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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).