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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Adult, Aged, Amyloid beta-Peptides, Amyloidosis, Apolipoproteins E, Brain, Brain Diseases, Brain Mapping, Cohort Studies, Disability Evaluation, Disease Progression, Female, Humans, Image Interpretation, Computer-Assisted, Imaging, Three-Dimensional, Magnetic Resonance Imaging, Male, Middle Aged, Neurodegenerative Diseases, Parkinson Disease, Peptide Fragments, Phenotype, Reference Values, Sensitivity and Specificity, Statistics as Topic.
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Does presence of cerebral amyloid modulate phenotype and pattern of neurodegeneration in early Parkinson 's disease? Context: To evaluate the frequency of cerebral amyloid in early Parkinson's disease (ePD) and provide a multimodal assessment of the influence of cerebral amyloid on disease phenotype. We performed a multicentre cohort study of the Parkinson's Progression Markers Initiative (PPMI), including 369 drug-naïve patients with ePD and 174 healthy controls (HC). Cerebrospinal fluid (CSF) amyloid-β levels were transformed using the linear regression procedure. A cut-off of >198 pg/mL was used to define amyloid-negative (PD-) and amyloid-positive (PD+) subgroups. Grey matter (GM) density and hippocampal volume from the MRI was measured using Advanced Normalisation Tools (ANTs). We compared demographic, genetic, CSF, behavioural, functional and imaging modalities across ePD- and ePD+ groups. We observed that 16.5% of ePD have CSF evidence of amyloidosis. PD+ was significantly older than PD-, had a higher frequency of APOE e4 alleles and all CSF measures (total-tau, phosphorylated-tau and α-synuclein) were reduced. PD+ had reduced cognitive performance relative to PD- on Symbol-Digit Matching, Verbal Category Fluency and Delayed Recall tests. Imaging analysis in a subset of individuals (PD+ =43; PD- =241) revealed overlapping GM atrophy relative to HC in medial temporal, frontal and brainstem structures. Direct comparisons revealed PD+ GM reductions predominantly located in the frontal cortex while PD- had GM reductions in subcortical structures. These observations remain when controlling for age and APOE e4 allele status.
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Cerebral amyloid in ePD yields a unique phenotype across all measured modalities that is consistent with a synergistic interaction between α-synuclein and amyloid pathology. Amyloid status should be considered when screening these individuals for trials involving disease-modifying agents. Final Decision: yes