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Forsgren, Lars
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Publications (10 of 108) Show all publications
Paslawski, W., Zareba-Paslawska, J., Zhang, X., Holzl, K., Wadensten, H., Shariatgorji, M., . . . Svenningsson, P. (2019). alpha-synuclein-lipoprotein interactions and elevated ApoE level in cerebrospinal fluid from Parkinson's disease patients. Proceedings of the National Academy of Sciences of the United States of America, 116(30), 15226-15235
Open this publication in new window or tab >>alpha-synuclein-lipoprotein interactions and elevated ApoE level in cerebrospinal fluid from Parkinson's disease patients
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2019 (English)In: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 116, no 30, p. 15226-15235Article in journal (Refereed) Published
Abstract [en]

The progressive accumulation, aggregation, and spread of alpha-synuclein (alpha SN) are common hallmarks of Parkinson's disease (PD) pathology. Moreover, numerous proteins interact with alpha SN species, influencing its toxicity in the brain. In the present study, we extended analyses of alpha SN-interacting proteins to cerebrospinal fluid (CSF). Using coimmunoprecipitation, followed by mass spectrometry, we found that alpha SN colocalize with apolipoproteins on lipoprotein vesicles. We confirmed these interactions using several methods, including the enrichment of lipoproteins with a recombinant alpha SN, and the subsequent uptake of prepared vesicles by human dopaminergic neuronal-like cells. Further, we report an increased level of ApoE in CSF from early PD patients compared with matched controls in 3 independent cohorts. Moreover, in contrast to controls, we observed the presence of ApoE-positive neuromelanin-containing dopaminergic neurons in substantia nigra of PD patients. In conclusion, the cooccurrence of alpha SN on lipoprotein vesicles, and their uptake by dopaminergic neurons along with an increase of ApoE in early PD, proposes a mechanism(s) for alpha SN spreading in the extracellular milieu of PD.

Place, publisher, year, edition, pages
NATL ACAD SCIENCES, 2019
Keywords
apolipoproteins, alpha-synuclein, Parkinson's disease, cerebrospinal fluid
National Category
Clinical Laboratory Medicine
Identifiers
urn:nbn:se:umu:diva-161992 (URN)10.1073/pnas.1821409116 (DOI)000476715500067 ()31270237 (PubMedID)
Available from: 2019-08-14 Created: 2019-08-14 Last updated: 2019-08-14Bibliographically approved
Patil, K. S., Basak, I., Dalen, I., Hoedt, E., Lange, J., Lunde, K. A., . . . Møller, S. G. (2019). Combinatory microRNA serum signatures as classifiers of Parkinson's disease. Parkinsonism & Related Disorders, 64, 202-210
Open this publication in new window or tab >>Combinatory microRNA serum signatures as classifiers of Parkinson's disease
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2019 (English)In: Parkinsonism & Related Disorders, ISSN 1353-8020, E-ISSN 1873-5126, Vol. 64, p. 202-210Article in journal (Refereed) Published
Abstract [en]

Introduction: As current clinical diagnostic protocols for Parkinson's disease (PD) may be prone to inaccuracies there is a need to identify and validate molecular biomarkers, such as circulating microRNAs, which will complement current practices and increase diagnostic accuracy. This study identifies, verifies and validates combinatory serum microRNA signatures as diagnostic classifiers of PD across different patient cohorts. Methods: 370 PD (drug naive) and control serum samples from the Norwegian ParkWest study were used for identification and verification of differential microRNA levels in PD which were validated in a blind study using 64 NY Parkinsonism in UMea (NYPUM) study serum samples and tested for specificity in 48 Dementia Study of Western Norway (DemWest) study Alzheimer's disease (AD) serum samples using miRNA-microarrays, and quantitative (q) RT-PCR. Proteomic approaches identified potential molecular targets for these microRNAs. Results: Using Affymetrix GeneChip (R) miRNA 4.0 arrays and qRT-PCR we comprehensively analyzed serum microRNA levels and found that the microRNA (PARKmiR)-combinations, hsa-miR-335-5p/hsa-miR-3613-3p (95% CI, 0.87-0.94), hsa-miR-335-5p/hsa-miR-6865-3p (95% CI, 0.87-0.93), and miR-335-5p/miR-3613-3p/miR-6865-3p (95% CI, 0.87-0.94) show a high degree of discriminatory accuracy (AUC 0.9-1.0). The PARKmiR signatures were validated in an independent PD cohort (AUC <= 0.71) and analysis in AD serum samples showed PARKmiR signature specificity to PD. Proteomic analyses showed that the PAFtKmiRs regulate key PD-associated proteins, including alpha-synuclein and Leucine Rich Repeat Kinase 2. Conclusions: Our study has identified and validated unique miRNA serum signatures that represent PD classifiers, which may complement and increase the accuracy of current diagnostic protocols.

