ArticleActa neuropathologica communications2019
Unique α-synuclein pathology within the amygdala in Lewy body dementia: implications for disease initiation and progression.
Article in Acta neuropathologica communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 89 citations in OpenAlex.
- Amygdalar nuclei vulnerability to protein aggregates in Lewy body diseases.Acta neuropathologica communications · 2026Article
- Modeling Parkinson's pathology in human iPSC dopaminergic neurons uncovers key mechanisms of Lewy body formation and heterogeneity.Science advances · 2026Article
- Frequency of mixed neuropathologies in individuals with down syndrome with and without Alzheimer's dementia.Acta neuropathologica · 2026Article
- Shared and distinct lipid profiles in amygdala from sporadic and GBA-associated Parkinson's diseases.NPJ Parkinson's disease · 2026Article
- Alpha-Synuclein in Neurodegeneration: From Shared Biology to Disease-Specific Phenotypes.Cells · 2026Review
- Where do PDD and DLB SYNdromes fit in neuronal alpha-SYNuclein biological frameworks?Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Alpha-synuclein seeding activity in postmortem tissues from patients with diffuse and isolated Lewy bodies.Acta neuropathologica communications · 2026Article
- Deep learning for FDG-PET classification in patients with Alzheimer's disease, dementia with Lewy bodies and their mixed pathology: a solution for diagnostic heterogeneity.Frontiers in aging neuroscience · 2026Article
- Robust immunohistochemical detection of α-synuclein, tau and amyloid-β in human brain tissue archived for up to 78 years.Free neuropathology · 2026Article
- Compensatory hallucinogenesis across three neuropsychiatric disorders: a Bayesian account.Brain communications · 2026Review
- Converging pathologies in neurodegeneration: the mechanistic interplay between α-Synuclein and Tau in Alzheimer's and Parkinson's.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- Amygdala-predominant Lewy bodies associate with cognitive decline and amygdala atrophy in Alzheimer's disease neuropathological change.Journal of neurology · 2025Article
- The Comorbidity of AD and PD: Exploring Clinical, Pathological, and Biomarker Interactions.Aging and disease · 2025Review
- Hippocampal subfields: volume, neuropathological vulnerability and cognitive decline in Alzheimer's and Parkinson's disease.Alzheimer's research & therapy · 2025Article
- Neuropathological stages of neuronal, astrocytic and oligodendrocytic alpha-synuclein pathology in Parkinson's disease.Acta neuropathologica communications · 2025Article
- RT-QuIC: a highly promising diagnostic method for neurodegenerative diseases-advantages and limitations.Frontiers in neurology · 2025Review
- Lewy body co-pathology in Alzheimer's disease and primary age-related tauopathy contributes to differential neuropathological, cognitive, and brain atrophy patterns.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Precision Medicine in Neurodegenerative Diseases: Genomic Approaches to Target Amyloid-β, Tau, and Alpha-Synuclein Pathways.Current genomics · 2025Review
- Cognitive decline profiles associated with lewy pathology in the context of Alzheimer's disease neuropathologic change.Alzheimer's research & therapy · 2024Article
- Pathologic subtyping of Alzheimer's disease brain tissue reveals disease heterogeneity.medRxiv : the preprint server for health sciences · 2024Article
2 more citing papers are in PubMed but not listed here.
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11 authors at 2 institutions in 1 country.
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Abstract
The protein α-synuclein (αsyn) forms pathologic aggregates in a number of neurodegenerative diseases including Lewy body dementia (LBD) and Parkinson's disease (PD). It is unclear why diseases such as LBD may develop widespread αsyn pathology, while in Alzheimer's disease with amygdala restricted Lewy bodies (AD/ALB) the αsyn aggregates remain localized. The amygdala contains αsyn aggregates in both LBD and in AD/ALB; to understand why αsyn pathology continues to progress in LBD but not in AD/ALB, tissue from the amygdala and other regions were obtained from 14 cases of LBD, 9 cases of AD/ALB, and 4 controls for immunohistochemical and biochemical characterization. Utilizing a panel of previously characterized αsyn antibodies, numerous unique pathologies differentiating LBD and AD/ALB were revealed; particularly the presence of dense neuropil αsyn aggregates, astrocytic αsyn, and αsyn-containing dystrophic neurites within senile plaques. Within LBD, these unique pathologies were predominantly present within the amygdala. Biochemically, the amygdala in LBD prominently contained specific carboxy-truncated forms of αsyn which are highly prone to aggregate, suggesting that the amygdala may be prone to initiate development of αsyn pathology. Similar to carboxy-truncated αsyn, it was demonstrated herein that the presence of aggregation prone A53T αsyn is sufficient to drive misfolding of wild-type αsyn in human disease. Overall, this study identifies within the amygdala in LBD the presence of unique strain-like variation in αsyn pathology that may be a determinant of disease progression.
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