In AD, these processes result in amyloid-beta plaques and tau neurofibrillary tangles; in PD, alpha-synuclein aggregates form Lewy bodies; in HD, mutant huntingtin proteins with polyglutamine expansions accumulate; and in ALS and frontotemporal dementia, TAR DNA-binding protein 43 (TDP-43) aggregates are involved [56,57]. The gene discussed is TARDBP; the disease is amyotrophic lateral sclerosis.