A study recently published in npj Parkinson’s Disease assessed if Parkinson’s disease (PD) patients present with an accelerated thinning rate in the parafoveal ganglion cell-inner plexiform layer (pfGCIPL) and peripapillary retinal nerve fiber layer (pRNFL) compared to controls.
Give me some background.
A previous study by the research team demonstrated that measuring macular GCIPL (mGCIPL) and pRNFL thickness with OCT can predict cognitive impairment and dementia in PD.
Understanding the timing between retinal changes and cognitive impairment in PD is critical to investigating the retina as a potential biomarker for monitoring PD and catching disease progression early.
Now talk about the study.
In this longitudinal study, researchers analyzed the data of 156 PD patients and 72 controls who underwent retinal optical coherence tomography (OCT) and visual and cognitive assessments.
In addition to confirming that the rates of pfGCIPL and pRNFL thinning were higher in PD patients, investigators also evaluated the relationship between the thinning rates and clinical progression in PD.
Findings?
The pfGCIPL thinning rate was twice as high in PD than in controls.
Further, in PD patients, the progression pattern of pfGCIPL atrophy depended on baseline thickness—slower thinning rates were reported in PD patients with a pfGCIPL below 89.9μm.
This result was validated with an external dataset from the Moorfield Eye Hospital National Health Service (NHS) Foundation Trust (i.e., the AlzEye study).
Anything else?
PD patients with greater baseline pfGCIPL atrophy had slower rates of thinning over time.
These individuals showed a threefold increase in the rate of cognitive decline compared to faster progressors and were characterized by:
- Older age at baseline
- Longer disease duration
- Greater disease severity
Additionally, pRNFL thinning in the temporal quadrant was accelerated in PD patients and showed a close association with cognitive score changes.
Expert opinion?
A notable finding from the study was the association between initial pfGCIPL atrophy and subsequent slower rate of pfGCIPL thinning with an accompanying faster decline in cognition in PD.
“It is plausible that patients with more pronounced baseline pfGCIPL atrophy have already experienced a substantial depletion of their neuronal pool that may contribute to an accelerated decline in cognitive abilities, outpacing those with high baseline pfGCIPL thickness and better-preserved cognitive functions,” explained the study authors.
Tie it together for me.
The cognitive and functional disability of PD patients with slow rates of pfGCIPL thinning were remarkably worse compared to PD patients with accelerated retinal tissue loss in the macula, although all patients exhibited altered cognitive and visual abilities compared to controls.
Limitations?
Key limitations of the study included:
- A relatively short follow-up time
- Limited number of follow-up visits per participant
- Inconsistent follow-up schedule across subjects
Additionally, the AlzEye dataset did not include pRNFL measurements and clinical data, so these results could not be validated.
Take home.
These findings suggest that retinal neurodegeneration (i.e., pfGCIPL thinning) could act as a biomarker to measure cognitive decline in PD, as a slower pattern of pfGCIPL tissue loss was linked to more rapid cognitive decline.
However: Further research into changes in temporal pRNFL is warranted to elucidate its potential role as a biomarker to track cognitive deterioration in PD.
Next steps?
The retinal changes reported in the study were below the resolution limit of OCTs, so advancements in OCT technology may be necessary before these findings can be implemented into clinical practice.