Repeat Mild Traumatic Brain Injury in Adolescent Rats Increases Subsequent β-Amyloid Pathogenesis

Area of Science:

• Neuroscience
• Pathology
• Neurodegenerative Diseases

Background:

• Single moderate-to-severe traumatic brain injuries (TBIs) are linked to increased neurodegenerative disease risk via beta-amyloid (Aβ) deposition.
• The impact of repetitive mild TBIs (rTBIs), common in young individuals, on chronic Aβ pathogenesis is not well understood.

Purpose of the Study:

• To investigate the long-term effects of adolescent rTBI on Aβ pathology.
• To determine if the interval between rTBIs influences Aβ deposition.

Main Methods:

• APP/PS1 transgenic rats received sham or four rTBIs at post-natal day 35.
• Injuries were separated by 24-hour or 72-hour intervals.
• Aβ plaque deposition was assessed via immunohistochemistry at 12 months of age.

Main Results:

• rTBI at 24-hour intervals significantly increased hippocampal Aβ plaque number and size compared to 72-hour intervals or sham injuries.
• Aβ deposition increased both ipsilaterally and contralaterally to the injury site.
• Similar, though less pronounced, effects were seen in extrahippocampal regions, affecting both sexes.

Conclusions:

• Adolescent rTBI promotes subsequent Aβ pathology deposition.
• The interinjury interval is a critical factor modulating the extent of Aβ deposition following rTBI.