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

Synaptophysin

α-synuclein

Soluble NSF attachment protein receptor

Synaptotagmin

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