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The motor neuron disease amyotrophic lateral sclerosis (ALS) typically beginswith localized muscle weakness. Progressive, widespread paralysis often followsover a few years. Does the disease begin with local changes in a small piece ofneural tissue and then spread? Or does neural decay happen independently acrossdiverse spatial locations? The distinction matters, because local initiationmay arise by local changes in a tissue microenvironment, by somatic mutation,or by various epigenetic or regulatory fluctuations in a few cells. A localtrigger must be coupled with a mechanism for spread. By contrast, independentdecay across spatial locations cannot begin by a local change, but must dependon some global predisposition or spatially distributed change that leads toapproximately synchronous decay. This article outlines the conceptual frame bywhich one contrasts local triggers and spread versus parallel spatiallydistributed decay. Various neurodegenerative diseases differ in theirmechanistic details, but all can usefully be understood as falling along acontinuum of interacting local and global processes. Cancer provides an exampleof disease progression by local triggers and spatial spread, setting aconceptual basis for clarifying puzzles in neurodegeneration. Heart diseasealso has crucial interactions between global processes, such as circulatinglipid levels, and local processes in the development of atheroscleroticplaques. The distinction between local and global processes helps to understandthese various age-related diseases.

Puzzles in modern biology. IV. Neurodegeneration, localized origin and widespread decay