scholarly journals The regulation of glycemia in the recovery phase after stroke counteracts the detrimental effect of obesity-induced type 2 diabetes on neurological recovery

2020 ◽  
Author(s):  
Ada Admin ◽  
Ingrid Lovise Augestad ◽  
Hiranya Pintana ◽  
Martin Larsson ◽  
Camilla Krizhanovskii ◽  
...  
Keyword(s):  
Chronic Phase ◽  
Clinical Situation ◽  
Recovery Phase ◽  
Artery Occlusion ◽  
Stroke Recovery ◽  
Neurological Recovery ◽  
Standard Diet ◽  
Dipeptidyl Peptidase 4 ◽  
Post Stroke ◽  
The Impact

The interplay between obesity and T2D in post-stroke recovery is unclear. Moreover, the impact of glucose control during the chronic phase after stroke is undetermined. <p>We investigated whether obesity-induced T2D impairs neurological recovery after stroke by using a clinically relevant experimental design. We also investigated the potential efficacy of two clinically-used T2D drugs: the dipeptidyl peptidase-4 inhibitor linagliptin and the sulfonylurea glimepiride.</p> <p>We induced transient middle cerebral artery occlusion (tMCAO) in T2D/obese mice (after 7 months of high-fat diet (HFD)) and age-matched controls. After stroke, we replaced HFD with standard diet for 8 weeks to mimic the post-stroke clinical situation. Linagliptin or glimepiride were administered daily from 3 days after tMCAO for 8 weeks.<b> </b>We assessed neurological recovery weekly by upper-limb grip strength. Brain damage, neuroinflammation, stroke-induced neurogenesis and atrophy of parvalbumin (PV)+ interneurons were quantified by immunohistochemistry.</p> <p>T2D/obesity impaired post-stroke neurological recovery in association with hyperglycemia, neuroinflammation and atrophy of PV+ interneurons. Both drugs counteracted these effects. In non-diabetic mice, only linagliptin accelerated recovery.</p> These findings shed light on the interplay between obesity and T2D in stroke recovery. Moreover, they promote the use of rehabilitative strategies based on efficacious glycemia regulation, even if initiated days after stroke.

scholarly journals The regulation of glycemia in the recovery phase after stroke counteracts the detrimental effect of obesity-induced type 2 diabetes on neurological recovery

2020 ◽  
Author(s):  
Ada Admin ◽  
Ingrid Lovise Augestad ◽  
Hiranya Pintana ◽  
Martin Larsson ◽  
Camilla Krizhanovskii ◽  
...  
Keyword(s):  
Chronic Phase ◽  
Clinical Situation ◽  
Recovery Phase ◽  
Artery Occlusion ◽  
Stroke Recovery ◽  
Neurological Recovery ◽  
Standard Diet ◽  
Dipeptidyl Peptidase 4 ◽  
Post Stroke ◽  
The Impact

The interplay between obesity and T2D in post-stroke recovery is unclear. Moreover, the impact of glucose control during the chronic phase after stroke is undetermined. <p>We investigated whether obesity-induced T2D impairs neurological recovery after stroke by using a clinically relevant experimental design. We also investigated the potential efficacy of two clinically-used T2D drugs: the dipeptidyl peptidase-4 inhibitor linagliptin and the sulfonylurea glimepiride.</p> <p>We induced transient middle cerebral artery occlusion (tMCAO) in T2D/obese mice (after 7 months of high-fat diet (HFD)) and age-matched controls. After stroke, we replaced HFD with standard diet for 8 weeks to mimic the post-stroke clinical situation. Linagliptin or glimepiride were administered daily from 3 days after tMCAO for 8 weeks.<b> </b>We assessed neurological recovery weekly by upper-limb grip strength. Brain damage, neuroinflammation, stroke-induced neurogenesis and atrophy of parvalbumin (PV)+ interneurons were quantified by immunohistochemistry.</p> <p>T2D/obesity impaired post-stroke neurological recovery in association with hyperglycemia, neuroinflammation and atrophy of PV+ interneurons. Both drugs counteracted these effects. In non-diabetic mice, only linagliptin accelerated recovery.</p> These findings shed light on the interplay between obesity and T2D in stroke recovery. Moreover, they promote the use of rehabilitative strategies based on efficacious glycemia regulation, even if initiated days after stroke.

scholarly journals Obesity-induced type 2 diabetes impairs neurological recovery after stroke in correlation with decreased neurogenesis and persistent atrophy of parvalbumin-positive interneurons

