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Article ; Online: Reply: More than a co-incidence? Exploring the increased frequency of amyotrophic lateral sclerosis in Huntington disease.

Hickman, Richard A / Traynor, Bryan J / Marder, Karen S / Vonsattel, Jean-Paul

2022 Volume 145, Issue 2, Page(s) 259–261

MeSH term(s)	Humans ; Amyotrophic Lateral Sclerosis/epidemiology ; Huntington Disease/epidemiology ; Huntington Disease/genetics ; Incidence
Language	English
Publishing date	2022-12-21
Publishing country	Germany
Document type	Research Support, Non-U.S. Gov't ; Letter ; Research Support, N.I.H., Intramural ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	1079-0
ISSN	1432-0533 ; 0001-6322
ISSN (online)	1432-0533
ISSN	0001-6322
DOI	10.1007/s00401-022-02532-2
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Article ; Online: Pathologically based criteria to distinguish essential tremor from controls: analyses of the human cerebellum.

Faust, Phyllis L / McCreary, Morgan / Musacchio, Jessica B / Kuo, Sheng-Han / Vonsattel, Jean-Paul G / Louis, Elan D

Annals of clinical and translational neurology

2024

Abstract: Objective: Essential tremor is among the most prevalent neurological diseases. Diagnosis is based entirely on neurological evaluation. Historically, there were few postmortem brain studies, hindering attempts to develop pathologically based criteria to ... ...

Abstract	Objective: Essential tremor is among the most prevalent neurological diseases. Diagnosis is based entirely on neurological evaluation. Historically, there were few postmortem brain studies, hindering attempts to develop pathologically based criteria to distinguish essential tremor from control brains. However, an intensive effort to bank essential tremor brains over recent years has resulted in postmortem studies involving >200 brains, which have identified numerous degenerative changes in the essential tremor cerebellar cortex. Although essential tremor and controls have been compared with respect to individual metrics of pathology, there has been no overarching analysis to derive a combination of metrics to distinguish essential tremor from controls. We asked whether there is a constellation of pathological findings that separates essential tremor from controls, and how well that constellation performs. Methods: Analyses included 100 essential tremor brains from the essential tremor centralized brain repository and 50 control brains. A standard tissue block from the cerebellar cortex was used to quantify 11 metrics of pathological change. Three supervised classification algorithms were investigated, with data divided into training and validation samples. Results: Using three different algorithms, we illustrate the ability to correctly predict a diagnosis of essential tremor, with sensitivity and specificity >87%, and in the majority of situations, >90%. We also provide a web-based application that uses these metric values, and based on specified cutoffs, determines the likely diagnosis. Interpretation: These analyses set the stage for use of pathologically based criteria to distinguish clinically diagnosed essential tremor cases from controls, at the time of postmortem.
Language	English
Publishing date	2024-04-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2740696-9
ISSN	2328-9503 ; 2328-9503
ISSN (online)	2328-9503
ISSN	2328-9503
DOI	10.1002/acn3.52068
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Article ; Online: The distribution and density of Huntingtin inclusions across the Huntington disease neocortex: regional correlations with Huntingtin repeat expansion independent of pathologic grade.

Hickman, Richard A / Faust, Phyllis L / Marder, Karen / Yamamoto, Ai / Vonsattel, Jean-Paul

Acta neuropathologica communications

2022 Volume 10, Issue 1, Page(s) 55

Abstract: Huntington disease is characterized by progressive neurodegeneration, especially of the striatum, and the presence of polyglutamine huntingtin (HTT) inclusions. Although HTT inclusions are most abundant in the neocortex, their neocortical distribution ... ...

Abstract	Huntington disease is characterized by progressive neurodegeneration, especially of the striatum, and the presence of polyglutamine huntingtin (HTT) inclusions. Although HTT inclusions are most abundant in the neocortex, their neocortical distribution and density in relation to the extent of CAG repeat expansion in the HTT gene and striatal pathologic grade have yet to be formally established. We immunohistochemically studied 65 brains with a pathologic diagnosis of Huntington disease to investigate the cortical distributions and densities of HTT inclusions within the calcarine (BA17), precuneus (BA7), motor (BA4) and prefrontal (BA9) cortices; in 39 of these brains, a p62 immunostain was used for comparison. HTT inclusions predominate in the infragranular cortical layers (layers V-VI) and layer III, however, the densities of HTT inclusions across the human cerebral cortex are not uniform but are instead regionally contingent. The density of HTT and p62 inclusions (intranuclear and extranuclear) in layers V-VI increases caudally to rostrally (BA17 < BA7 < BA4 < BA9) with the median burden of HTT inclusions being 38-fold greater in the prefrontal cortex (BA9) than in the calcarine cortex (BA17). Conversely, intranuclear HTT inclusions prevail in the calcarine cortex irrespective of HTT CAG length. Neocortical HTT inclusion density correlates with CAG repeat expansion, but not with the neuropathologic grade of striatal degeneration (Vonsattel grade) or with the duration of clinical disease since motor onset. Extrapolation of these findings suggest that HTT inclusions are at a regionally-contingent, CAG-dependent, density during the advanced stages of HD. The distribution and density of HTT inclusions in HD therefore does not provide a measure of pathologic disease stage but rather infers the degree of pathogenic HTT expansion.
MeSH term(s)	Animals ; Disease Models, Animal ; Humans ; Huntingtin Protein/genetics ; Huntington Disease/genetics ; Huntington Disease/pathology ; Intranuclear Inclusion Bodies/pathology ; Neocortex/pathology ; Nerve Tissue Proteins/metabolism ; Neurons/metabolism
Chemical Substances	Huntingtin Protein ; Nerve Tissue Proteins
Language	English
Publishing date	2022-04-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-022-01364-1
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Article ; Online: Amyotrophic lateral sclerosis is over-represented in two Huntington's disease brain bank cohorts: further evidence to support genetic pleiotropy of pathogenic HTT gene expansion.

Hickman, Richard A / Dewan, Ramita / Cortes, Etty / Traynor, Bryan J / Marder, Karen / Vonsattel, Jean-Paul

Acta neuropathologica

2021 Volume 143, Issue 1, Page(s) 105–108

MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/pathology ; Cohort Studies ; Female ; Genetic Pleiotropy ; Humans ; Huntingtin Protein/genetics ; Huntington Disease/genetics ; Huntington Disease/pathology ; Male ; Middle Aged ; Tissue Banks ; Trinucleotide Repeat Expansion
Chemical Substances	HTT protein, human ; Huntingtin Protein
Language	English
Publishing date	2021-11-20
Publishing country	Germany
Document type	Case Reports ; Letter ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1079-0
ISSN	1432-0533 ; 0001-6322
ISSN (online)	1432-0533
ISSN	0001-6322
DOI	10.1007/s00401-021-02385-1
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Article: The New York Brain Bank of Columbia University: practical highlights of 35 years of experience.

Ramirez, Etty Paola Cortes / Keller, Christian Ernst / Vonsattel, Jean Paul

Handbook of clinical neurology

2018 Volume 150, Page(s) 105–118

Abstract: The New York Brain Bank processes brains and organs of clinically well-characterized patients with age-related neurodegenerative diseases, and for comparison, from individuals without neurologic or psychiatric impairments. The donors, either patients or ... ...

Abstract	The New York Brain Bank processes brains and organs of clinically well-characterized patients with age-related neurodegenerative diseases, and for comparison, from individuals without neurologic or psychiatric impairments. The donors, either patients or individuals, were evaluated at healthcare facilities of the Columbia University of New York. Each source brain yields four categories of samples: fresh frozen blocks and crushed parenchyma, and formalin-fixed wet blocks and histology sections. A source brain is thoroughly evaluated to determine qualitatively and quantitatively any changes it might harbor using conventional neuropathologic techniques. The clinical and pathologic diagnoses are integrated to determine the distributive diagnosis assigned to the samples obtained from a source brain. The gradual standardization of the protocol was developed in 1981 in response to the evolving requirements of basic investigations on neurodegeneration. The methods assimilate long-standing experience from multiple centers. The resulting and current protocol includes a constant central core applied to all brains with conditional flexibility around it. The New York Brain Bank is an integral part of the department of pathology, where the expertise, teaching duties, and hardware are shared. Since details of the protocols are available online, this chapter focuses on practical issues in professionalizing brain banking.
MeSH term(s)	Academies and Institutes ; Brain/pathology ; History, 20th Century ; History, 21st Century ; Humans ; Information Systems/history ; Information Systems/trends ; New York ; Tissue Banks/history ; Tissue Banks/organization & administration ; Universities
Language	English
Publishing date	2018
Publishing country	Netherlands
Document type	Historical Article ; Journal Article ; Review
ISSN	0072-9752
ISSN	0072-9752
DOI	10.1016/B978-0-444-63639-3.00008-6
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Article ; Online: Characterizing Lewy Pathology in 231 Essential Tremor Brains From the Essential Tremor Centralized Brain Repository.

Louis, Elan D / Iglesias-Hernandez, Daniella / Hernandez, Nora C / Flowers, Xena / Kuo, Sheng-Han / Vonsattel, Jean Paul G / Faust, Phyllis L

Journal of neuropathology and experimental neurology

2022 Volume 81, Issue 10, Page(s) 796–806

Abstract: The Essential Tremor Centralized Brain Repository is the largest repository of prospectively collected essential tremor (ET) brains (n = 231). Hence, we are uniquely poised to address several questions: What proportion of ET cases has Lewy pathology (LP)? ...

Abstract	The Essential Tremor Centralized Brain Repository is the largest repository of prospectively collected essential tremor (ET) brains (n = 231). Hence, we are uniquely poised to address several questions: What proportion of ET cases has Lewy pathology (LP)? What is the nature of that pathology and how does it relate to other comorbidities? Each brain had a complete neuropathological assessment, including α-synuclein immunostaining. We created a 10-category classification scheme to fully encapsulate the patterns of LP observed. Four metrics of cerebellar pathology were also quantified. Mean age at death = 89.0 ± 6.4 years. Fifty-eight (25.1%) had LP and 46 (19.9%) had early to late stages of Parkinson disease (PD). LP was very heterogeneous. Of 58 cases with LP, 14 (24.1%) clinically developed possible PD or PD after a latency of 5 or more years. There was a similar degree of cerebellar pathology in ET cases both with and without LP. In summary, 1 in 4 ET cases had LP-a proportion that seems higher than expected based on studies among control populations. Heterogeneous LP likely reflects clinical associations between ET and PD, and ET with Alzheimer disease-type neuropathology. These data further our understanding of ET and its relatedness to other degenerative diseases.
MeSH term(s)	Brain/pathology ; Essential Tremor/pathology ; Humans ; Lewy Bodies/pathology ; Parkinson Disease/pathology ; alpha-Synuclein
Chemical Substances	alpha-Synuclein
Language	English
Publishing date	2022-07-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3088-0
ISSN	1554-6578 ; 0022-3069
ISSN (online)	1554-6578
ISSN	0022-3069
DOI	10.1093/jnen/nlac068
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Article ; Online: Authors' replies to the comments of Koga et al. on "Movement disorders rounds: A case of missing pathology in a patient with LRRK2 Parkinson's disease".

Hickman, Richard A / Vonsattel, Jean-Paul / Agin-Liebes, Julian / Marder, Karen / Alcalay, Roy N

Parkinsonism & related disorders

2020 Volume 79, Page(s) 131–132

MeSH term(s)	Humans ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics ; Parkinson Disease/complications ; Parkinson Disease/genetics ; alpha-Synuclein
Chemical Substances	alpha-Synuclein ; LRRK2 protein, human (EC 2.7.11.1) ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1)
Language	English
Publishing date	2020-09-05
Publishing country	England
Document type	Letter ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	1311489-x
ISSN	1873-5126 ; 1353-8020
ISSN (online)	1873-5126
ISSN	1353-8020
DOI	10.1016/j.parkreldis.2020.08.037
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Article ; Online: Histopathology of the cerebellar cortex in essential tremor and other neurodegenerative motor disorders: comparative analysis of 320 brains.

Louis, Elan D / Martuscello, Regina T / Gionco, John T / Hartstone, Whitney G / Musacchio, Jessica B / Portenti, Marisa / McCreary, Morgan / Kuo, Sheng-Han / Vonsattel, Jean-Paul G / Faust, Phyllis L

Acta neuropathologica

2023 Volume 145, Issue 3, Page(s) 265–283

Abstract: In recent years, numerous morphologic changes have been identified in the essential tremor (ET) cerebellar cortex, distinguishing ET from control brains. These findings have not been fully contextualized within a broader degenerative disease spectrum, ... ...

Abstract	In recent years, numerous morphologic changes have been identified in the essential tremor (ET) cerebellar cortex, distinguishing ET from control brains. These findings have not been fully contextualized within a broader degenerative disease spectrum, thus limiting their interpretability. Building off our prior study and now doubling the sample size, we conducted comparative analyses in a postmortem series of 320 brains on the severity and patterning of cerebellar cortex degenerative changes in ET (n = 100), other neurodegenerative disorders of the cerebellum [spinocerebellar ataxias (SCAs, n = 47, including 13 SCA3 and 34 SCA1, 2, 6, 7, 8, 14); Friedreich's ataxia (FA, n = 13); multiple system atrophy (MSA), n = 29], and other disorders that may involve the cerebellum [Parkinson's disease (PD), n = 62; dystonia, n = 19] versus controls (n = 50). We generated data on 37 quantitative morphologic metrics, grouped into 8 broad categories: Purkinje cell (PC) loss, heterotopic PCs, PC dendritic changes, PC axonal changes (torpedoes), PC axonal changes (other than torpedoes), PC axonal changes (torpedo-associated), basket cell axonal hypertrophy, and climbing fiber-PC synaptic changes. Principal component analysis of z scored raw data across all diagnoses (11,651 data items) revealed that diagnostic groups were not uniform with respect to pathology. Dystonia and PD each differed from controls in only 4/37 and 5/37 metrics, respectively, whereas ET differed in 21, FA in 10, SCA3 in 10, MSA in 21, and SCA1/2/6/7/8/14 in 27. Pathological changes were generally on the milder end of the degenerative spectrum in ET, FA and SCA3, and on the more severe end of that spectrum in SCA1/2/6/7/8/14. Comparative analyses across morphologic categories demonstrated differences in relative expression, defining distinctive patterns of changes in these groups. In summary, we present a robust and reproducible method that identifies somewhat distinctive signatures of degenerative changes in the cerebellar cortex that mark each of these disorders.
MeSH term(s)	Humans ; Cerebellar Cortex/pathology ; Cerebellum/pathology ; Dystonia/pathology ; Dystonic Disorders/pathology ; Essential Tremor/metabolism ; Motor Disorders ; Multiple System Atrophy/pathology ; Parkinson Disease/pathology ; Purkinje Cells/pathology ; Spinocerebellar Ataxias/pathology
Language	English
Publishing date	2023-01-06
Publishing country	Germany
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1079-0
ISSN	1432-0533 ; 0001-6322
ISSN (online)	1432-0533
ISSN	0001-6322
DOI	10.1007/s00401-022-02535-z
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Article ; Online: Patterns of TDP-43 Deposition in Brains with LRRK2 G2019S Mutations.

Agin-Liebes, Julian / Hickman, Richard A / Vonsattel, Jean Paul / Faust, Phyllis L / Flowers, Xena / Utkina Sosunova, Irina / Ntiri, Joel / Mayeux, Richard / Surface, Matthew / Marder, Karen / Fahn, Stanley / Przedborski, Serge / Alcalay, Roy N

Movement disorders : official journal of the Movement Disorder Society

2023 Volume 38, Issue 8, Page(s) 1541–1545

Abstract: Objective: To assess for TDP-43 deposits in brains with and without a LRRK2 G2019S mutation.: Background: LRRK2 G2019S mutations have been associated with parkinsonism and a wide range of pathological findings. There are no systematic studies ... ...

Abstract	Objective: To assess for TDP-43 deposits in brains with and without a LRRK2 G2019S mutation. Background: LRRK2 G2019S mutations have been associated with parkinsonism and a wide range of pathological findings. There are no systematic studies examining the frequency and extent of TDP-43 deposits in neuropathological samples from LRRK2 G2019S carriers. Methods: Twelve brains with LRRK2 G2019S mutations were available for study from the New York Brain Bank at Columbia University; 11 of them had samples available for TDP-43 immunostaining. Clinical, demographic, and pathological data are reported for 11 brains with a LRRK2 G2019S mutation and compared to 11 brains without GBA1 or LRRK2 G2019S mutations with a pathologic diagnosis of Parkinson's disease (PD) or diffuse Lewy body disease. They were frequency matched by age, gender, parkinsonism age of onset, and disease duration. Results: TDP-43 aggregates were present in 73% (n = 8) of brains with a LRRK2 mutation and 18% (n = 2) of brains without a LRRK2 mutation (P = 0.03). In one brain with a LRRK2 mutation, TDP-43 proteinopathy was the primary neuropathological change. Conclusions: Extranuclear TDP-43 aggregates are observed with greater frequency in LRRK2 G2019S autopsies compared to PD cases without a LRRK2 G2019S mutation. The association between LRRK2 and TDP-43 should be further explored. © 2023 International Parkinson and Movement Disorder Society.
MeSH term(s)	Humans ; Brain ; DNA-Binding Proteins/genetics ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics ; Mutation/genetics ; Parkinson Disease/genetics ; Parkinsonian Disorders/genetics ; Protein Serine-Threonine Kinases/genetics
Chemical Substances	DNA-Binding Proteins ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1) ; LRRK2 protein, human (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; TARDBP protein, human
Language	English
Publishing date	2023-05-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	607633-6
ISSN	1531-8257 ; 0885-3185
ISSN (online)	1531-8257
ISSN	0885-3185
DOI	10.1002/mds.29449
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Article ; Online: Neuropathological Findings in a Case of Parkinsonism and Developmental Delay Associated with a Monoallelic Variant in PLXNA1.

O'Shea, Sarah A / Hickman, Richard A / Cortes, Etty / Vonsattel, Jean Paul / Fahn, Stanley / Okur, Volkan / Alcalay, Roy N / Chung, Wendy K

Movement disorders : official journal of the Movement Disorder Society

2021 Volume 36, Issue 11, Page(s) 2681–2687

Abstract: Background: PLXNA1 encodes for Plexin-A, a transmembrane protein expressed in the developing nervous system. Mutations in this gene have been associated with developmental delay but have not been previously associated with the development of ... ...

Abstract	Background: PLXNA1 encodes for Plexin-A, a transmembrane protein expressed in the developing nervous system. Mutations in this gene have been associated with developmental delay but have not been previously associated with the development of parkinsonism. Objectives: To describe the case of a 38-year-old patient with developmental delay who developed parkinsonism later in life. Methods: Post-mortem exome sequencing was performed with confirmation by Sanger sequencing. Brain autopsy was also performed. Results: Post-mortem exome sequencing on the proband identified a heterozygous predicted nonsense PLXNA1 variant (c.G3361T:p.Glu1121Ter). Pathology demonstrated arhinencephaly with brainstem heterotopia, diffuse Lewy body disease, and frontotemporal lobar dementia-tau. Conclusions: This case of a patient with developmental delay and parkinsonism with PLXNA1 mutation highlights a need for assessing long-term outcomes of individuals with neurodevelopmental disorders, as well as the need for genetic testing in adults. It also suggests that the link between PLXNA1 and α-synuclein should be explored in the future. © 2021 International Parkinson and Movement Disorder Society.
MeSH term(s)	Adult ; Brain/pathology ; Frontotemporal Dementia/pathology ; Humans ; Lewy Body Disease/pathology ; Mutation/genetics ; Nerve Tissue Proteins/genetics ; Parkinsonian Disorders/genetics ; Parkinsonian Disorders/pathology ; Receptors, Cell Surface
Chemical Substances	Nerve Tissue Proteins ; PLXNA1 protein, human ; Receptors, Cell Surface
Language	English
Publishing date	2021-08-20
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	607633-6
ISSN	1531-8257 ; 0885-3185
ISSN (online)	1531-8257
ISSN	0885-3185
DOI	10.1002/mds.28756
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