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. 2017 Jun 22;74(20):3769–3787. doi: 10.1007/s00018-017-2550-9

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

[156159]

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]