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Ferman, Tanis J.

https://orcid.org/0000-0001-8377-6194

Mayo Clinic

Mayo Clinic

Citations 181

Excessive Daytime Sleepiness in Major Dementia Syndromes
Boeve, Angelica, Ferman, Tanis J. , Aakre, Jeremiah A. , Silber, Michael H. , Fields, Julie A. , Graff‐Radford, Neill R. , Geda, Yonas E. , Graff-Radford, Jonathon, Petersen, Ronald C. , Aakre, Jeremiah, St Louis, Erik, Silber, Michael , Mielke, Michelle, Geda, Yonas, Boeve, Brad , Geda, Yonas E , Ferman, Tanis J , Louis, Erik K. St. , Machulda, Mary M. , Mielke, Michelle M. , Jones, David T. , Knopman, David S. , Boeve, Bradley F.

American Journal of Alzheimer's Disease & Other Dementias® | February 11, 2019 | Volume: 34 | Issue: 4 | Pages: 261-264

10.1177/1533317519828046 Get It

There has been no comparison of excessive daytime sleepiness (EDS) in patients with Alzheimer’s disease dementia (AD), dementia with Lewy bodies (DLB), and behavioral variant frontotemporal dementia (bvFTD). We identified patients with mild dementia who met criteria for these disorders who also had the Epworth Sleepiness Scale (ESS) completed. The sample included 17 bvFTD, 111 AD, and 31 DLB. An ESS score ≥10 was considered abnormal and consistent with EDS. Analyses with age and sex as covariates revealed higher mean ESS scores for DLB compared to the other groups (DLB 13.9 [5], bvFTD 9.6 [8], AD 8.8 [5], P < .05). An ESS score ≥10 was significantly more likely to occur in DLB compared to bvFTD or AD (DLB 81% vs bvFTD 47% vs AD 45%, P < .01). In patients with mild dementia, EDS is greatest in DLB and comparably lower in bvFTD and AD.
F1‐01‐04: DEMENTIA WITH LEWY BODIES
Lowe, Val J. , Kantarci, Kejal , Boeve, Bradley F. , Ferman, Tanis J. , Dickson, Dennis W.

Alzheimer's & Dementia | October 22, 2018 | Volume: 14 | Issue: 7S_Part_3 | Pages: No page available

10.1016/j.jalz.2018.06.2306 Get It

IC‐P‐019: LONGITUDINAL ACCUMULATION OF β‐AMYLOID ON PET IN DEMENTIA WITH LEWY BODIES AND RELATIONSHIP TO CLINICAL DISEASE PROGRESSION
Lesnick, Timothy G. , Przybelski, Scott A. , Lowe, Val J. , Gunter, Jeffrey L. , Radford, Jonathan Graff, Petersen, Ronald C. , Nedelská, Zuzana , Schwarz, Christopher G. , Boeve, Bradley F. , Kremers, Walter K. , Senjem, Matthew L. , Ferman, Tanis J. , Knopman, David S. , Jack, Clifford R. , Kantarci, Kejal

Alzheimer's & Dementia | October 22, 2018 | Volume: 14 | Issue: 7S_Part_1 | Pages: No page available

10.1016/j.jalz.2018.06.2083 Get It

P3‐424: LONGITUDINAL ACCUMULATION OF β‐AMYLOID ON PET IN DEMENTIA WITH LEWY BODIES AND RELATIONSHIP TO CLINICAL DISEASE PROGRESSION
Lesnick, Timothy G. , Przybelski, Scott A. , Lowe, Val J. , Gunter, Jeffrey L. , Graff‐Radford, Jonathan , Petersen, Ronald C. , Nedelská, Zuzana , Schwarz, Christopher G. , Boeve, Bradley F. , Kremers, Walter K. , Senjem, Matthew L. , Ferman, Tanis J. , Knopman, David S. , Jack, Clifford R. , Kantarci, Kejal

Alzheimer's & Dementia | October 22, 2018 | Volume: 14 | Issue: 7S_Part_24 | Pages: No page available

10.1016/j.jalz.2018.06.1787 Get It

P1‐492: SELECTIVE VULNERABILITY OF THE CHOLINERGIC SYSTEM IN ALZHEIMER'S DISEASE SUBTYPES
Al‐Shaikh, Fadi S. Hanna , Graff‐Radford, Neill R. , Liesinger, Amanda M., Ertekin‐Taner, Nilüfer , Pedraza, Otto , Duara, Ranjan , Ferman, Tanis J. , Ross, Owen A. , Duara, Ranjan , Dickson, Dennis W. , Murray, Melissa E.

Alzheimer's & Dementia | October 22, 2018 | Volume: 14 | Issue: 7S_Part_9 | Pages: No page available

10.1016/j.jalz.2018.06.502 Get It

Full sequencing and haplotype analysis of MAPT in Parkinson's disease and rapid eye movement sleep behavior disorder
Li, Jiao , Ruskey, Jennifer A. , Arnulf, Isabelle , Dauvilliers, Yves , Hu, Michele T.M., Högl, Birgit , Leblond, Claire S. , Ambalavanan, Amirthagowri , Ross, Jay P. , Bourassa, Cynthia V., Spiegelman, Dan , Laurent, Sandra B., Stefani, Ambra , Monaca, Christelle, Boivin, Michel , Antelmi, Elena , Young, Peter, Heidbreder, Anna , Ferman, Tanis J. , Dion, Patrick A. , Désautels, Alex , Gagnon, Jean‐François, Dupré, Nicolas , Montplaisir, Jacques , Boeve, Bradley F., Ross, Owen A. , Shulman, Joshua , Labbé, Catherine, Antelmi, Elena , Ross, Owen A , Dauvilliers, Yves , Ferman, Tanis J , Stefani, Ambra , Zhou, Sirui , Cochen De Cock, Valérie , Ferini-Strambi, Luigi , Plazzi, Giuseppe , Labbé, Catherine , Fan, Dongsheng , Fon, Edward A , Boeve, Bradley F. , Postuma, Ronald B. , Rouleau, Guy Armand , Gan‐Or, Ziv , Arnulf, Isabelle , Hu, Michele T M , Högl, Birgit , Heidbreder, Anna

