The Health-Promoting Effects and the Mechanism of Intermittent Fasting

Table 5

Information about IF and neurological diseases.

Information	Method	Sample feature	Results	Discussion
Zhang [59]	Nonrandomized controlled experiments on animals	APPswe/PSIdE9 double transgenic mice	ADF improved AQP4 polarity	IF caused the loss of AQP4 polarity in the cerebral cortex of the target mice, inhibited the expression of AQP4 and AQP4-M1 and the increase of AQP4-M1/M23, and decreased the expression of SnTA1.
Zhang [60]	Nonrandomized controlled experiments on animals	C57BL/6 mice with acute PD randomly divided into four groups: NS+AL group, NS+ADF group, MPTP+AL group, MPTP+ADF group	ADF: motor dysfunction, DA, 5-HT, TH, Prakk1, Tjp1 ↑; DOPAC, HVA, 5-HIAA↓	ADF has protective effects on intestinal barrier and nerves and maintains the integrity of intestinal epithelium in PD mice.
Rubovitch [61]	Nonrandomized controlled experiments on animals	ICR male mouse control group TBI group (AL group, IF group, CR group)	IF: prevented the significant decrease of preference index, SIRT1 in TBI mice	IF is effective in ameliorating cognitive deficits in a TBI model when initiated after the brain injury.

Note: AL: fed ad libitum; NS: normal saline; ADF: alternate-day fasting; MPTP: 1-methyl-4-phenyl-1, 2, 3, 6-tetrathydropyridine; transgenic mice were transferred to both the amyloid precursor protein gene (APP) K670N mutant gene and the early ageing protein 1 gene (PS1) E9 mutant gene. APPswe/Pside9 double transgenic mice; Prakk1: mRNA of AMPK; Tjp1: mRNA of ZO-1; DOPAC: 3,4-dihydroxyphenylacetic acid; HVA: homovanillic acid; 5-HIAA: 5-hydroxyindoleacetic acid; ICR: Institute of Cancer Research; TBI: traumatic brain injury.