Table 1.
T2DM | Drugs | AD |
---|---|---|
↑ glucose uptake and regulation | INSULIN | ↑ deactivation of GSK-3β ↑ Aβ clearance |
↑ insulin secretion |
GLP1-RA (Exenatide-4, liraglutide, lixisenatide) |
↑ deactivation of GSK-3β ↓ neuronal Tau hyperphoshorylation |
↑ insulin sensitivity, ↑ transcription of insulin sensitive genes |
TZDs (rosiglitazone, pioglitazone) |
↓ Aβ generation and deposition |
↑ insulin sensitivity |
GSK-3β INHIBITORS (Tideglusib, NP12, TDZD-8) |
↑ deactivation of GSK-3β ↓ Tau hyperphosh ↓ Aβ deposition |
↓ RAGE expression ↑ glucose uptake ↑ insulin sensitivity |
RESVERATROL | ↑ AMPK ↓ mTOR ↑autophagy ↓ Aβ deposition |
↑ insulin sensitivity ↓ glucose plasma levels |
CURCUMIN | ↓ IAPP amyloid fibrils ↑ deactivation of GSK-3β |
↑ insulin sensitivity | ZERUMBONE | AChE inhibitor |
↓ intestinal glucose absorption | CAPSAICIN | ↓ RAGE activation ↓ blood–brain Aβ |
↓ free radicals | LYCOPENE | ↓ free radicals |
J147 | ↑ AMPK ↓ mTOR ↑autophagy ↓ Aβ deposition |
|
THIAMET G | O-GlcNAcase inhibitor ↓ Aβ and Tau pathology | |
MITOCHONDRIA ANTIOXIDANTS (MitoQ and MitoVitE) |
↓ free radicals ↓ Aβ neurotoxicity |
|
RAPAMYCIN | ↓ mTOR ↑autophagy/mitophagy |
|
LATREPIRDINE | ↑autophagy/mitophagy ↓Aβ toxicity | |
NICOTINAMIDE | ↑ autophagy ↓Aβ and Tau pathology. |
Abbreviations: GLP-1 RA: glucagon-like peptide-1 receptor agonists; TZDs: thiazolidinediones; AChE: Acetylcholinesterase; RAGE: Receptor advanced glycation end products. ↑ increase, ↓ decrease.