Office of Rare Diseases Neuropathologic Criteria for Corticobasal Degeneration
Abstract
A working group supported by the Office of Rare Diseases of the National Institutes of Health formulated neuropathologic criteria for corticobasal degeneration (CBD) that were subsequently validated by an independent group of neuropathologists. The criteria do not require a specific clinical phenotype, since CBD can have diverse clinical presentations, such as progressive asymmetrical rigidity and apraxia, progressive aphasia, or frontal lobe dementia. Cortical atrophy, ballooned neurons, and degeneration of the substantia nigra have been emphasized in previous descriptions and are present in CBD, but the present criteria emphasize tau-immunoreactive lesions in neurons, glia, and cell processes in the neuropathologic diagnosis of CBD. The minimal pathologic features for CBD are cortical and striatal tau-positive neuronal and glial lesions, especially astrocytic plaques and thread-like lesions in both white matter and gray matter, along with neuronal loss in focal cortical regions and in the substantia nigra. The methods required to make this diagnosis include histologic stains to assess neuronal loss, spongiosis and ballooned neurons, and a method to detect tau-positive neuronal and glial lesions. Use of either the Gallyas silver staining method or immunostains with sensitive tau antibodies is acceptable. In cases where ballooned neurons are sparse or difficult to detect, immunostaining for phospho-neurofilament or alpha-B-crystallin may prove helpful. Methods to assess Alzheimer-type pathology and Lewy body pathology are necessary to rule out other causes of dementia and Parkinsonism. Using these criteria provides good differentiation of CBD from other tauopathies, except frontotemporal dementia and Parkinsonism linked to chromosome 17, where additional clinical or molecular genetic information is required to make an accurate diagnosis.
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CBD is a late-onset neurodegenerative disorder that can only be diagnosed upon neuropathologic examination.
“CBD is a late-onset neurodegenerative disorder that can only be diagnosed upon neuropathologic examination, which has impeded the ability to conduct genome-wide association studies (GWASs).”
From Genome-wide association study of corticobasal degeneration identifies risk variants shared with progressive supranuclear palsy (2015) · cites this paper as [1]
Neuropathologic diagnostic criteria for CBD require tau inclusions in neurons and glia, with tau astrocytic plaques, and extensive thread-like pathology in grey and white matter.
“Neuropathologic diagnostic criteria for CBD are based on tau immunohistochemistry, requiring tau inclusions in neurons and glia, with tau astrocytic plaques, and extensive thread-like pathology in both grey matter and white matter1.”
From Genome-wide association study of corticobasal degeneration identifies risk variants shared with progressive supranuclear palsy (2015) · cites this paper as [1]
CBD is a tauopathy with abnormal aggregates of microtubule-associated protein tau in the brain.
“Similar to progressive supranuclear palsy (PSP), Alzheimer’s disease (AD), and chronic traumatic encephalopathy, CBD is a tauopathy, having abnormal aggregates of microtubule-associated protein tau in the brain1.”
From Genome-wide association study of corticobasal degeneration identifies risk variants shared with progressive supranuclear palsy (2015) · cites this paper as [1]
The scarcity of pathologically characterized samples has prompted efforts to enrich cohorts with FTD syndromes highly correlated with a specific underlying neuropathology and/or to jointly analyze data from combined cohorts of sporadic and familial cases with the same neuropathology background.
“The scarcity of these samples has prompted efforts to enrich cohorts with FTD syndromes that are highly correlated with a specific underlying neuropathology (e.g., FTD‐ALS for FTLD‐TDP 22 or PSP and CBS for FTLD‐tau 119 , 120 ) and/or to jointly analyze data from both combined cohorts of sporadic and familial cases with the same neuropathology background.”
From New developments of biofluid‐based biomarkers for routine diagnosis and disease trajectories in frontotemporal dementia (2022) · cites this paper as [120]
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- Authors
- Dickson, D. W., Bergeron, C., Chin, S. S., Duyckaerts, C., Horoupian, D., Ikeda, K., Jellinger, K., Lantos, P. L., Lippa, C. F., Mirra, S. S., Tabaton, M., Vonsattel, J. P., Wakabayashi, K., & Litvan, I.
- Affiliations
- Mayo Clinic in Florida (US)
- Mayo Clinic (US)
- Corresponding author
- Dickson, D. W.
- Venue
- Journal of Neuropathology & Experimental Neurology
- Publisher
- Oxford University Press (OUP)
- Published
- 2002-11
- Volume
- 61
- Issue
- 11
- Pages
- 935-946
- ISSN
- 0022-3069 (ISSN-L)
- 1554-6578
- OpenAlex
- W69591616
- Cited by
- 724
- References
- 86
- Citations by year
- 2026: 30 · 2025: 31 · 2024: 50 · 2023: 37 · 2022: 42 · 2021: 35 · 2020: 32 · 2019: 34 · 2018: 21 · 2017: 32 · 2016: 26 · 2015: 26 · 2014: 32 · 2013: 33 · 2012: 18
- FWCI
- 12.59
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuropathology & Experimental Neurology (publishedVersion)
- PubMed (publishedVersion)
- CINECA IRIS Institutial Research Information System (University of Genoa) (submittedVersion)
- Funders
- University of Pennsylvania
- School of Medicine, Boston University
- Johns Hopkins University
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- corticobasal degeneration, tauopathy, ballooned neurons, spongiosis, substantia nigra degeneration, tau antibodies, alphaB-crystallin, differential diagnosis, frontotemporal dementia, rare diseases
- MeSH terms
- Atrophy, Brain, Inclusion Bodies, Humans, Neuroglia, Neurons, Silver Staining, Neurofibrillary Tangles, Neurodegenerative Diseases
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