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Zhornitsky et al., 2013)

These findings offer a mechanism by which OL deficiencies trigger amyloid pathology rather than the reverse

Results: We included 197 participants with mean age 68.8 years, 66% male and 68% functionally independent at 1 year

Researchers have explored BPC-157 in experimental settings to better understand: Cellular signalling pathways Tissue repair mechanisms Inflammatory response modulation Gastrointestinal tissue integrity in models It is important to emphasise that much of the available data originates from non-human studies , and outcomes observed in laboratory or animal models cannot be assumed to translate to humans

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