A more recent, modern and thorough model of amyloid fibril formation involves the intervention of secondary events, such as 'fragmentation', in which a fibril breaks into two or more shorter fibrils, and 'secondary nucleation', in which fibril surfaces (not fibril ends) catalyze the formation of new nuclei. Both secondary events increase the number of fibril ends able to recruit new monomers or oligomers, therefore accelerating fibril formation. These events add to the well recognised steps of primary nucleation (formation of the nucleus from the mnonomers through one of models described above), fibril elongation (addition of monomers or oligomers to growing fibril ends) and dissociation (opposite process).