Place, publisher, year, edition, pages
Elsevier, 2019
Keywords
microRNA, Biomarker, Parkinson's disease, Alzheimer's disease
National Category
Neurology
Identifiers
urn:nbn:se:umu:diva-164077 (URN)10.1016/j.parkreldis.2019.04.010 (DOI)000487567800030 ()31003905 (PubMedID)
Available from: 2019-10-14 Created: 2019-10-14 Last updated: 2019-10-14Bibliographically approved
Riso, L., Kaaks, R., Kuehn, T., Sookthai, D., Forsgren, L., Trupp, M., . . . Katzke, V. A. (2019). General and abdominal adiposity and the risk of Parkinson's disease: A prospective cohort study. Parkinsonism & Related Disorders, 62, 98-104
Open this publication in new window or tab >>General and abdominal adiposity and the risk of Parkinson's disease: A prospective cohort study
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2019 (English)In: Parkinsonism & Related Disorders, ISSN 1353-8020, E-ISSN 1873-5126, Vol. 62, p. 98-104Article in journal (Refereed) Published
Abstract [en]

Introduction: Due to demographic change, an increase in the frequency of Parkinson's disease (PD) patients is expected in the future and, thus, the identification of modifiable risk factors is urgently needed. We aimed to examine the associations of body mass index (BMI) and waist circumference (WC) with incident PD. Methods: In 13 of the 23 centers of the European Prospective Investigation into Cancer and Nutrition (EPIC) study, a total of 734 incident cases of PD were identified between 1992 and 2012 with a mean follow-up of 12 years. Cox proportional hazards regression was used to calculate hazard ratios (HR) with 95% confidence intervals (CI). We modelled anthropometric variables as continuous and categorical exposures and performed subgroup analyses by potential effect modifiers including sex and smoking. Results: We found no association between BMI, WC and incident PD, neither among men nor among women. Among never and former smokers, BMI and waist circumference were also not associated with PD risk. For male smokers, however, we observed a statistically significant inverse association between BMI and PD risk (HR 0.51, 95%CI: 0.30, 0.84) and the opposite for women, i.e. a significant direct association of BMI (HR 1.79, 95%CI: 1.04, 3.08) and waist circumference (HR 1.64, 95%CI: 1.03, 2.61) with risk of PD. Conclusion: Our data revealed no association between excess weight and PD risk but a possible interaction between anthropometry, sex and smoking.

Place, publisher, year, edition, pages
ELSEVIER SCI LTD, 2019
Keywords
Parkinson, Overweight, BMI, Smoking, Cohort, EPIC
National Category
General Practice
Identifiers
urn:nbn:se:umu:diva-162023 (URN)10.1016/j.parkreldis.2019.01.019 (DOI)000476961700016 ()30772279 (PubMedID)
Available from: 2019-08-12 Created: 2019-08-12 Last updated: 2019-08-12Bibliographically approved
Lunde, K. A., Chung, J., Dalen, I., Pedersen, K. F., Linder, J., Domellöf, M. E., . . . Maple-Grødem, J. (2018). Association of glucocerebrosidase polymorphisms and mutations with dementia in incident Parkinson's disease. Alzheimer's & Dementia, 14(10), 1293-1301
Open this publication in new window or tab >>Association of glucocerebrosidase polymorphisms and mutations with dementia in incident Parkinson's disease
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2018 (English)In: Alzheimer's & Dementia, ISSN 1552-5260, E-ISSN 1552-5279, ISSN 1552-5260, Vol. 14, no 10, p. 1293-1301Article in journal (Refereed) Published
Abstract [en]

Introduction

Both polymorphisms and mutations in glucocerebrosidase (GBA) may influence the development of dementia in patients with Parkinson's disease.

