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Apathy linked to higher amyloid burden and cognitive deterioration in Parkinson's disease.

Authors: Gasca-Salas C, Fernández-Fernández R, Rodríguez-Rojas R, Fernández-Rodríguez B, García-Cañamaque L, Lahera G, Trompeta C
Journal: Journal of Parkinson's disease
mental health psychology open access

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by motor symptoms such as bradykinesia, rigidity, and (resting-)tremor. In addition, mild cognitive impairment in PD (PD-MCI) is a common and early manifestation, with up to 50% of PD patients experiencing some degree of cognitive decline. This condition often precedes dementia, which significantly impacts quality of life and the healthcare burden. Despite extensive research, the factors influencing the progression from PD-MCI to PD dementia (PDD) remain unclear. Genetic factors have been implicated in the etiology and progression of many neuro­degenerative diseases, including PD. Genome-wide association studies (GWAS) have identified numerous single nucleotide polymorphisms (SNPs) associated with PD susceptibility, providing insights into the genetic underpinnings of the disease. SNPs are the most common type of genetic variation and may serve as biomarkers for disease risk, prognosis, and therapeutic response. While numerous studies have successfully identified genetic variants associated with PD onset and motor symptoms, the genetic basis of cognitive impairment within PD remains poorly understood. Previous research has highlighted several genetic loci linked to cognitive decline in the general population and Alzheimer's disease (AD), suggesting a possible overlap with PD. However, the distinct pathophysiological mechanisms underlying PD necessitate a focused investigation.