Stroke is a major cause of death in the elderly, and risk of dementia increases after stroke. Poststroke dementia （PSD） covers all types of dementia after stroke, and is an important cause of disability in the elderly. The prevalence of PSD varies from 31.4% to 21.5% in 3 months to 4 years after the stroke. Its incidence increases with time after the stroke. Stroke and dementia share a number of risk factors. Stroke can be the direct cause of dementia and may also produce dementia by precipitating the onset of degenerative disease.

Key words: 
stroke ;  dementia ;  Alzheimer＇s disease ; risk factor

Poststroke Dementia

http://manuscript.elsevier.com/S1568163722001027/pdf/S1568163722001027.pdf

Cortical excitability and plasticity in Alzheimer’s disease and mild cognitive impairment: A systematic review and meta-analysis of transcranial magnetic stimulation studies

Objective Post-stroke cognitive impairment (PSCI) is resistant to treatment. Recent studies have widely applied repetitive transcranial magnetic stimulation (rTMS) to treat various brain dysfunctions, such as post-stroke syndromes. Nonetheless, a protocol for PSCI has not been established. Therefore, this study is aimed to evaluate the therapeutic effect of our high-frequency rTMS protocol for PSCI during the chronic phase of stroke. Methods In this prospective study, ten patients with PSCI were enrolled and received high-frequency rTMS on the ipsilesional dorsolateral prefrontal cortex (DLPFC) for 10 sessions (5 days per week for 2 weeks). Cognitive and affective abilities were assessed at baseline and 2 and 14 weeks after rTMS initiation. To investigate the therapeutic mechanism of rTMS, the mRNA levels of pro-inflammatory cytokines (interleukin (IL)-6, IL-1β, transforming growth factor beta [TGF-β], and tumor necrosis factor alpha [TNF-α]) in peripheral blood samples were quantified using reverse transcription polymerase chain reaction, and cognitive functional magnetic resonance imaging (fMRI) was conducted at baseline and 14 weeks in two randomly selected patients after rTMS treatment. Results The scores of several cognitive evaluations, i.e., the Intelligence Quotient (IQ) of Wechsler Adult Intelligence Scale, auditory verbal learning test (AVLT), and complex figure copy test (CFT), were increased after completion of the rTMS session. After 3 months, these improvements were sustained, and scores on the Mini-Mental Status Examination and Montreal Cognitive Assessment (MoCA) were also increased (p < 0.05). While the Geriatric Depression Scale (GeDS) did not show change among all patients, those with moderate-to-severe depression showed amelioration of the score, with marginal significance. Expression of pro-inflammatory cytokines was decreased immediately after the ten treatment sessions, among which, IL-1β remained at a lower level after 3 months. Furthermore, strong correlations between the decrease in IL-6 and increments in AVLT (r = 0.928) and CFT (r = 0.886) were found immediately after the rTMS treatment (p < 0.05). Follow-up fMRI revealed significant activation in several brain regions, such as the medial frontal lobe, hippocampus, and angular area. Conclusions High-frequency rTMS on the ipsilesional DLPFC may exert immediate efficacy on cognition with the anti-inflammatory response and changes in brain network in PSCI, lasting at least 3 months.

/pdf/therapeutic-effect-of-repetitive-transcranial-magnetic-1n10au33.pdf

Therapeutic Effect of Repetitive Transcranial Magnetic Stimulation for Post-stroke Vascular Cognitive Impairment: A Prospective Pilot Study

Many stroke survivors experience persisting episodic memory disturbances. Since hippocampal and para-hippocampal areas are usually spared from the infarcted area, alterations of memory processing networks remote from the ischemic brain region might be responsible for the observed clinical symptoms. To pinpoint changes in activity of hippocampal connections and their role in post-stroke cognitive impairment, we induced ischemic stroke by occlusion of the middle cerebral artery (MCAO) in adult rats and analyzed the functional and structural consequences using activity-dependent manganese (Mn2+) enhanced MRI (MEMRI) along with behavioral and histopathological analysis. MCAO caused stroke lesions of variable extent along with sensorimotor and cognitive deficits. Direct hippocampal injury occurred in some rats, but was no prerequisite for cognitive impairment. In healthy rats, injection of Mn2+ into the entorhinal cortex resulted in distribution of the tracer within the hippocampal subfields into the lateral septal nuclei. In MCAO rats, Mn2+ accumulated in the ipsilateral thalamus. Histopathological analysis revealed secondary thalamic degeneration 28 days after stroke. Our findings provide in vivo evidence that remote sensorimotor stroke modifies the activity of hippocampal-thalamic networks. In addition to potentially reversible alterations in signaling of these connections, structural damage of the thalamus likely reinforces dysfunction of hippocampal-thalamic circuitries.

