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. 2016 Jan 27;283(1823):20152397. doi: 10.1098/rspb.2015.2397

Figure 2.

Figure 2.

Microscopic pathology of chronic dietary l-BMAA exposures in vervets. Representative low-power images (5× magnification) of hyperphosphorylated tau (AT8) immunostained coronal hemisections from control (a,c) and l-BMAA-fed vervets (b,d). AT8 immunostaining is seen in the amygdala (Amy), entorhinal (EC), perirhinal (PrC), primary motor (M1) and temporal cortices of l-BMAA-fed vervets. Higher-power images show predominant tau AT8 staining in superficial cortical layers II and III with more robust staining over the entorhinal and perirhinal cortices (25× magnification) (d). Microscopic images (original magnification ×120) show NFT in vervets fed l-BMAA. Tangle-like tau aggregates are seen in the temporal gyrus (e,f). Dense intracellular tau immunolabelling (gi) and extracellular deposits (j,k) were seen in the parahippocampal gyrus. Abundant neuropil threads, tangles and dystrophic neuronal processes are observed in layers II and III of the perirhinal cortex (I, high-power images shown in l,m) and the paralaminar nucleus of the amygdala (n). Tau plaques were seen in l-BMAA-fed vervets ranging from large and diffuse (o) to small dense aggregates (p). ac, anterior commissure; Amy, amygdala; Bmc, basal nucleus of the amygdala, magnocellular region; Bpc, basal nucleus of the amygdala, parvicellular subdivision; Cd, caudate; cgs, cingulate gyrus sulcus; EC, entorhinal cortex; L, lateral nucleus of the amygdala; LF, lateral fissure; M1, primary motor cortex; PrC, perirhinal cortex; PL, paralaminar nucleus; Pu, putamen; STS, superior temporal sulcus.