Methods

Four hundred forty-two patients and 419 controls were followed for 7 years. Dementia was diagnosed using established criteria. Participants were analyzed for GBA genetic variants, including E326K, T369M, and L444P. Associations between GBA carrier status and dementia were assessed with Cox survival analysis.

Results

A total of 12.0% of patients with Parkinson's disease carried a GBA variant, and nearly half (22/53) of them progressed to dementia during follow-up. Carriers of deleterious GBA mutations (adjusted hazard ratio 3.81, 95% confidence interval 1.35 to 10.72; P = .011) or polymorphisms (adjusted hazard ratio 1.79; 95% confidence interval 1.07 to 3.00; P = .028) progressed to dementia more rapidly than noncarriers.

Discussion

GBA variants are of great clinical relevance for the development of dementia in Parkinson's disease, especially due to the relatively higher frequency of these alleles compared with other risk alleles.

Place, publisher, year, edition, pages
Elsevier, 2018
Keywords
Parkinson's Disease
National Category
Neurology
Research subject
Genetics; Neurology
Identifiers
urn:nbn:se:umu:diva-148814 (URN)10.1016/j.jalz.2018.04.006 (DOI)000446086000006 ()
Projects
NYPUM projectParkWest studyPINE study
Funder
The Kempe FoundationsVästerbotten County CouncilThe Kempe FoundationsVästerbotten County Council
Available from: 2018-06-12 Created: 2018-06-12 Last updated: 2019-05-07Bibliographically approved
Johansson, C., Lindström, B., Forsgren, L. & Johansson, G. M. (2018). Balance and mobility in patients with newly diagnosed Parkinson's disease - a five-year follow-up of a cohort in northern Sweden. Disability and Rehabilitation, 1-10
Open this publication in new window or tab >>Balance and mobility in patients with newly diagnosed Parkinson's disease - a five-year follow-up of a cohort in northern Sweden
2018 (English)In: Disability and Rehabilitation, ISSN 0963-8288, E-ISSN 1464-5165, p. 1-10Article in journal (Refereed) Epub ahead of print
Abstract [en]

BACKGROUND: The presence of early balance impairment in patients with Parkinson's disease has not been fully investigated.

PURPOSE: The purpose of this study was to examine balance and mobility, self-perceived unsteadiness, self-reported falls, and effects of medication on balance among patients at their first visit to a neurological clinic and during the ensuing five years.

MATERIALS AND METHODS: The participants were collected from a prospective longitudinal study. One hundred and forty-five patients with idiopathic Parkinson's disease and 31 healthy controls were included. The outcome measures were the Berg Balance Scale, the Timed Up and Go, the Postural Stability test and a questionnaire.

RESULTS: At their first visit to the neurological clinic, the patients performed less well on the Berg Balance Scale (p < 0.001, r = 0.36), the Timed Up and Go (p < 0.001, r = 0.32), and the Postural Stability test (p < 0.001, r = 0.35) compared with the controls. In addition, a higher percentage of the patients reported self-perceived unsteadiness (p < 0.001, phi = 0.47). During the ensuing five years, balance and mobility worsened both with and without medication (p < 0.01, r = 0.24-0.37), although with small median differences.

CONCLUSIONS: Further studies are needed to confirm that minor balance impairments exist even at the time of diagnosis and worsen during the ensuing five years. IMPLICATIONS FOR REHABILITATION Impairments in balance and mobility may occur early in Parkinson's disease, especially in the elderly patients, and seem to worsen during the first five years. There is a need to use sensitive outcome measures and to ask the patients about unsteadiness and falls to detect balance impairment in this cohort. Parkinsonian medication has a limited effect on balance and may preferably be complemented with balance exercises to target balance impairment early in Parkinson's disease.

Place, publisher, year, edition, pages
Taylor & Francis Group, 2018
Keywords
Parkinson’s disease, balance, exercise, falls, parkinsonism, postural instability
National Category
Neurology
Research subject
Neurology
Identifiers
urn:nbn:se:umu:diva-155392 (URN)10.1080/09638288.2018.1509240 (DOI)30451551 (PubMedID)
Available from: 2019-01-15 Created: 2019-01-15 Last updated: 2019-04-05
Blomstedt, P., Stenmark Persson, R., Hariz, G.-M., Linder, J., Fredricks, A., Häggström, B., . . . Hariz, M. (2018). Deep brain stimulation in the caudal zona incerta versus best medical treatment in patients with Parkinson's disease: a randomised blinded evaluation. Journal of Neurology, Neurosurgery and Psychiatry, 89(7), 710-716
Open this publication in new window or tab >>Deep brain stimulation in the caudal zona incerta versus best medical treatment in patients with Parkinson's disease: a randomised blinded evaluation
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2018 (English)In: Journal of Neurology, Neurosurgery and Psychiatry, ISSN 0022-3050, E-ISSN 1468-330X, Vol. 89, no 7, p. 710-716Article in journal (Refereed) Published
Abstract [en]

