Heparin sustains the brain

Amyloid plaque formation can be inhibited by an unlikely culprit, according to work by Scholefield et al. on page 97. The group finds that heparan sulfate (HS)—normally a part of the cell surface and extracellular matrix—functions in cells to slow the production of the plaque components of Alzheimer's disease.

Amyloid plaques are aggregates of the amyloid β-peptide (Aβ). Aβ is produced upon intracellular cleavage of the amyloid precursor protein (APP) by the BACE1 β-secretase and subsequent processing of one of the resulting fragments by γ-secretase. Plaque aggregation in the extracellular matrix is promoted by HS. Scholefield et al. now show that HS also has an anti-plaque activity: it inhibits BACE1.

The group finds that HS and BACE1 colocalize at the cell surface and in the Golgi—both regions that have been suggested...