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Occlusion/occlusion-like syndromes

The collagenase model replicates the matrix disorganization and degenerative pathology of clinical tendinopathy more closely than transection models, strengthening the relevance of the findings to the human chronic tendinopathy condition

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While familial AD, a less prevalent form, is driven by genetic mutations affecting $A\beta$ metabolism, most sporadic AD cases are attributed to inefficient A clearance (76) (Figure 2)

Surprisingly, increased p21 level was observed in the FOXO4-DRI pre-treatment groups, suggesting senolytics might be a potential stressor to cells

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