Sensorimotor stroke alters hippocampo-thalamic network activity

Repetitive Transcranial Magnetic Stimulation of the Brain After Ischemic Stroke: Mechanisms from Animal Models

Different combinations of high-frequency rTMS and cognitive training improve the cognitive function of cerebral ischemic rats.

Objective(s): This study aimed to determine the effect of ischemic occlusion duration and recovery time course on motor and cognitive function, identify optimal conditions for assessing cognitive function with minimal interference from motor deficits, and elucidate the underlying mechanism of axonal inhibitors.Materials and Methods: Sprague-Dawley (SD) rats were randomly allocated to the transient middle cerebral artery occlusion (tMCAO) 60-min (tMCAO60min), tMCAO90min, tMCAO120min, and sham groups. We conducted forelimb grip strength, two-way shuttle avoidance task, and novel object recognition task (NORT)tests at three time points (14, 21, and 28 days). Expression of Nogo receptor-1 (NgR1), the endogenous antagonist lateral olfactory tract usher substance, ras homolog family member A (Rho-A), and RhoA-activated Rho kinase (ROCK) was examined in the ipsilateral thalamus.Results: There was no difference in grip strength between sham and tMCAO90min rats at 28 days. tMCAO90min and tMCAO120min rats showed lower discrimination indices in the NORT than sham rats on day 28. Compared with that in sham rats, the active avoidance response rate was lower in tMCAO90min rats on days 14, 21, and 28 and in tMCAO120min rats on days 14 and 21. Furthermore, 50-54% of rats in the tMCAO90min group developed significant cognitive impairment on day 28, and thalamic NgR1, RhoA, and ROCK expression were greater in tMCAO90min rats than in sham rats.Conclusion: Employing 90-min tMCAO in SD rats and assessing cognitive function 28 days post-stroke could minimize motor dysfunction effects in cognitive function assessments. Axonal inhibitor deregulation could be involved in poststroke cognitive impairment.

https://ijbms.mums.ac.ir/article_18025_4fd54193b3e5b4408fb44531600ca4b5.pdf

NgR1 pathway expression in cerebral ischemic Sprague-Dawley rats with cognitive impairment

Poststroke cognitive impairment (PSCI) is one of the most severe sequelae of stroke and lacks effective treatment. Previous studies have shown that high-frequency repetitive transcranial magnetic stimulation (rTMS) may be a promising PSCI therapeutic approach, but the underlying mechanism is unclear. To uncover the effect of rTMS on PSCI, a transient middle cerebral artery occlusion (tMCAO) model was established. Modified Neurological Severity Score (mNSS) test and Morris Water Maze (MWM) test were performed to assess the neurological and cognitive function of rats. Furthermore, to explore the underlying mechanism, differentially expressed genes (DEGs) in the hippocampus of rats in the rTMS group and tMCAO group were compared using RNA sequencing. Then, bioinformatics analysis, including gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis and protein-protein interaction (PPI) network analysis, was conducted to elaborate these DEGs. Our results indicated that high-frequency rTMS could significantly improve neurological and cognitive function, according to mNSS and MWM tests. We found 85 DEGs, including 71 upregulated genes and 14 downregulated genes, between the rTMS group and tMCAO group. The major functional category was related to chemical synaptic transmission modulation and several DEGs were significantly upregulated in processes related to synaptic plasticity, such as glutamatergic synapses. Calb2, Zic1, Kcnk9, and Grin3a were notable in PPI analysis. These results demonstrate that rTMS has a beneficial effect on PSCI, and its mechanism may be related to the regulation of synaptic plasticity and functional genes such as Calb2, Zic1, Kcnk9, and Grin3a in the hippocampus.

High-Frequency rTMS Improves Cognitive Function by Regulating Synaptic Plasticity in Cerebral Ischemic Rats

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Different combinations of high-frequency rTMS and cognitive training improve the cognitive function of cerebral ischemic rats.

NgR1 pathway expression in cerebral ischemic Sprague-Dawley rats with cognitive impairment

High-Frequency rTMS Improves Cognitive Function by Regulating Synaptic Plasticity in Cerebral Ischemic Rats