Background: Several open-label studies have shown good effect of deep brain stimulation (DBS) in the caudal zona incerta (cZi) on tremor, including parkinsonian tremor, and in some cases also a benefit on akinesia and axial symptoms. The aim of this study was to evaluate objectively the effect of cZi DBS in patients with Parkinson's disease (PD).

Method: 25 patients with PD were randomised to either cZi DBS or best medical treatment. The primary outcomes were differences between the groups in the motor scores of the Unified Parkinson's Disease Rating Scale (UPDRS-III) rated single-blindly at 6 months and differences in the Parkinson's Disease Questionnaire 39 items (PDQ-39). 19 patients, 10 in the medical arm and 9 in the DBS arm, fulfilled the study.

Results: The DBS group had 41% better UPDRS-III scores off-medication on-stimulation compared with baseline, whereas the scores of the non-surgical patients off-medication were unchanged. In the on-medication condition, there were no differences between the groups, neither at baseline nor at 6 months. Subitems of the UPDRS-III showed a robust effect of cZi DBS on tremor. The PDQ-39 domains 'stigma' and 'ADL' improved only in the DBS group. The PDQ-39 summary index improved in both groups.

Conclusion: This is the first randomised blinded evaluation of cZi DBS showing its efficacy on PD symptoms. The most striking effect was on tremor; however, the doses of dopaminergic medications could not be decreased. cZi DBS in PD may be an addition to existing established targets, enabling tailoring the surgery to the needs of the individual patient.

Place, publisher, year, edition, pages
BMJ Publishing Group Ltd, 2018
National Category
Neurology
Identifiers
urn:nbn:se:umu:diva-150375 (URN)10.1136/jnnp-2017-317219 (DOI)000438044100010 ()29386253 (PubMedID)
Available from: 2018-08-08 Created: 2018-08-08 Last updated: 2019-05-07Bibliographically approved
Bäckström, D., Granåsen, G., Eriksson Domellöf, M., Linder, J., Jakobson Mo, S., Riklund, K., . . . Forsgren, L. (2018). Early predictors of mortality in parkinsonism and Parkinson disease: A population-based study. Neurology, 91(22), E2045-E2056
Open this publication in new window or tab >>Early predictors of mortality in parkinsonism and Parkinson disease: A population-based study
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2018 (English)In: Neurology, ISSN 0028-3878, E-ISSN 1526-632X, Vol. 91, no 22, p. E2045-E2056Article in journal (Refereed) Published
Abstract [en]

Objective To examine mortality and associated risk factors, including possible effects of mild cognitive impairment, imaging, and CSF abnormalities, in a community-based population with incident parkinsonism and Parkinson disease. Methods One hundred eighty-two patients with new-onset, idiopathic parkinsonism were diagnosed from January 2004 through April 2009, in a catchment area of 142,000 inhabitants in Sweden. Patients were comprehensively investigated according to a multimodal research protocol and followed prospectively for up to 13.5 years. A total of 109 patients died. Mortality rates in the general Swedish population were used to calculate standardized mortality ratio and expected survival, and Cox proportional hazard models were used to investigate independent predictors of mortality. Results The standardized mortality ratio for all patients was 1.84 (95% confidence interval 1.50-2.22, p < 0.001). Patients with atypical parkinsonism (multiple system atrophy or progressive supranuclear palsy) had the highest mortality. In early Parkinson disease, a mild cognitive impairment diagnosis, freezing of gait, hyposmia, reduced dopamine transporter activity in the caudate, and elevated leukocytes in the CSF were significantly associated with shorter survival. Conclusion Although patients presenting with idiopathic parkinsonism have reduced survival, the survival is highly dependent on the type and characteristics of the parkinsonian disorder. Patients with Parkinson disease presenting with normal cognitive function seem to have a largely normal life expectancy. The finding of a subtle CSF leukocytosis in patients with Parkinson disease with short survival may have clinical implications.

