Secondary Logo

Journal Logo

Institutional members access full text with Ovid®

Distinguishing Dementia With Lewy Bodies From Alzheimer Disease

What is the Influence of the GBA Genotype in Ashkenazi Jews?

Bregman, Noa MD*,†; Kavé, Gitit PhD*,‡; Mirelman, Anat PhD*,†,§,∥; Thaler, Avner MD, PhD†,∥; Gana Weisz, Mali PhD; Bar-Shira, Anat PhD; Orr-Urtreger, Avi MD, PhD†,§,¶; Giladi, Nir MD†,§,∥; Shiner, Tamara MBChB, PhD*,†,§,∥

Alzheimer Disease & Associated Disorders: July–September 2019 - Volume 33 - Issue 3 - p 279–281
doi: 10.1097/WAD.0000000000000283
Brief Reports

Cognitive deficits beyond memory impairment, such as those affecting language production or executive functioning, can be useful in clinically distinguishing between dementia syndromes. We tested the hypothesis that Ashkenazi Jewish (AJ) patients who have dementia with Lewy bodies (DLB) and carry glucocerebrosidase (GBA) mutations will have verbal fluency deficits different from those found in Alzheimer disease (AD), whereas AJ patients with DLB who have no GBA mutations will have similar deficits in verbal fluency to those found in AD. We compared performance in phonemic and semantic verbal fluency tasks in 44 AJ patients with DLB and 20 patients with AD, matched for age, education, and age of immigration. All groups were found to have a deficit in semantic verbal fluency. On conducting the phonemic task, patients with DLB who carried GBA mutations scored more poorly than patients with AD, whereas DLB-noncarriers performed similarly to patients with AD. We suggest that verbal fluency tasks could serve as a possible clinical marker to subtype patients with DLB, with phonemic fluency being a marker for GBA-associated DLB.

*Center for Memory and Attention Disorders

Movement Disorders Unit, Neurological Institute

Genetic Institute, Tel Aviv Sourasky Medical Center

Sackler School of Medicine

§Sagol School of Neuroscience, Tel Aviv University, Tel Aviv

Department of Education and Psychology, The Open University, Raanana, Israel

N.G. reports serving as a member of the editorial board for the Journal of Parkinson’s Disease; serving as a consultant to Teva-Lundbeck, IntecPharma, NeuroDerm, Armon Neuromedical Ltd, Dexel, Monfort, and Lysosomal Therapeutic Inc.; receiving payment for lectures at Teva-Lundbeck, Novartis, UCB, AbbVie, Shaier, and Genzyme; and receiving research support from the Michael J. Fox Foundation, the National Parkinson Foundation, the European Union Seventh Framework Program, the Israel Science Foundation, Teva NNE program, LTI, AbbVie, and CHDI. The remaining authors declare no conflicts of interest.

Reprints: Tamara Shiner, MBChB, PhD, Tel Aviv Sourasky Medical Center, 6 Weizman street, Tel Aviv 6423906, Israel (e-mail:

Received May 28, 2018

Accepted September 25, 2018

Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved