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Fig. 1 | Cell & Bioscience

Fig. 1

From: Abnormal protein post-translational modifications induces aggregation and abnormal deposition of protein, mediating neurodegenerative diseases

Fig. 1

The role of PPTMs in neurodegenerative diseases. Take increased phosphorylation as an example: (a) AD: Phosphorylation affects the aggregation and stability of tau protein, which can lead to its abnormal aggregation and formation of neurofibrillary tangles, and ultimately the death of neurons [125]. (b) PD: Abnormal phosphorylation of α-synuclein may promote the formation of Lewy bodies in patients with Parkinson’s disease [126]. (c) HD: Toxic mHTT can be phosphorylated, and this can protect against the toxicity of polyQ-expanded HTT thus reducing neuronal damage [127]. (d) ALS: Phosphorylation of TDP-43 is one of the important factors leading to its abnormal aggregation. TDP-43 deposits exist in the brain and spinal cord of ALS patients as inclusion bodies, resulting in neuronal damage and death [128,129,130,131,132,133,134]

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