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Table 1 Rodent models of neuroinflammation

From: Rodent models of neuroinflammation for Alzheimer’s disease

Models Predisposing factors/causes Time of appearance of lesions Signs (time detectable) SLC reading key Reference
hp-Tau Aβ depositions
LPS Peripheral immune challenge, chronic neuroinflammation ? ? Fear memory (?) S1L0C1 [165]
Spatial memory (?)
PolyI:C Peripheral immune challenge, chronic neuroinflammation 3m 12m Spatial memory (20 m) S1L1C1 [5]
(PHF, but not NFTs) (APP depositions)
ICV-STZ Disrupted insulin signaling, chronic neuroinflammation 6-7w 12w Spatial memory S1L1C1 [85]
Visual recognition memory (3w)   
ICV-OKA Inhibition of serine/threonine phosphatases 1 and 2A 2w 6w Spatial memory (?) S1L1C0 [102] [104]
(PHF, but not NFTs) (Non-fibrillar Aβ deposits)
ICV-colchicine Inhibition of tubulin formation/microtubule breakdown ? (Tau dephosphorylation) ? (Amyloid plaque) Spatial memory (14d to 21d) S1L0C1 [113] [117]
p25 Tg Upregulation of cPLA2, neuroinflammation 4w 8w Contextual fear memory (6w) S1L1C1 [145]
IL-1 β Tg Chronic neuroinflammation ? ? (Increased clearance of amyloid plaques) Contextual fear memory (12w) S1L0C0 [39]
Anti-NGF antibody Tg Blockade of NGF signaling pathway ? (Neurofibrillary pathology) ? (Amyloid plaques) Visual recognition memory (4 m); Spatial memory (9 m) S1L1C0 [148] [149]
  1. This table summarizes the suggested models of late-onset AD (LOAD) displaying neuroinflammation as one of the prominent pathological events. The SLC reading key is a scoring system that represents the compatibility of an animal model with the disease in humans with respect to signs (S), lesions (L), and causes (C) [7]. Compatibility is indicated by 1 and incompatibility by 0. Based on SLC reading key, p25 tg, PolyI:C-, and STZ-induced neuroinflammation models are compatible with the inflammation hypothesis of LOAD [13]. (Abbreviations: ? unavailable data; LPS lipopolysaccharide; PolyI:C polyriboinosinic-polyribocytidilic acid; p25 Tg p25 transgenic model; NGF nerve growth factor; IL-1β Tg interleukin-1β transgenic model; ICV intracerebroventricular; STZ streptozotocin; OKA okadaic acid; hp-Tau hyperphosphorylated tau; amyloid β; PHF paired helical filaments; NFT neurofibrillary tangles; cPLA2 cytosolic phospholipase 2; SLC Signs, Lesions, Causes; w week; m month).