Pattern of cortical thinning associated with the BDNF Val66Met polymorphism in Parkinson’s disease

The objective was to investigate if high cadence cycling altered non-motor cognition and depression symptoms in individuals with Parkinson’s disease (PD) and whether exercise responses were influenced by brain-derived neurotrophic factor (BDNF) Val66Met polymorphism. Individuals with idiopathic PD who were ≥50 years old and free of surgical procedures for PD were recruited. Participants were assigned to either a cycling (n = 20) or control (n = 15) group. The cycling group completed three sessions of high cadence cycling on a custom motorized stationary ergometer. The primary outcome was cognition (attention, executive function, and emotion recognition were assessed via WebNeuro® and global cognition via Montreal Cognitive Assessment). Depression symptoms were assessed via Beck Depression Inventory-II. There was a main effect of time for emotional recognition (p = 0.048), but there were no other changes in cognition or depression symptoms. Regardless of intervention or Val66Met polymorphism, high cadence cycling does not alter cognition or depression symptoms after three sessions in one week.

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Association of brain-derived neurotrophic factor (BDNF) Val66Met polymorphism with Parkinson’s disease in a Greek population

Journal of Clinical Neuroscience ◽

10.1016/j.jocn.2011.03.015 ◽

2011 ◽

Vol 18 (12) ◽

pp. 1744-1745 ◽

Cited By ~ 14

Author(s):

Charalambos Karakasis ◽

Kallirhoe Kalinderi ◽

Zoe Katsarou ◽

Liana Fidani ◽

Sevasti Bostantjopoulou

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Neurotrophic Factor ◽

Brain Derived Neurotrophic Factor ◽

Greek Population ◽

Val66met Polymorphism ◽

Bdnf Val66met Polymorphism

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Cortical Thinning Associated with Age and CSF Biomarkers in Early Parkinson’s Disease Is Modified by the SNCA rs356181 Polymorphism

Neurodegenerative Diseases ◽

10.1159/000493103 ◽

2018 ◽

Vol 18 (5-6) ◽

pp. 233-238

Author(s):

Frederic Sampedro ◽

Juan Marín-Lahoz ◽

Saul Martínez-Horta ◽

Javier Pagonabarraga ◽

Jaime Kulisevsky

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Cognitive Decline ◽

De Novo ◽

Brain Regions ◽

Cortical Atrophy ◽

Csf Biomarkers ◽

Gene Encoding ◽

Cortical Thinning ◽

Age Related

The role of cerebrospinal fluid (CSF) biomarkers such as CSF α-synuclein and CSF tau in predicting cognitive decline in Parkinson’s disease (PD) continues to be inconsistent. Here, using a cohort of de novo PD patients with preserved cognition from the Parkinson’s Progression Markers Initiative (PPMI), we show that the SNCA rs356181 single nucleotide polymorphism (SNP) modulates the effect of these CSF biomarkers on cortical thinning. Depending on this SNP’s genotype, cortical atrophy was associated with either higher or lower CSF biomarker levels. Additionally, this SNP modified age-related atrophy. Importantly, the integrity of the brain regions where this phenomenon was observed correlated with cognitive measures. These results suggest that this genetic variation of the gene encoding the α-synuclein protein, known to be involved in the development of PD, also interferes in its subsequent neurodegeneration. Overall, our findings could shed light on the so far incongruent association of common CSF biomarkers with cognitive decline in PD.

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