Movement Disorders | May 14, 2018 | Volume: 33 | Issue: 6 | Pages: 1016-1020

10.1002/mds.27385 Get It

ABSTRACT Background: MAPT haplotypes are associated with PD, but their association with rapid eye movement sleep behavior disorder is unclear. Objective: To study the role of MAPT variants in rapid eye movement sleep behavior disorder. Methods: Two cohorts were included: (A) PD (n = 600), rapid eye movement sleep behavior disorder (n = 613) patients, and controls (n = 981); (B) dementia with Lewy bodies patients with rapid eye movement sleep behavior disorder (n = 271) and controls (n = 950). MAPT ‐associated variants and the entire coding sequence of MAPT were analyzed. Age‐, sex‐, and ethnicity‐adjusted analyses were performed to examine the association between MAPT , PD, and rapid eye movement sleep behavior disorder. Results: MAPT‐ H2 variants were associated with PD (odds ratios: 0.62‐0.65; P = 0.010‐0.019), but not with rapid eye movement sleep behavior disorder. In PD, the H1 haplotype odds ratio was 1.60 (95% confidence interval: 1.12‐2.28; P = 0.009), and the H2 odds ratio was 0.68 (95% confidence interval: 0.48‐0.96; P = 0.03). The H2/H1 haplotypes were not associated with rapid eye movement sleep behavior disorder. Conclusions: Our results confirm the protective effect of the MAPT ‐H2 haplotype in PD, and define its components. Furthermore, our results suggest that MAPT does not play a major role in rapid eye movement sleep behavior disorder, emphasizing different genetic background than in PD in this locus. © 2018 International Parkinson and Movement Disorder Society
Clinicopathological and 123I‐FP‐CIT SPECT correlations in patients with dementia
Jung, Youngsin, Jordan, Lennon, Lowe, Val J. , Kantarci, Kejal , Parisi, Joseph E. , Murray, Melissa E. , Reichard, Ross R., Ferman, Tanis J. , Graff‐Radford, Jonathan , Savica, Rodolfo , Fields, Julie A. , Allen, Laura A., Drubach, Daniel A., Louis, Erik K. St. , Silber, Michael H. , Jack, Clifford R. , Petersen, Ronald C. , Jordan, Lennon G, St Louis, Erik K, Jack, Clifford R , St Louis, E K , Kantarci, Kejal , Murray, Melissa E , Ferman, Tanis J , Dickson, Dennis W. , Jones, David T. , Machulda, Mary M. , Knopman, David S. , Boeve, Bradley F.

Annals of Clinical and Translational Neurology | January 24, 2018 | Volume: 5 | Issue: 3 | Pages: 376-381

10.1002/acn3.521 Get It

AbstractThe relationship between clinicopathologic diagnosis and 123I‐FP‐CIT SPECT in 18 patients with dementia (12 with Lewy body disease) from one center in the United States was assessed. The sensitivity and specificity of abnormal 123I‐FP‐CIT SPECT with reduced striatal uptake on visual inspection for predicting Lewy body disease were 91.7% and 83.3%, respectively. The mean calculated putamen to occipital ratio (mPOR) based on regions of interest was significantly reduced in Lewy body disease compared to non‐Lewy body disease cases (P = 0.002). In this study, abnormal 123I‐FP‐CIT SPECT was strongly associated with underlying Lewy body disease pathology, supporting the utility of 123I‐FP‐CIT SPECT in the clinical diagnosis of dementia with Lewy bodies.
The limbic and neocortical contribution of α‐synuclein, tau, and amyloid β to disease duration in dementia with Lewy bodies
Ferman, Tanis J. , Aoki, Naoya , Murray, Melissa E. , Graff‐Radford, Neill R. , Gerpen, Jay A. van, Uitti, Ryan J. , Graff‐Radford, Jonathan, Pedraza, Otto , Kantarci, Kejal , Crook, Julia E. , Van Gerpen, Jay A, Kantarci, Kejal , Murray, Melissa E , Ferman, Tanis J , Wszołek, Zbigniew K. , Graff‐Radford, Jonathan , Boeve, Bradley F. , Dickson, Dennis W.

Alzheimer's & Dementia | October 31, 2017 | Volume: 14 | Issue: 3 | Pages: 330-339

10.1016/j.jalz.2017.09.014 Get It

AbstractIntroductionWe sought to assess the individual and combined contribution of limbic and neocortical α‐synuclein, tau, and amyloid β (Aβ) to duration of illness in dementia with Lewy bodies (DLB).MethodsQuantitative digital pathology of limbic and neocortical α‐synuclein, tau, and Aβ was assessed in 49 patients with clinically probable DLB. Regression modeling examined the unique and shared contribution of each pathology to the variance of illness duration.ResultsPatients with diffuse Lewy body disease had more severe pathology of each type and a shorter duration of illness than individuals with transitional Lewy body disease. The three pathologies accounted for 25% of the total variance of duration of illness, with 19% accounted for by α‐synuclein alone or in combination with tau and Aβ. When the diffuse Lewy body disease group was examined separately, α‐synuclein deposition significantly exceeded that of tau and Aβ. In this model, 20% of 24% total variance in the model for duration of illness was accounted for independently by α‐synuclein.DiscussionIn DLB, α‐synuclein is an important predictor of disease duration, both independently and synergistically with tau and Aβ.