2019 ◽  
Vol 133 (13) ◽  
pp. 1367-1386 ◽  
Author(s):  
Hiranya Pintana ◽  
Grazyna Lietzau ◽  
Ingrid Lovise Augestad ◽  
Fausto Chiazza ◽  
Thomas Nyström ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Recovery Phase ◽  
Artery Occlusion ◽  
Stroke Recovery ◽  
Neurological Recovery ◽  
Repair Mechanisms ◽  
Induced Neural Stem Cell ◽  
Cerebral Artery Occlusion

Abstract Type 2 diabetes (T2D) hampers stroke recovery though largely undetermined mechanisms. Few preclinical studies have investigated the effect of genetic/toxin-induced diabetes on long-term stroke recovery. However, the effects of obesity-induced T2D are mostly unknown. We aimed to investigate whether obesity-induced T2D worsens long-term stroke recovery through the impairment of brain’s self-repair mechanisms – stroke-induced neurogenesis and parvalbumin (PV)+ interneurons-mediated neuroplasticity. To mimic obesity-induced T2D in the middle-age, C57bl/6j mice were fed 12 months with high-fat diet (HFD) and subjected to transient middle cerebral artery occlusion (tMCAO). We evaluated neurological recovery by upper-limb grip strength at 1 and 6 weeks after tMCAO. Gray and white matter damage, stroke-induced neurogenesis, and survival and potential atrophy of PV-interneurons were quantitated by immunohistochemistry (IHC) at 2 and 6 weeks after tMCAO. Obesity/T2D impaired neurological function without exacerbating brain damage. Moreover, obesity/T2D diminished stroke-induced neural stem cell (NSC) proliferation and neuroblast formation in striatum and hippocampus at 2 weeks after tMCAO and abolished stroke-induced neurogenesis in hippocampus at 6 weeks. Finally, stroke resulted in the atrophy of surviving PV-interneurons 2 weeks after stroke in both non-diabetic and obese/T2D mice. However, after 6 weeks, this effect selectively persisted in obese/T2D mice. We show in a preclinical setting of clinical relevance that obesity/T2D impairs neurological functions in the stroke recovery phase in correlation with reduced neurogenesis and persistent atrophy of PV-interneurons, suggesting impaired neuroplasticity. These findings shed light on the mechanisms behind impaired stroke recovery in T2D and could facilitate the development of new stroke rehabilitative strategies for obese/T2D patients.

scholarly journals Delayed Administration of Angiotensin Receptor (AT2R) Agonist C21 Improves Survival and Preserves Sensorimotor Outcomes in Female Diabetic Rats Post-Stroke through Modulation of Microglial Activation

2021 ◽  
Vol 22 (3) ◽  
pp. 1356
Author(s):  
LaDonya Jackson-Cowan ◽  
Wael Eldahshan ◽  
Selin Dumanli ◽  
Guangkuo Dong ◽  
Sarah Jamil ◽  
...  
Keyword(s):  
Therapeutic Option ◽  
Young Female ◽  
Artery Occlusion ◽  
Diabetic Rats ◽  
Stroke Recovery ◽  
Fine Motor ◽  
Post Stroke ◽  
The Impact

About 70% of stroke victims present with comorbid diseases such as diabetes and hypertension. The integration of comorbidities in pre-clinical experimental design is important in understanding the mechanisms involved in the development of stroke injury and recovery. We recently showed that administration of compound C21, an angiotensin II type 2 receptor agonist, at day 3 post-stroke improved sensorimotor outcomes by lowering neuroinflammation in diabetic male animals. In the current study, we hypothesized that a delayed administration of C21 would also lower chronic inflammation post-stroke in diabetic female animals. Young female diabetic rats were subjected to 1 h of middle cerebral artery occlusion (MCAO). Three days post-stroke, rats were administered C21 or vehicle in drinking water at a dose of 0.12 mg/kg/day for 4 weeks. The impact of C21 on microglial polarization was analyzed by flow cytometry in vivo and in vitro. Compound 21 treatment improved fine motor skills after MCAO through modulation of the microglia/macrophage inflammatory properties. In addition, C21 increased M2 polarization and reduced the M1:M2 ratio in vitro. In conclusion, delayed administration of C21 downregulates post-stroke inflammation in female diabetic animals. C21 may be a useful therapeutic option to lower neuro-inflammation and improve the post-stroke recovery in diabetes.

