Following this analytical approach, it has become apparent that the lag phase does not correspond necessarily to only nucleus formation, but rather results from a combination of various steps. Similarly, the exponential phase is not only fibril elongation, but results from a combination of various steps, involving primary nucleation, fibril elongation, but also secondary events. A significant quantity of fibrils resulting from primary nucleation and fibril elongation may be formed during the lag phase and secondary steps, rather than only fibril elongation, can be the dominant processes contributing to fibril growth during the exponential phase. With this new model, any perturbing agents of amyloid fibril formation, such as putative drugs, metabolites, mutations, chaperones, etc., can be assigned to a specific step of fibril formation. Amino acid sequence and amyloid formation
In general, amyloid polymerization (aggregation or non-covalent polymerization) is sequence-sensitive, that is mutations in the sequence can induce or prevent self-assembly. For example, humans produce amylin, an amyloidogenic peptide associated with type II diabetes, but in rats and mice prolines are substituted in critical locations and amyloidogenesis does not occur. Studies comparing synthetic to recombinant β amyloid peptide in assays measuring rate of fibrillation, fibril homogeneity, and cellular toxicity showed that recombinant β amyloid peptide has a faster fibrillation rate and greater toxicity than synthetic β amyloid peptide.There are multiple classes of amyloid-forming polypeptide sequences. Glutamine-rich polypeptides are important in the amyloidogenesis of Yeast and mammalian prions, as well as trinucleotide repeat disorders including Huntingtons disease.
Recent research by Krystel R. Huxlin and others on the relearning of complex visual motion following V1 damage has offered potentially promising treatments for individuals with acquired cortical blindness. These treatments focus on retraining and retuning certain intact pathways of the visual cortex which are more or less preserved in individuals who sustained damage to V1. Huxlin and others found that specific training focused on utilizing the "blind field" of individuals who had sustained V1 damage improved the patients ability to perceive simple and complex visual motion. This sort of relearning therapy may provide a good workaround for patients with acquired cortical blindness in order to better make sense of the visual environment. See also
Blindsight

References
Further reading
Books
Vighetto, A., & Krolak-Salmon, P. (2007). Cortical blindness. New York, NY: Cambridge University Press. Papers
Balliet, R., Blood, K. M., & Bach-y-Rita, P. (1985). Visual field rehabilitation in the cortically blind? : Journal of Neurology, Neurosurgery & Psychiatry Vol 48(11) Nov 1985, 1113-1124. Trevethan, C. T., & Sahraie, A. (2003). Spatial and temporal processing in a subject with cortical blindness following occipital surgery: Neuropsychologia Vol 41(10) 2003, 1296-1306. == External links ==