Gut microenvironmental changes as a potential trigger in Parkinson’s disease through the gut–brain axis

Table 2 Double-hit rodent models of Parkinson’s disease

PD model	Environmental toxin	Intestinal pathological change		Brain pathological change		Clinical symptoms		Study
PD model	Environmental toxin	Enteric α-syn^a	Impaired epithelial barrier	Central α-syn^a	Neuropathology^b	GI	Motor
SNCA A53T	Oral paraquat	+		−			−	Naudet [169]
SNCA A53T	DSS	+		+	+		+	Kishimoto [77]
SNCA A53T	IP LPS				+		−	Vitola [170]
LRRK2 G2019S, LRRK2 R1441G	IP LPS				+			Kozina [171]
LRRK2 G2019S	DSS	+	+	−	+		+	Lin [76]
PINK1^±	IP rotenone				+			Martella [172]
PINK1^−/−	Oral bacteria				+		+	Matheoud [173]
Thy1-αSyn	Oral SCFAs			+	+		+	Sampson [113]
Thy1-αSyn	Oral bacteria	+		+	+	+	+	Sampson [122]

DSS, dextran sulfate sodium; GI, gastrointestinal; IP, intraperitoneal; LPS, lipopolysaccharide; PD, Parkinson’s disease; SCFAs, short chain fatty acids; α-syn, α-synuclein. + and − indicates positive and negative results. Blank indicates items not shown
^aPathologic α-synuclein deposition at tissue
^bNeuroinflammation, neuronal loss, and/or synaptopathy at brain

ISSN: 1423-0127