Place, publisher, year, edition, pages
Wolters Kluwer, 2018
National Category
Neurology
Identifiers
urn:nbn:se:umu:diva-154849 (URN)10.1212/WNL.0000000000006576 (DOI)000452519500002 ()30381367 (PubMedID)
Available from: 2019-01-04 Created: 2019-01-04 Last updated: 2019-05-07Bibliographically approved
Håglin, L., Bäckman, L., Linder, J., Forsgren, L. & Domellöf, M. (2018). Early Recognition of Cognitive Ability and Nutritional Markers for Dementia in Parkinson’s Disease. Journal of Aging Research & Clinical Practice, 7, 156-162
Open this publication in new window or tab >>Early Recognition of Cognitive Ability and Nutritional Markers for Dementia in Parkinson’s Disease
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2018 (English)In: Journal of Aging Research & Clinical Practice, ISSN 2258-8094, Vol. 7, p. 156-162Article in journal (Refereed) Published
Abstract [en]

Background: Cognitive decline and dementia are common non-motor problems in Parkinson’s disease (PD). The underlying aetiology is multifaceted and both chronic and reversible causes for cognitive decline are likely to be present. Malnutrition is frequent in the Parkinson population, both early and late in the disease, and nutritional deficiencies could play a role in some cognitive deficits. Objectives: The objective is to study the association between nutritional status with focus on iron intake and homeostasis, mild cognitive impairment (MCI), and PD dementia (PDD). Setting and Participants: This study included 73 out of 145 patients with PD participating in a population-based study in northern Sweden. Measurements: Registration of nutritional status by laboratory analyses of blood plasma and neuropsychological assessments at time of diagnosis were performed. MCI and PDD were assessed yearly up to ten years after diagnosis. Mini Nutritional Assessments (Full-MNA score) and plasma variables detecting iron homeostasis were compared between patients with MCI and patients with normal cognition (NC). Motor severity was measured using the Unified Parkinson´s disease rating scale III, (UPDRS III) and Hoehn and Yahr (H&Y) staging scale. Cox proportional Hazard model were performed to see if any variables that differed between MCI and NC could predict PDD at follow-up. Results: Patients with MCI at time of diagnosis had lower levels of plasma iron (P-Fe) and albumin (P-Albumin) as well as a lower score on Full-MNA score. Dietary intake of iron was higher in patients with MCI than in patients with NC (p = 0.012). In logistic regression models adjusted for age, sex, and UPDRS III, lower levels of P-Fe (p = 0.025) and P-Albumin (p = 0.011) and higher dietary iron intake (p = 0.019) were associated with MCI at baseline. A Cox regression model with dementia as endpoint revealed that lower levels of P-Fe increase the risk of dementia at follow-up with adjustments for age, sex, UPDRS III, and MCI at baseline (HR 95% CI = 0.87 (0.78-0.98), p = 0.021). Conclusions: Low P-Fe was associated with cognitive disturbance at baseline and predicted dementia up to ten years after diagnosis in patients with PD. Low P-Albumin and malnutrition assessed with Full-MNA score were associated with MCI at baseline but did not predict dementia at follow-up.

Place, publisher, year, edition, pages
Auzeville-Tolosane: SERDI, 2018
Keywords
Cognition, dementia, iron deficiency, Parkinson’s disease
National Category
Neurology
Identifiers
urn:nbn:se:umu:diva-159274 (URN)10.14283/jarcp.2018.26 (DOI)
Available from: 2019-05-23 Created: 2019-05-23 Last updated: 2019-05-24Bibliographically approved
Gallo, V., Vineis, P., Cancellieri, M., Chiodini, P., Barker, R. A., Brayne, C., . . . Riboli, E. (2018). Exploring causality of the association between smoking and Parkinson's disease. International Journal of Epidemiology
Open this publication in new window or tab >>Exploring causality of the association between smoking and Parkinson's disease
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2018 (English)In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685Article in journal (Refereed) Epub ahead of print
Abstract [en]

Background: The aim of this paper is to investigate the causality of the inverse association between cigarette smoking and Parkinson's disease (PD). The main suggested alternatives include a delaying effect of smoking, reverse causality or an unmeasured confounding related to a low-risk-taking personality trait.

