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Revealing subcellular retinal alterations in 5xFAD B6SJLF1/J mice
A Giani1, C A Musi1, E C Priori1
1Department of Pharmacological and Biomolecular Sciences, University of Milan, Milan, Italy; Department of Neuroscience, IRCCS-Mario Negri Institute for Pharmacological Research, Milan, Italy.
Experimental Neurology
|April 3, 2026
Summary
Alzheimer
Area of Science:
- Neuroscience
- Ophthalmology
- Pathology
Background:
- Alzheimer's disease (AD) pathology involves neurodegeneration.
- The 5xFAD mouse model exhibits AD hallmarks.
- Investigating shared pathogenic mechanisms between brain and retina is crucial for AD monitoring.
Purpose of the Study:
- To determine if JNK activation is a common mechanism in both retinal and cerebral neurodegeneration in 5xFAD mice.
- To assess the retina's potential as an accessible window for monitoring AD progression.
Main Methods:
- Western blotting and immunofluorescence staining on retinal tissues from 5xFAD and wild-type mice at various ages.
- Analysis of JNK signaling markers, synaptic integrity markers, gliosis, and amyloid pathology.
- Comparison of retinal layer thickness between 5xFAD and wild-type mice.
Main Results:
- No significant JNK signaling activation was detected in total retinal homogenates.
- Synaptic dysfunction was indicated by increased PSD95 phosphorylation in 5xFAD retinas.
- Elevated JNK3 immunoreactivity and gliosis were observed in 5xFAD retinas.
- Retinal layer thickness showed distinct age-related changes in 5xFAD mice compared to controls.
Conclusions:
- Fundamental differences exist in AD pathology between the retina and brain in 5xFAD mice.
- Limited JNK activation in retinal tissue suggests challenges in developing retinal AD biomarkers.
- Further technical refinement and careful interpretation are needed for using the retina as a CNS disease monitor.
