Imagine if the eye had a sneak peek into the brain, like a window revealing its secrets. Well, it turns out that Reelin protein, known for its involvement in brain development and memory, may also play a role in ocular degeneration. Scientists conducted experiments on mice lacking Reelin protein and discovered some exciting results. At a certain stage of development, these mice showed an increase in markers associated with Alzheimer’s disease, such as Amyloid Precursor Protein (APP), its amyloidogenic peptide (Aβ1-42), and a truncated tau fragment called NH2htau. Additionally, they found increased levels of inflammatory mediators and oxidative stress biomarkers. These findings suggest that the absence of functional Reelin signaling leads to the expression of key pathological features commonly seen in Alzheimer’s disease. This research not only sheds light on the connection between brain and eye degeneration but also suggests that the Reeler mouse could be a valuable model for studying other neurodegenerative diseases like Age-related Macular Degeneration. Dive deeper into this fascinating study by exploring the underlying research!

The neurosensory retina is an outgrowth of the Central Nervous System (CNS), and the eye is considered “a window to the brain.” Reelin glycoprotein is directly involved in neurodevelopment, in synaptic plasticity, learning and memory. Consequently, abnormal Reelin signaling has been associated with brain neurodegeneration but its contributing role in ocular degeneration is still poorly explored. To this aim, experimental procedures were assayed on vitreous or retinas obtained from Reeler mice (knockout for Reelin protein) at different postnatal days (p) p14, p21 and p28. At p28, a significant increase in the expression of Amyloid Precursor Protein (APP) and its amyloidogenic peptide (Aβ1-42 along with truncated tau fragment (i.e., NH2htau)- three pathological hallmarks of Alzheimer’s disease (AD)-were found in Reeler mice when compared to their age-matched wild-type controls. Likewise, several inflammatory mediators, such as Interleukins, or crucial biomarkers of oxidative stress were also found to be upregulated in Reeler mice by using different techniques such as ELLA assay, microchip array or real-time PCR. Taken together, these findings suggest that a dysfunctional Reelin signaling enables the expression of key pathological features which are classically associated with AD neurodegenerative processes. Thus, this work suggests that Reeler mouse might be a suitable animal model to study not only the pathophysiology of developmental processes but also several neurodegenerative diseases, such as AD and Age-related Macular Degeneration (AMD), characterized by accumulation of APP and/or Aβ1-42, NH2htau and inflammatory markers.

Read Full Article (External Site)