Abstract W MP41: Potentiation of Gaba-Mediated Synaptic Inhibition in the Recovery Phase: A Novel Therapeutic Target for Stroke

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Takeshi Hiu ◽  
Tonya Bliss ◽  
Jeanne Paz ◽  
Eric Wang ◽  
Zoya Farzampour ◽  
...  
Keyword(s):  
Pyramidal Cells ◽  
Recovery Phase ◽  
Synaptic Activity ◽  
Stroke Recovery ◽  
Functional Changes ◽  
Post Stroke ◽  
Array Tomography ◽  
Neuronal Inhibition ◽  
Gaba Signaling ◽  
Novel Therapeutic

Background: Stroke is a major cause of disability yet pharmacotherapy targeting the recovery phase is lacking. Cortical circuit reorganization adjacent to the stroke site promotes recovery, thus elucidating mechanisms that promote this plasticity could lead to new therapeutics. Tonic neuronal inhibition, mediated by extrasynaptic GABA A receptors,inhibits post-stroke recovery. However, effects of phasic (synaptic) GABA signaling - which promotes plasticity during development - are unknown. Here we use a combined approach of i) array tomography to determine the composition of GABA synapses in the post-stroke mouse brain, ii) electrophysiology to determine whether stroke leads to functional changes in GABA-mediated phasic inhibition, and (iii) treatment with zolpidem, an FDA-approved GABA agonist, to modulate recovery. Results: We found, using array tomography, a 1.7-fold increase in the number of GABAergic synapses containing the α1 receptor subunit in layer 5 of the peri-infarct cortex (synapse number/μm 3 : 0.039±0.006 (control) vs 0.064±0.006 (stroke); P<0.01), but not in layer 2/3. There was an associated increase in spontaneous inhibitory post-synaptic currents (sIPSC) specific to layer 5 pyramidal neurons (sIPSC charge (fC): -403±27.8 (control) vs -724±166 (stroke); p=0.03). This effect was transient, occurring during the onset of functional recovery. To test whether the increased phasic inhibitory GABAergic signaling promotes stroke recovery, we treated animals with zolpidem, an agonist with high affinity for α1 subunit-containing GABA A receptors. Low dose zolpidem increased GABA A phasic signaling in layer 5 pyramidal cells and notably increased the rate and extent of behavioral recovery without altering infarct size. Conclusions: These data provide the first evidence that enhanced GABA A -mediated synaptic activity during the recovery phase improves stroke outcome. These data identify modulation of phasic GABA signaling as a novel therapeutic strategy for stroke, indicate zolpidem as a potential drug to improve recovery, and underscore the necessity to distinguish the role of tonic and phasic GABA inhibition in stroke recovery.

scholarly journals Dynamics of language reorganization after left temporo-parietal and frontal stroke

Brain ◽  
2020 ◽  
Vol 143 (3) ◽  
pp. 844-861 ◽  
Author(s):  
Anika Stockert ◽  
Max Wawrzyniak ◽  
Julian Klingbeil ◽  
Katrin Wrede ◽  
Dorothee Kümmerer ◽  
...  
Keyword(s):  
Functional Mri ◽  
Chronic Phase ◽  
Global Network ◽  
Lesion Location ◽  
Post Stroke ◽  
Language Functions ◽  
Language Recovery ◽  
Patient Groups ◽  
The Impact ◽  
General Networks

Abstract The loss and recovery of language functions are still incompletely understood. This longitudinal functional MRI study investigated the neural mechanisms underlying language recovery in patients with post-stroke aphasia putting particular emphasis on the impact of lesion site. To identify patterns of language-related activation, an auditory functional MRI sentence comprehension paradigm was administered to patients with circumscribed lesions of either left frontal (n = 17) or temporo-parietal (n = 17) cortex. Patients were examined repeatedly during the acute (≤1 week, t1), subacute (1–2 weeks, t2) and chronic phase (&gt;6 months, t3) post-stroke; healthy age-matched control subjects (n = 17) were tested once. The separation into two patient groups with circumscribed lesions allowed for a direct comparison of the contributions of distinct lesion-dependent network components to language reorganization between both groups. We hypothesized that activation of left hemisphere spared and perilesional cortex as well as lesion-homologue cortex in the right hemisphere varies between patient groups and across time. In addition, we expected that domain-general networks serving cognitive control independently contribute to language recovery. First, we found a global network disturbance in the acute phase that is characterized by reduced functional MRI language activation including areas distant to the lesion (i.e. diaschisis) and subsequent subacute network reactivation (i.e. resolution of diaschisis). These phenomena were driven by temporo-parietal lesions. Second, we identified a lesion-independent sequential activation pattern with increased activity of perilesional cortex and bilateral domain-general networks in the subacute phase followed by reorganization of left temporal language areas in the chronic phase. Third, we observed involvement of lesion-homologue cortex only in patients with frontal but not temporo-parietal lesions. Fourth, irrespective of lesion location, language reorganization predominantly occurred in pre-existing networks showing comparable activation in healthy controls. Finally, we detected different relationships of performance and activation in language and domain-general networks demonstrating the functional relevance for language recovery. Our findings highlight that the dynamics of language reorganization clearly depend on lesion location and hence open new perspectives for neurobiologically motivated strategies of language rehabilitation, such as individually-tailored targeted application of neuro-stimulation.

