Table 1: Cysteinet deregulation in AD.

1. Mitochondrial SCCPs dysfunctions

Complex I, IV and V disruption; TCAc disturbance  

Reactive species overproduction  

Mitochondrial biogenesis  

MPTP (mitocondrial permeability transition pore) dysfunction


2. Cytosolic SCCPs dysfunctions  

Glyceraldehyde-3-phosphate dehydrogenase  

Pyruvate kinase; Phosphofructokinase  

Glucose 6-phosphate isomerase   

Glycogen phosphorylase

Phosphoglycerate mutase 1

Phosphoglucomutase 2   

Protein tyrosine kinases 


3. Synaptic proteins  

Cysteine string protein α   



Soluble NSF attachment protein receptor  



4. APP processing and Aβ aggregation  

APP mutations and palmitoylation  

Presenilin 1 mutations  

Presenilin 2 tertiary structure alteration  

γ-secretase dysfunction


5. Tau protein aggregation  

Tau cross-link  

Tau self-acetylation  

Microtubule associated protein-2 (MAP2)


6. Calcium homeostasis  

Sarco-endoplasmic reticulum Ca2+ ATPase (SERCA) pump

Inositol 1,4,5-trisphosphate receptor (IP3R)  

Ryanodine receptor (RYR)


 7. Protein misfolding  

Reduced/oxidized disulfide bonds in proteins  

Protein disulfide isomerase (PDI)  

Mitochondrial import and assembly (MIA) pathway  

Other redox-dependent chaperone-like mechanisms (thioredoxin)


8. Ubiquitin-proteasome pathway  

E1, E2 and E3 enzymes  

Other proteins of the proteasome machinery  

Keap1-Cullin-3 ubiquitination system


9. Cysteine proteases  

Calpains, cathepsins, and caspases  

X-linked inhibitor of apoptosis (XIAP)


10. Transcription factors and genes expression  

Heat shock transcription factor 1 (HSF1)  

Nuclear factor (erythroid-derived 2)-like 2 (Nrf2)  

NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells)  

Ras-ERK pathway