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The in-vitro seeded fibrils are unlikely to be disease-relevant and representative of the diverse alpha-synuclein polymorphs in the brain.

Dendrites of pyramidal neurons in piriform cortex can initiate NMDA spikes, which may serve to amplify odor responses, and provide combination selectivity underlying 'discontinuous' odor receptive fields in these neurons.

In bacteria, frequent adaptive copy-number mutations can hinder the fixation of beneficial point mutations and hence the divergence of duplicated DNA sequences.

Transposable elements and gene amplifications can provide variation needed for novel trait refinement and adaptation to new niches, though a recalcitrant organism-environment mismatch may persist.

The olfactory mucosa of patients with fatal familial insomnia contains traces of infectious prions, and their analyses could support the clinical diagnosis and elucidate disease-specific mechanisms.

Somatically derived genomic mosaicism in the form of increased DNA content and APP copy number in single neurons plausibly has a function in sporadic Alzheimer’s disease and points to functions for single-neuron gene copy number changes.

A DNA transposon, or ‘jumping gene’, controls its amplification within a genome through a competition between the enzyme multimers that are responsible for its mobility.

Experimental evolution reveals how adaptation by increased expression of a gene depends on a combination of simple genetic properties of the gene's neighbors on the DNA.

SIMR-1 acts downstream of the piRNA pathway to promote siRNA amplification by the Mutator complex and localizes to perinuclear foci distinct from Mutator foci, P granules and Z granules.

Bacteriophage can rapidly evolve resistance to anti-phage defense elements in bacteria by amplifying latent counter-defense genes, though this amplification comes at a cost of compensatory deletions that eliminate other counter-defense genes.