Table 1.
Summary of the effect of specific probiotics on neurological disorders
Probiotic strain | Model | Neurological effect | Reference |
---|---|---|---|
Neuroprotection | |||
Clostridium butyricum | Male ICR mice (cerebral I/R injury; stroke) |
C. butyricum improved neurological deficits Improved anti-oxidant capacity (increase in SOD and decrease in MDA levels) Decreased apoptosis (caspase-3 and Bax levels decreased, Bcl-2/Bax ratio increased) |
[152] |
L. helveticus R0052 B. longum R0175 |
WT mice stressed with water avoidance stress (WAS) |
Probiotic treatment attenuated HPA axis and ANS activities in response to WAS Prevented WAS-induced decrease in hippocampal neurogenesis and expression changes in hypothalamic genes involved in synaptic plasticity |
[153] |
Multiple sclerosis | |||
B. animalis | Rat model of EAE: autoimmune encephalomyelitis |
Probiotic reduced duration of clinical symptoms Improved body weight gain Reduced cytokine expression |
[154] |
B. fragilis PSA |
In vivo mouse model of EAE |
Prophylactic treatment delayed EAE symptom onset and reduced symptom severity Reduced expression of cytokines (IL-17), IFNγ and RORγt Therapeutic treatment reduced disease severity |
[155] |
L. paracasei DSM 13434 L. plantarum DSM 15312 L. plantarum DSM 15313 |
In vivo mouse model of EAE |
Probiotic treatment reduced neuroinflammation Induced regulatory T cells in mesenteric lymph nodes Enhanced TGFβ1 expression Combination of three strains suppressed progression and reversed clinical histological signs of EAE |
[156–159] |
L. casei L. acidophilus L. reuteri B. bifidum S. thermophilus |
Mouse model of EAE: MOG35055 peptide in CFA containing Mycobacterium tuberculosis and pertussis toxin |
Prophylactic treatment suppressed EAE development and delayed progression Inhibited proinflammatory Th1/Th17 polarization Induced IL-10 and/or Foxp3(+) regulatory T cells |
[158] |
Anxiety and memory deficits | |||
L. helveticus R0052 | WT and IL-10 deficient 129/SvEv mice on normal or Western-style diet |
Prevented anxiety-like behavior and memory impairment in mice with proinflammatory state and western diet Decreased inflammation and fecal corticosterone in WT mice on western diet |
[160] |
L. helveticus L. rhamnosus |
Streptozocin injected mice (diabetes model) |
Probiotics improved the impaired special memory in the diabetic animals Recovered declined basic synaptic transmission Restored hippocampal long-term potentiation |
[161] |
L. rhamnosus R0011 L. helveticus R0052 L. casei Shirota |
Female SPF mice | Memory impairment induced by C. rodentium infection was prevented by daily probiotic treatment | [162] |
Patients with chronic fatigue syndrome | Probiotic treatment significantly reduced anxiety symptoms | [163] | |
Neurodegeneration | |||
L. fermentum NCIMB 5221 |
Strains of L. fermentum potently secrete FA, a molecule that has potent anti-AD activity FA reduced Aβ fibril formation, neuroinflammation and restores learning and memory deficits in AD models |
[61, 164] | |
VSL#3 | Aged (20–22 months) Wistar rats |
Probiotic treatment attenuated the age-related deficits in long-term potentiation Decreased markers of microglial activation Increased expression of BDNF and synapsin Strong downregulation of genes involved in neurodegeneration (Alox15, Nid2,PLA2G3) |
[165] |
L. rhamnosus R0011 L. helveticus R0052 |
Myocardial infarction rats |
Prophylactic probiotic treatment reduced the Bax/Bcl-2 ratio and caspase-3 proapoptotic activity in the amygdala and dendrite gyrus Akt activity was increased in similar areas |
[166] |
L. helveticus R0052 B. longum R0175 |
WT mice stressed with water avoidance stress (WAS) |
Probiotic treatment attenuated HPA axis and ANS activation in response to WAS Prevented WAS-induced decrease in hippocampal neurogenesis and expression changes in hypothalamic genes involved in synaptic plasticity |
[153] |
C. butyricum | Mouse model of vascular dementia (permanent right unilateral common carotid arteries occlusion) |
Significantly attenuated the cognitive dysfunction and histopathological changes Increased levels of BDNF and Bcl-2, decreased levels of Bax supporting anti-apoptotic state Induced Akt phosphorylation Reduced neuronal apoptosis |
[167] |