Skip to main content
. Author manuscript; available in PMC: 2014 Mar 24.
Published in final edited form as: Nature. 2013 Sep 5;501(7465):45–51. doi: 10.1038/nature12481

Figure 1. Commonalities among age-related neurodegenerative diseases.

Figure 1

The deposited proteins adopt an amyloid conformation and show prion-like self-propagation and spreading in experimental settings, consistent with the progressive appearance of the lesions in the human diseases. a, Aβ deposits (senile plaques) in the neocortex of a patient with Alzheimer’s disease. b, Tau inclusion as a neurofibrillary tangle in a neocortical neuron of a patient with Alzheimer’s disease. c, α-Synuclein inclusion (Lewy body) in a neocortical neuron from a patient with Parkinson’s disease/Lewy body dementia. d, TDP-43 inclusion in a motoneuron of the spinal cord from a patient with amyotrophic lateral sclerosis. Scale bars are 50 µm in a and 20 µm in b–d. e–h, Characteristic progression of specific proteinaceous lesions in neurodegenerative diseases over time (t, black arrows), inferred from post-mortem analyses of brains. Aβ deposits and tau inclusions in brains of patients with Alzheimer’s disease (e and f), α-synuclein inclusions in brains of patients with Parkinson’s disease (g), and TDP-43 inclusions in brains of patients with amyotrophic lateral sclerosis (h). Three stages are shown for each disease, with white arrows indicating the putative spread of the lesions (for details see refs 58). Panels e and f are reproduced, with permission, from ref. 61.