Methods: A total of 715 incident PD cases were ascertained in a cohort of 220 494 individuals from NeuroEPIC4PD, a prospective European population-based cohort study including 13 centres in eight countries. Smoking habits were recorded at recruitment. We analysed smoking status, duration, and intensity and exposure to passive smoking in relation to PD onset.

Results: Former smokers had a 20% decreased risk and current smokers a halved risk of developing PD compared with never smokers. Strong dose-response relationships with smoking intensity and duration were found. Hazard ratios (HRs) for smoking <20 years were 0.84 [95% confidence interval (CI) 0.67-1.07], 20-29 years 0.73 (95% CI 0.56-0.96) and >30 years 0.54 (95% CI 0.43-0.36) compared with never smokers. The proportional hazard assumption was verified, showing no change of risk over time, arguing against a delaying effect. Reverse causality was disproved by the consistency of dose-response relationships among former and current smokers. The inverse association between passive smoking and PD, HR 0.70 (95% CI 0.49-0.99) ruled out the effect of unmeasured confounding.

Conclusions: These results are highly suggestive of a true causal link between smoking and PD, although it is not clear which is the chemical compound in cigarette smoking responsible for the biological effect.

Place, publisher, year, edition, pages
Oxford University Press, 2018
National Category
Neurology
Research subject
Neurology
Identifiers
urn:nbn:se:umu:diva-156190 (URN)10.1093/ije/dyy230 (DOI)30462234 (PubMedID)
Available from: 2019-02-07 Created: 2019-02-07 Last updated: 2019-04-05
Machaczka, M., Paucar, M., Kämpe Björkvall, C., Smith, N. J. C., Cox, T. M., Forsgren, L. & Svenningsson, P. (2018). Novel hyperkinetic dystonia-like manifestation and neurological disease course of Swedish Gaucher patients. Blood Cells, Molecules & Diseases, 68(S1), 86-92
Open this publication in new window or tab >>Novel hyperkinetic dystonia-like manifestation and neurological disease course of Swedish Gaucher patients
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2018 (English)In: Blood Cells, Molecules & Diseases, ISSN 1079-9796, E-ISSN 1096-0961, Vol. 68, no S1, p. 86-92Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Neuronopathic Gaucher disease type 3 (GD3) is frequent in northern Sweden, whereas GD1 is found throughout the country. In a nation-wide study, we examined neurological manifestations and clinical course in 12 patients with GD3 and 13 patients with GD1.

METHODS: The patients were evaluated by standardized neurological assessments. Every sixth month, the GD3 patients were rated with the modified Severity Scoring Tool. At baseline and at the 3years follow-up, patients underwent University of Pennsylvania Smell Identification Test, Montreal Cognitive Assessment and Hospital Anxiety and Depression Scale. When clinical signs were present, additional examinations were undertaken.

RESULTS: Marked clinical heterogeneity was evident in both GD3 and GD1 groups. Several GD3 patients had a hitherto unreported rapid and repetitive dystonia-like hyperkinetic movement disorder. Most patients with GD3 have abnormalities of horizontal gaze, ataxia and focal epilepsy, some also had cognitive impairment, anxiety and hyposmia. Six GD3 patients, all homoallelic for L444P GBA1 mutations, have lived beyond 40years of age; and none has developed Parkinsonism. Two of the GD1 patients suffer from Parkinsonism; mild to complete hyposmia was present in six GD3 and five GD1 patients. Neither the group of GD3 nor GD1 patients had detectable progression of their neurological manifestations.

CONCLUSIONS: These middle-aged and older Swedish GD3 or GD1 patients are clinically stable over time. However, we have identified unusual clinical features, discordant phenotypes and a hyperkinetic dystonia-like movement disorder which appears unique to this Swedish disease variant and expands the phenotype for GD.

Place, publisher, year, edition, pages
San Diego: Academic Press, 2018
Keywords
Dystonia, GBA1, Gaucher disease, Glucocerebrosidase, Parkinson's disease
National Category
Neurosciences
Identifiers
urn:nbn:se:umu:diva-134976 (URN)10.1016/j.bcmd.2016.10.011 (DOI)000417147400017 ()27789132 (PubMedID)
Available from: 2017-05-15 Created: 2017-05-15 Last updated: 2018-06-09Bibliographically approved
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