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. 2024 Jan 2;6(1):fcad356. doi: 10.1093/braincomms/fcad356

Table 1.

ND, for example, of different pathogenesis of cell deregulation, aberrant proteins and genetic associations, highlighting the different areas of the brain that are affected in the disorders adapted from Bernaus et al.80 and Li et al.81

Neurodegenerative disorder
Alzheimer’s disease Parkinson’s disease Huntington’s disease Motor neuron disease (amyotrophic lateral sclerosis)
Agent OS OS OS OS
Glial deregulation Phagocytic clearance, NI, autophagy, microgliosis, BBB dysregulation
Epigenetic factors DNA methylation, chromatin remodelling and histone post-translational modifications
Mode of action Activation of macromolecule, glial cell and tau phosphorylation Lipid peroxidation and mutation in α-synuclein Lipid peroxidation SOD1 activation, inflammation
Familial form has SOD1 mutation
Aberrant protein and cause of neuronal deregulation Aβ plaques, tau neurofibril tangles α-Synuclein misfolding protein Huntingtin (Htt) protein Multiple impaired protein homeostasis due to ER stress
Gene association ApoE4, amyloid precursor protein (APP), presenilin 1/2 (PSEN1/2) SNCA, LRRK2 HTT (IT15) SOD1, TDP-43, FUS
Area of the brain affected Hippocampus Basal ganglia and substantia nigra Caudate nucleus, putamen and globus pallidus Lower and upper motor