Affiliations: [a]
Department of Clinical Neurosciences, Division of Neurology, Geneva University Hospitals and Faculty of Medicine, University of Geneva, Geneva, Switzerland | [b]
Department of Neurology, Division of Cognitive and Motor Aging, Albert Einstein College of Medicine, Yeshiva University, Bronx, NY, USA | [c]
Department of Genetics, Laboratory Medicine and Pathology, Geneva University Hospitals and Faculty of Medicine, University of Geneva, Geneva, Switzerland | [d]
Willy Taillard Laboratory of Kinesiology, Geneva University Hospitals and University of Geneva, Geneva, Switzerland
Correspondence:
[*]
Correspondence to: Gilles Allali, MD, PhD, Department of Neurology, Geneva University Hospitals, 4 rue Gabrielle-Perret-Gentil, 1211 Geneva, Switzerland. Tel.: +41 22 372 83 18; Fax: +41 22 372 83 33; gilles.allali@hcuge.ch.
Abstract: Background:Central neurological gait abnormalities (CNGA) are frequently associated with parkinsonism in older adults. However, the neuropathological substrates and the clinical impact of parkinsonism have been not described in CNGA. Objective:This cross-sectional study aims to compare the CSF total tau, Aβ1-42, and phosphorylated tau levels in non-Parkinson’s disease (PD) patients with CNGA with and without parkinsonism and to study the clinical impact of parkinsonism on gait and cognition. Methods:CSF biomarkers were measured by ELISA in 49 non-PD patients with CNGA (77.7±6.6 years; 32.7% women). Gait was quantified with an optoelectronic system and cognition with a comprehensive neuropsychological assessment. Parkinsonism was defined by presence of bradykinesia and at least one of the following signs among muscular rigidity, rest tremor, or postural instability. Results:Parkinsonism was identified in 14 CNGA patients (28.6% ). CSF Aβ1-42 level was decreased in CNGA patients with parkinsonism (β: – 189.4; 95% CI [– 352.3; – 26.6]; p = 0.024) even after adjusting for age, gender, comorbidities, and total white matter burden; while CSF total tau and phosphorylated tau levels were similar between CNGA patients with and without parkinsonism. CNGA patients with parkinsonism presented decreased attentional and executive performances but similar gait parameters than those without parkinsonism. Conclusion:Parkinsonism represents a phenotype related with amyloidopathy—decreased CSF Aβ1-42 level—in non-PD patients with CNGA. This phenotype is clinically associated with impaired cognition, but similar quantitative gait parameters in comparison to CNGA patients without parkinsonism.
