It is increasingly clear that certain combinations of pathologic changes tend to coexist in aging brains. Although "pure" LATE-NC is not rare, LATE-NC often coexists in the same brains with Alzheimer disease neuropathologic change, brain arteriolosclerosis, hippocampal sclerosis of aging, and/or age-related tau astrogliopathy (ARTAG). The patterns of pathologic comorbidities provide circumstantial evidence of mechanistic interactions ("synergies") between the pathologies, and also suggest common upstream influences. As to primary mediators of vulnerability to neuropathologic changes, genetics may play key roles. Genes associated with LATE-NC include TMEM106B, GRN, APOE, SORL1, ABCC9, and others. Although the anatomic distribution of TDP-43 pathology defines the condition, important cofactors for LATE-NC may include Tau pathology, endolysosomal pathways, and blood-brain barrier dysfunction. A review of the human phenomenology offers insights into disease-driving mechanisms, and may provide clues for diagnostic and therapeutic targets.
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