Table 2.
Neuroprotective effects of trehalose in in vivo PD models
| Reference | Animal model | Route of administration | Doses | Treatment duration | Main finding |
|---|---|---|---|---|---|
| Ferguson, Law, and Sarkar (2015) | Adult male C57Bl/6 mice (MPTP‐induced PD) | In drinking water | 1% (1.90–2.34 g·kg−1) | 38 days |
No improvement in the MPTPp‐induced behavioural alterations. Attenuation in the striatal reduction of DA, DOPAC, HVA, and 5‐HIAA levels. |
| Sarkar et al. (2014) | Adult male C57Bl/6 mice (MPTP‐induced PD) | In drinking water | 2% | Twice a week for 5 weeks and started at 3 days prior to the start of MPTP + probenecid administration | Decrease in the loss of TH and DA transporter in the ventral midbrain SNpc and CPu and dopamine levels in CPu. Reduction in microglial activation and astrocytic hypertrophy, amelioration of motor deficits, protecting ZO‐1 and occluding (two tight junctional proteins), and glucose transporter‐1 in brain endothelial cells from MPTP‐induced down‐regulation. |
| He et al. (2016) | Female SD rats (injected with AAV1/2 expressing human A53T α‐synuclein) | In drinking water | 5, 2, and 0.5% | 6 weeks |
0.5% trehalose: fail to improve the behavioural and neurochemical deficits. 5% and 2% trehalose: reduction in α‐synuclein‐mediated deficits in motor asymmetry and DA neurodegeneration and α‐synuclein aggregation in the nigrostriatal, enhancement of autophagy in the striatum by increasing formation of LC3‐II. |
| Rodríguez‐Navarro et al. (2010) | PK−/−/TauVLW transgenic mice | In drinking water | 1% |
Twice a week for 2.5 months (in 3‐month‐old mice) 4 months (in 3‐month‐old mice) 3‐week treatment (in 14‐month‐old mice) |
2.5 months: improvement in the motor and cognitive behaviours, increase in the number of dopamine neurons in the ventral midbrain and the dopamine‐related protein levels in the midbrain and striatum, and decrease in the number of phosphorylated tau‐positive neuritic plaques, the levels of phosphorylated tau protein, and the astrogliosis. 4 months: maintained the amelioration of the tau pathology and astrogliosis and failed to revert DA‐related pathology in the striatum. 3 weeks (at the limit of their life expectancy): improving in the motor behaviour and anxiety and reducing in the levels of phosphorylated tau and the number of murine β‐amyloid plaques. |
| Tanji et al. (2015) | LBD model mice (overexpressed A53T α‐synuclein) | Oral intake and intraperitoneal injection | 2% (wt/vol) |
Short period (1‐week intake) Long period (3‐ or 12‐week intake) |
I.p. injection: no effect on autophagy in the brain. Oral intake: (a) in short period: induction of autophagy and increase in the levels of a heat shock protein, HSP90, and an ER stress chaperone, SigmaR1. (b) In long period: The effect of trehalose was obscured. |
| Kaur and Nazir (2015) | Transgenic Caenorhabditis elegans model (expressing human α‐synuclein) | Seeded onto the nematode growth medium plates | 5 and 10 mM | 48 hr |
5 mM concentration: no reduction in α‐synuclein levels. 10 mM concentration: reduction in ROS and α‐synuclein levels, increase in motility and dopamine levels, and up‐regulation of autophagic and chaperonic genes bec‐1, lgg‐1, epg‐8, hsp‐60, and hsp‐4. |
| Wu, Xu, et al. (2015) | Male Lewis rats (rotenone‐induced PD) | In drinking water | 2% (wt/vol) | Daily, for 56 days | Reduction in the loss of SNpc DA neurons. |
5‐HIAA: 5‐hydroxyindoleacetic acid; CPu: caudate putamen; DA: dopamine; DOPAC: 3,4‐dihydroxyphenylacetic acid; HVA: homovanillic acid; LBD: Lewy body disease; MPTP: 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine; PD: Parkinson's disease; SD: Sprague–Dawley; SNpc: substantia nigra pars compacta; WT: wild‐type.