Abstract P746: Sex Differences in Cognitive and Psychological Outcomes of Stroke: Impact of Diabetes

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Victoria L Wolf ◽  
Aunay Miller ◽  
Raghavendar Chandran ◽  
Weiguo Li ◽  
Adviye Ergul
Keyword(s):  
Artery Occlusion ◽  
Psychological Outcomes ◽  
Experimental Stroke ◽  
Dark Light ◽  
Stroke Outcomes ◽  
Post Stroke ◽  
Stroke Research ◽  
Y Maze ◽  
Male Animal ◽  
The Impact

Diabetes increases risk and severity of post-stroke cognitive impairment (PSCI), a major cause of disability worldwide. While it is known that females suffer more from PSCI, psychological outcomes and underlying reasons are poorly understood. From a preclinical perspective, potential explanations include 1) use of otherwise healthy animals in experimental stroke research without integration of common comorbid diseases like diabetes into the study design, and 2) optimization of most behavioral tests for sensorimotor and cognitive functions using only male animal models. Our hypothesis is that post-stroke outcomes are sex and comorbid disease-dependent. To test this, we validated the Novel Object Recognition (NOR), Y-maze, and Passive Avoidance (PAT) behavioral paradigms in Ctrl and Diabetic (DM) male (M) and female (F) rats pre- and post-stroke (S) via 60 min. middle cerebral artery occlusion (MCAO). We tested the PAT paradigm with a multi-trial method where the animals were habituated to the dark/light chambers without foot shock and then trained in 3 trials where they received foot shock upon entering the dark. We then tested retention following MCAO for their memory of foot shock 2 weeks prior. Multitrial results suggested that there was no difference between groups in learning to associate the dark chamber with the shock, so we revised the multitrial method into a single-trial method for ongoing retention tests to compare the impact of stroke on shock memory recall. PAT revealed (Table 1) disease- and sex-dependent responses to aversive stimulus. NOR revealed that M-DM-S and F-DM-S rats have decreased exploration time, suggesting that they are unmotivated or depressed. Y-maze indicated that males displayed spatial memory recovery, while females remained impaired. In summary, we have observed numerous sex- and disease-dependent post-stroke outcomes with standard behavioral paradigms, causing us to carefully consider how we evaluate preclinical outcomes.

scholarly journals Impact of Key Nicotinic AChR Subunits on Post-Stroke Pneumococcal Pneumonia

Vaccines ◽  
2020 ◽  
Vol 8 (2) ◽  
pp. 253
Author(s):  
Sandra Jagdmann ◽  
Claudia Dames ◽  
Daniel Berchtold ◽  
Katarzyna Winek ◽  
Luis Weitbrecht ◽  
...  
Keyword(s):  
Artery Occlusion ◽  
Experimental Stroke ◽  
Medical Complication ◽  
Α7 Nicotinic Acetylcholine Receptor ◽  
Post Stroke ◽  
Cholinergic Signaling ◽  
Cerebral Artery Occlusion ◽  
Pathogen Clearance ◽  
The Impact ◽  
Alveolar Capillary

Pneumonia is the most frequent severe medical complication after stroke. An overactivation of the cholinergic signaling after stroke contributes to immunosuppression and the development of spontaneous pneumonia caused by Gram-negative pathogens. The α7 nicotinic acetylcholine receptor (α7nAChR) has already been identified as an important mediator of the anti-inflammatory pathway after stroke. However, whether the α2, α5 and α9/10 nAChR expressed in the lung also play a role in suppression of pulmonary innate immunity after stroke is unknown. In the present study, we investigate the impact of various nAChRs on aspiration-induced pneumonia after stroke. Therefore, α2, α5, α7 and α9/10 nAChR knockout (KO) mice and wild type (WT) littermates were infected with Streptococcus pneumoniae (S. pneumoniae) three days after middle cerebral artery occlusion (MCAo). One day after infection pathogen clearance, cellularity in lung and spleen, cytokine secretion in bronchoalveolar lavage (BAL) and alveolar-capillary barrier were investigated. Here, we found that deficiency of various nAChRs does not contribute to an enhanced clearance of a Gram-positive pathogen causing post-stroke pneumonia in mice. In conclusion, these findings suggest that a single nAChR is not sufficient to mediate the impaired pulmonary defense against S. pneumoniae after experimental stroke.

scholarly journals Impaired meningeal lymphatic vessel development worsens stroke outcome

2019 ◽  
Vol 40 (2) ◽  
pp. 263-275 ◽  
Author(s):  
Pavel Yanev ◽  
Katherine Poinsatte ◽  
Devon Hominick ◽  
Noor Khurana ◽  
Kielen R Zuurbier ◽  
...  
Keyword(s):  
Lymphatic Vessels ◽  
Growth Factor Receptor ◽  
Young Male ