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Article ; Online: Late-Onset Alcohol Abuse as a Presenting Symptom of Neurodegenerative Diseases.

de Paula França Resende, Elisa / Ketelle, Robin / Karydas, Anna / Allen, Isabel / Grinberg, Lea T / Spina, Salvatore / Seeley, William W / Perry, David C / Miller, Bruce / Naasan, Georges

Journal of Alzheimer's disease : JAD

2022 Volume 86, Issue 3, Page(s) 1073–1080

Abstract: Background: The association between lifetime alcohol abuse and a higher risk to develop dementia is well known. However, it is unknown whether older adults who begin abusing alcohol late in life have an underlying neurodegenerative disease.: Objective! ...

Abstract	Background: The association between lifetime alcohol abuse and a higher risk to develop dementia is well known. However, it is unknown whether older adults who begin abusing alcohol late in life have an underlying neurodegenerative disease. Objective: Identify the frequency of lifelong alcohol abuse (L-AA), late-onset alcohol abuse (LO-AA), and alcohol abuse as a first symptom of dementia (AA-FS) in patients with neurodegenerative diseases. Methods: Cross-sectional retrospective study of patients evaluated at an academic referral center with a clinical diagnosis of behavioral variant frontotemporal dementia (bvFTD), Alzheimer-type dementia (AD), and semantic variant primary progressive aphasia (svPPA) (n = 1,518). The presence of alcohol abuse was screened with the National Alzheimer's Coordinating Center questionnaire. L-AA was defined as onset < 40 years, LO-AA as onset ≥40 years, and AA-FS was defined when the abuse started within the first three years from symptom onset. Results: The frequency of LO-AA was 2.2% (n = 33/1,518). LO-AA was significantly more frequent in patients with bvFTD than AD (7.5%, n = 13/173 versus 1.3%, n = 16/1,254, CI:1.0;11.4%), but not svPPA (4.4%, n = 4/91, CI: -4.4;10.7%). Similarly, AA-FS was more frequent in bvFTD patients than AD (5.7%, n = 10/173 versus 0.7%, n = 9/1,254, CI:0.5%;9.5%), but not svPPA (2.2%, n = 2/91, CI:-2.4;9.1%). Conclusion: LO-AA can be a presenting symptom of dementia, especially bvFTD. Alcohol abuse onset later in life should prompt a clinical investigation into the possibility of an underlying neurodegenerative process because delay in diagnosis and treatment may increase patient and caregiver burden. The results need to be interpreted with caution due to the limitations of the study.
MeSH term(s)	Aged ; Alcoholism/diagnosis ; Alcoholism/epidemiology ; Alzheimer Disease/diagnosis ; Alzheimer Disease/epidemiology ; Cross-Sectional Studies ; Frontotemporal Dementia/diagnosis ; Frontotemporal Dementia/epidemiology ; Humans ; Neurodegenerative Diseases/diagnosis ; Neurodegenerative Diseases/epidemiology ; Neuropsychological Tests ; Retrospective Studies
Language	English
Publishing date	2022-02-18
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-215369
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Article ; Online: Postmortem Human Dura Mater Cells Exhibit Phenotypic, Transcriptomic and Genetic Abnormalities that Impact their Use for Disease Modeling.

Argouarch, Andrea R / Schultz, Nina / Yang, Andrew C / Jang, Yeongjun / Garcia, Kristle / Cosme, Celica G / Corrales, Christian I / Nana, Alissa L / Karydas, Anna M / Spina, Salvatore / Grinberg, Lea T / Miller, Bruce / Wyss-Coray, Tony / Abyzov, Alexej / Goodarzi, Hani / Seeley, William W / Kao, Aimee W

Stem cell reviews and reports

2022 Volume 18, Issue 8, Page(s) 3050–3065

Abstract: Patient-derived cells hold great promise for precision medicine approaches in human health. Human dermal fibroblasts have been a major source of cells for reprogramming and differentiating into specific cell types for disease modeling. Postmortem human ... ...

Abstract	Patient-derived cells hold great promise for precision medicine approaches in human health. Human dermal fibroblasts have been a major source of cells for reprogramming and differentiating into specific cell types for disease modeling. Postmortem human dura mater has been suggested as a primary source of fibroblasts for in vitro modeling of neurodegenerative diseases. Although fibroblast-like cells from human and mouse dura mater have been previously described, their utility for reprogramming and direct differentiation protocols has not been fully established. In this study, cells derived from postmortem dura mater are directly compared to those from dermal biopsies of living subjects. In two instances, we have isolated and compared dermal and dural cell lines from the same subject. Notably, striking differences were observed between cells of dermal and dural origin. Compared to dermal fibroblasts, postmortem dura mater-derived cells demonstrated different morphology, slower growth rates, and a higher rate of karyotype abnormality. Dura mater-derived cells also failed to express fibroblast protein markers. When dermal fibroblasts and dura mater-derived cells from the same subject were compared, they exhibited highly divergent gene expression profiles that suggest dura mater cells originated from a mixed mural lineage. Given their postmortem origin, somatic mutation signatures of dura mater-derived cells were assessed and suggest defective DNA damage repair. This study argues for rigorous karyotyping of postmortem derived cell lines and highlights limitations of postmortem human dura mater-derived cells for modeling normal biology or disease-associated pathobiology.
MeSH term(s)	Humans ; Animals ; Mice ; Transcriptome ; Dura Mater/metabolism ; Dura Mater/pathology ; Cell Differentiation/genetics ; Fibroblasts ; Cells, Cultured
Language	English
Publishing date	2022-07-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2495577-2
ISSN	2629-3277 ; 1558-6804 ; 1550-8943
ISSN (online)	2629-3277 ; 1558-6804
ISSN	1550-8943
DOI	10.1007/s12015-022-10416-x
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Article ; Online: Psychosis in neurodegenerative disease: differential patterns of hallucination and delusion symptoms.

Naasan, Georges / Shdo, Suzanne M / Rodriguez, Estrella Morenas / Spina, Salvatore / Grinberg, Lea / Lopez, Lucia / Karydas, Anna / Seeley, William W / Miller, Bruce L / Rankin, Katherine P

Brain : a journal of neurology

2021 Volume 144, Issue 3, Page(s) 999–1012

Abstract: Although psychosis is a defining feature of Lewy body disease, psychotic symptoms occur in a subset of patients with every major neurodegenerative disease. Few studies, however, have compared disease-related rates of psychosis prevalence in a large ... ...

Abstract	Although psychosis is a defining feature of Lewy body disease, psychotic symptoms occur in a subset of patients with every major neurodegenerative disease. Few studies, however, have compared disease-related rates of psychosis prevalence in a large autopsy-based cohort, and it remains unclear how diseases differ with respect to the nature or content of the psychosis. We conducted a retrospective chart review of 372 patients with autopsy-confirmed neurodegenerative pathology: 111 with Alzheimer's disease, 59 with Lewy body disease and concomitant Alzheimer's disease, 133 with frontotemporal lobar degeneration (FTLD) with tau inclusions (including progressive supranuclear palsy, corticobasal degeneration or Pick's disease), and 69 with FTLD and TDP inclusions (FTLD-TDP, including types A-C). Psychosis content was classified by subtype, and the frequency of each subtype was compared among pathological diagnoses using logistic regression. A total of 111 of 372 patients had psychosis. Compared to other groups, patients with Lewy body disease/Alzheimer's disease pathology were significantly more likely to have hallucinations and were more likely to have more than one subtype of hallucination. Patients with Braak Parkinson stage 5-6 Lewy body disease were significantly more likely than those with no Lewy body disease to have visual hallucinations of misperception, peripheral hallucinations, hallucinations that moved, hallucinations of people/animals/objects, as well as delusions regarding a place and delusions of misidentification. The feeling of a presence occurred significantly more frequently in patients with Lewy body disease/Alzheimer's disease than all other pathologies. Patients with FTLD-TDP were significantly more likely to have delusions, and for the delusions to occur in the first 3 years of the disease, when compared to patients with Alzheimer's disease and FTLD-tau, though rates were not significantly greater than patients with Lewy body disease/Alzheimer's disease. Paranoia occurred more frequently in the FTLD-TDP and Lewy body disease/Alzheimer's disease categories compared to patients with Alzheimer's disease or FTLD-tau. Patients with FTLD-TDP pathology had delusions of misidentification as frequently as patients with Lewy body disease/Alzheimer's disease, and were significantly more likely to have self-elevating delusions such as grandiosity and erotomania compared to patients with other pathologies including FTLD-tau. These data show that the nature and content of psychosis can provide meaningful information about the underlying neurodegenerative pathology, emphasizing the importance of characterizing patients' psychoses for prediction of the neuropathological diagnosis, regardless of a patient's clinical syndrome.
MeSH term(s)	Aged ; Delusions/epidemiology ; Delusions/etiology ; Female ; Hallucinations/epidemiology ; Hallucinations/etiology ; Humans ; Male ; Middle Aged ; Neurodegenerative Diseases/complications ; Prevalence ; Psychotic Disorders/epidemiology ; Psychotic Disorders/etiology
Language	English
Publishing date	2021-01-27
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awaa413
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Article ; Online: Genetic counseling for FTD/ALS caused by the C9ORF72 hexanucleotide expansion.

Fong, Jamie C / Karydas, Anna M / Goldman, Jill S

Alzheimer's research & therapy

2012 Volume 4, Issue 4, Page(s) 27

Abstract: Frontotemporal degeneration (FTD) and amyotrophic lateral sclerosis (ALS) are related but distinct neurodegenerative diseases. The identification of a hexanucleotide repeat expansion in a noncoding region of the chromosome 9 open reading frame 72 ( ... ...

Abstract	Frontotemporal degeneration (FTD) and amyotrophic lateral sclerosis (ALS) are related but distinct neurodegenerative diseases. The identification of a hexanucleotide repeat expansion in a noncoding region of the chromosome 9 open reading frame 72 (C9ORF72) gene as a common cause of FTD/ALS, familial FTD, and familial ALS marks the culmination of many years of investigation. This confirms the linkage of disease to chromosome 9 in large, multigenerational families with FTD and ALS, and it promotes deeper understanding of the diseases' shared molecular FTLD-TDP pathology. The discovery of the C9ORF72 repeat expansion has significant implications not only for familial FTD and ALS, but also for sporadic disease. Clinical and pathological correlates of the repeat expansion are being reported but remain to be refined, and a genetic test to detect the expansion has only recently become clinically available. Consequently, individuals and their families who are considering genetic testing for the C9ORF72 expansion should receive genetic counseling to discuss the risks, benefits, and limitations of testing. The following review aims to describe genetic counseling considerations for individuals at risk for a C9ORF72 repeat expansion.
Language	English
Publishing date	2012-07-19
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2506521-X
ISSN	1758-9193 ; 1758-9193
ISSN (online)	1758-9193
ISSN	1758-9193
DOI	10.1186/alzrt130
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Article ; Online: Lack of Association Between the CCR5-delta32 Polymorphism and Neurodegenerative Disorders.

Wojta, Kevin J / Ayer, Ariane H / Ramos, Eliana M / Nguyen, Peter D / Karydas, Anna M / Yokoyama, Jennifer S / Kramer, Joel / Lee, Suzee E / Boxer, Adam / Miller, Bruce L / Coppola, Giovanni

Alzheimer disease and associated disorders

2020 Volume 34, Issue 3, Page(s) 244–247

Abstract: Objective: Recent studies have suggested that diminished Ccr5 functioning has an effect on synaptic plasticity and hippocampal memory in mouse models. CCR5-delta32, a 32-bp frameshift deletion in human CCR5 encoding a nonfunctional receptor, has been ... ...

Abstract	Objective: Recent studies have suggested that diminished Ccr5 functioning has an effect on synaptic plasticity and hippocampal memory in mouse models. CCR5-delta32, a 32-bp frameshift deletion in human CCR5 encoding a nonfunctional receptor, has been reported to have a protective effect against human immunodeficiency virus infection but its role as a modifier of neurodegenerative disease has been minimally explored. We investigated whether the CCR5-delta32 polymorphism could have an effect in the context of human neurodegenerative diseases. Methods: We examined the frequency of the CCR5-delta32 polymorphism in a large and well-characterized cohort including 1425 patients with neurodegenerative dementias and 2032 controls. Results: We did not observe a significant association between the CCR5-delta32 polymorphism and any of the neurodegenerative diseases screened in this study. However, we observed an earlier age of onset among neurodegenerative disease patients carrying the CCR5-delta32 allele. Conclusions: Although our findings were inconclusive, the earlier age of onset observed among neurodegenerative disease patients carrying the CCR5-delta32 allele suggests that the deletion may have a detrimental effect in the context of neurodegeneration.
MeSH term(s)	Adult ; Age of Onset ; Alleles ; California ; Cohort Studies ; Humans ; Middle Aged ; Neurodegenerative Diseases/genetics ; Polymorphism, Genetic ; Receptors, CCR5/genetics
Chemical Substances	CCR5 protein, human ; Receptors, CCR5
Language	English
Publishing date	2020-08-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	1002700-2
ISSN	1546-4156 ; 0893-0341
ISSN (online)	1546-4156
ISSN	0893-0341
DOI	10.1097/WAD.0000000000000367
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Article ; Online: Elevated levels of extracellular vesicles in progranulin-deficient mice and FTD-GRN Patients.

Arrant, Andrew E / Davis, Skylar E / Vollmer, Rachael M / Murchison, Charles F / Mobley, James A / Nana, Alissa L / Spina, Salvatore / Grinberg, Lea T / Karydas, Anna M / Miller, Bruce L / Seeley, William W / Roberson, Erik D

Annals of clinical and translational neurology

2020 Volume 7, Issue 12, Page(s) 2433–2449

Abstract: Objective: The goal of this study was to investigate the effect of progranulin insufficiency on extracellular vesicles (EVs), a heterogeneous population of vesicles that may contribute to progression of neurodegenerative disease. Loss-of-function ... ...

Abstract	Objective: The goal of this study was to investigate the effect of progranulin insufficiency on extracellular vesicles (EVs), a heterogeneous population of vesicles that may contribute to progression of neurodegenerative disease. Loss-of-function mutations in progranulin (GRN) are a major cause of frontotemporal dementia (FTD), and brains from GRN carriers with FTD (FTD-GRN) exhibit signs of lysosomal dysfunction. Lysosomal dysfunction may induce compensatory increases in secretion of exosomes, EVs secreted from the endolysosomal system, so we hypothesized that progranulin insufficiency would increase EV levels in the brain. Methods: We analyzed levels and protein contents of brain EVs from Grn Results: Grn Interpretation: These data show that symptomatic FTD-GRN patients have elevated levels of brain and plasma EVs, and that this effect is modeled in the brain of Grn
MeSH term(s)	Aged ; Aged, 80 and over ; Animals ; Disease Progression ; Extracellular Vesicles/metabolism ; Female ; Frontal Lobe/metabolism ; Frontotemporal Dementia/blood ; Frontotemporal Dementia/genetics ; Frontotemporal Dementia/metabolism ; Humans ; Male ; Mice ; Middle Aged ; Progranulins/deficiency ; Progranulins/genetics ; Progranulins/metabolism ; Proteomics ; Single-Blind Method
Chemical Substances	GRN protein, human ; Grn protein, mouse ; Progranulins
Language	English
Publishing date	2020-11-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2740696-9
ISSN	2328-9503 ; 2328-9503
ISSN (online)	2328-9503
ISSN	2328-9503
DOI	10.1002/acn3.51242
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Article ; Online: Promoting tau secretion and propagation by hyperactive p300/CBP via autophagy-lysosomal pathway in tauopathy.

Chen, Xu / Li, Yaqiao / Wang, Chao / Tang, Yinyan / Mok, Sue-Ann / Tsai, Richard M / Rojas, Julio C / Karydas, Anna / Miller, Bruce L / Boxer, Adam L / Gestwicki, Jason E / Arkin, Michelle / Cuervo, Ana Maria / Gan, Li

Molecular neurodegeneration

2020 Volume 15, Issue 1, Page(s) 2

Abstract: Background: The trans-neuronal propagation of tau has been implicated in the progression of tau-mediated neurodegeneration. There is critical knowledge gap in understanding how tau is released and transmitted, and how that is dysregulated in diseases. ... ...

Abstract	Background: The trans-neuronal propagation of tau has been implicated in the progression of tau-mediated neurodegeneration. There is critical knowledge gap in understanding how tau is released and transmitted, and how that is dysregulated in diseases. Previously, we reported that lysine acetyltransferase p300/CBP acetylates tau and regulates its degradation and toxicity. However, whether p300/CBP is involved in regulation of tau secretion and propagation is unknown. Method: We investigated the relationship between p300/CBP activity, the autophagy-lysosomal pathway (ALP) and tau secretion in mouse models of tauopathy and in cultured rodent and human neurons. Through a high-through-put compound screen, we identified a new p300 inhibitor that promotes autophagic flux and reduces tau secretion. Using fibril-induced tau spreading models in vitro and in vivo, we examined how p300/CBP regulates tau propagation. Results: Increased p300/CBP activity was associated with aberrant accumulation of ALP markers in a tau transgenic mouse model. p300/CBP hyperactivation blocked autophagic flux and increased tau secretion in neurons. Conversely, inhibiting p300/CBP promoted autophagic flux, reduced tau secretion, and reduced tau propagation in fibril-induced tau spreading models in vitro and in vivo. Conclusions: We report that p300/CBP, a lysine acetyltransferase aberrantly activated in tauopathies, causes impairment in ALP, leading to excess tau secretion. This effect, together with increased intracellular tau accumulation, contributes to enhanced spreading of tau. Our findings suggest that inhibition of p300/CBP as a novel approach to correct ALP dysfunction and block disease progression in tauopathy.
MeSH term(s)	Animals ; Autophagy/physiology ; Humans ; Lysosomes/metabolism ; Mice ; Mice, Transgenic ; Neurons/metabolism ; Rats, Sprague-Dawley ; Tauopathies/metabolism ; p300-CBP Transcription Factors/metabolism ; tau Proteins/metabolism
Chemical Substances	tau Proteins ; p300-CBP Transcription Factors (EC 2.3.1.48)
Language	English
Publishing date	2020-01-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2244557-2
ISSN	1750-1326 ; 1750-1326
ISSN (online)	1750-1326
ISSN	1750-1326
DOI	10.1186/s13024-019-0354-0
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Article ; Online: Interbatch Reliability of Blood-Based Cytokine and Chemokine Measurements in Community-Dwelling Older Adults: A Cross-Sectional Study.

Lindbergh, Cutter A / Asken, Breton M / Casaletto, Kaitlin B / Elahi, Fanny M / Goldberger, Lauren A / Fonseca, Corrina / You, Michelle / Apple, Alexandra C / Staffaroni, Adam M / Fitch, Ryan / Rivera Contreras, Will / Wang, Paul / Karydas, Anna / Kramer, Joel H

The journals of gerontology. Series A, Biological sciences and medical sciences

2021 Volume 76, Issue 11, Page(s) 1954–1961

Abstract: Blood-based inflammatory markers hold considerable promise for diagnosis and prognostication of age-related neurodegenerative disease, though a paucity of research has empirically tested how reliably they can be measured across different experimental ... ...

Abstract	Blood-based inflammatory markers hold considerable promise for diagnosis and prognostication of age-related neurodegenerative disease, though a paucity of research has empirically tested how reliably they can be measured across different experimental runs ("batches"). We quantified the interbatch reliability of 13 cytokines and chemokines in a cross-sectional study of 92 community-dwelling older adults (mean age = 74; 48% female). Plasma aliquots from the same blood draw were parallelly processed in 2 separate batches using the same analytic platform and procedures (high-performance electrochemiluminescence by Meso Scale Discovery). Interbatch correlations (Pearson's r) ranged from small and nonsignificant (r = .13 for macrophage inflammatory protein-1 alpha [MIP-1α]) to very large (r > .90 for interferon gamma [IFNγ], interleukin-10 [IL-10], interferon gamma-induced protein 10 [IP-10], MIP-1β, thymus and activation-regulated chemokine [TARC]) with most markers falling somewhere in between (.67 ≤ r ≤ .90 for IL-6, tumor necrosis factor alpha [TNF-α], Eotaxin, Eotaxin-3, monocyte chemoattractant protein-1 [MCP-1], MCP-4, macrophage-derived chemokine [MDC]). All markers, except for IL-6 and MCP-4, showed significant differences in absolute values between batches, with discrepancies ranging in effect size (Cohen's d) from small to moderate (0.2 ≤ \|d\| ≤ 0.5 for IL-10, IP-10, MDC) to large or very large (0.68 ≤ \|d\| ≤ 1.5 for IFNγ, TNF-α, Eotaxin, Eotaxin-3, MCP-1, MIP-1α, MIP-1β, TARC). Relatively consistent associations with external variables of interest (age, sex, systolic blood pressure, body mass index, cognition) were observed across batches. Taken together, our results suggest heterogeneity in measurement reliability of blood-based cytokines and chemokines, with some analytes outperforming others. Future work is needed to evaluate the generalizability of these findings while identifying potential sources of batch effect measurement error.
MeSH term(s)	Aged ; Chemokine CCL26 ; Chemokine CCL3 ; Chemokine CCL4 ; Chemokine CXCL10 ; Cross-Sectional Studies ; Cytokines ; Female ; Humans ; Independent Living ; Interferon-gamma ; Interleukin-10 ; Interleukin-6 ; Male ; Neurodegenerative Diseases ; Reproducibility of Results ; Tumor Necrosis Factor-alpha
Chemical Substances	Chemokine CCL26 ; Chemokine CCL3 ; Chemokine CCL4 ; Chemokine CXCL10 ; Cytokines ; Interleukin-6 ; Tumor Necrosis Factor-alpha ; Interleukin-10 (130068-27-8) ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2021-06-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1223643-3
ISSN	1758-535X ; 1079-5006
ISSN (online)	1758-535X
ISSN	1079-5006
DOI	10.1093/gerona/glab162
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Article: Youthful Processing Speed in Older Adults: Genetic, Biological, and Behavioral Predictors of Cognitive Processing Speed Trajectories in Aging.

Bott, Nicholas T / Bettcher, Brianne M / Yokoyama, Jennifer S / Frazier, Darvis T / Wynn, Matthew / Karydas, Anna / Yaffe, Kristine / Kramer, Joel H

Frontiers in aging neuroscience

2017 Volume 9, Page(s) 55

Abstract: Objective: ...

Abstract	Objective:
Language	English
Publishing date	2017-03-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2017.00055
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Article ; Online: Gyrification abnormalities in presymptomatic

Caverzasi, Eduardo / Battistella, Giovanni / Chu, Stephanie A / Rosen, Howie / Zanto, Theodore P / Karydas, Anna / Shwe, Wendy / Coppola, Giovanni / Geschwind, Daniel H / Rademakers, Rosa / Miller, Bruce L / Gorno-Tempini, Maria Luisa / Lee, Suzee E

Journal of neurology, neurosurgery, and psychiatry

2019 Volume 90, Issue 9, Page(s) 1005–1010

Abstract: Objective: To investigate in-vivo cortical gyrification patterns measured by the local gyrification index (lGI) in presymptomatic : Methods: We assessed cortical gyrification and thickness patterns in a cohort of 15 presymptomatic : Results: ... ...

Abstract	Objective: To investigate in-vivo cortical gyrification patterns measured by the local gyrification index (lGI) in presymptomatic Methods: We assessed cortical gyrification and thickness patterns in a cohort of 15 presymptomatic Results: Compared with controls, presymptomatic carriers showed significantly lower lGI in left frontal and right parieto-occipital regions. Interestingly, those areas with abnormal gyrification in presymptomatic carriers showed no concomitant cortical thickness abnormality. Overall, for both presymptomatic carriers and healthy controls, gyrification and cortical thickness measures were not correlated, suggesting that gyrification captures a feature distinct from cortical thickness. Conclusions: Presymptomatic
MeSH term(s)	Adult ; Age Factors ; Asymptomatic Diseases ; C9orf72 Protein/genetics ; Case-Control Studies ; Cerebral Cortex/abnormalities ; Cerebral Cortex/diagnostic imaging ; Female ; Heterozygote ; Humans ; Magnetic Resonance Imaging ; Male ; Neuroimaging
Chemical Substances	C9orf72 Protein ; C9orf72 protein, human
Language	English
Publishing date	2019-05-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3087-9
ISSN	1468-330X ; 0022-3050
ISSN (online)	1468-330X
ISSN	0022-3050
DOI	10.1136/jnnp-2018-320265
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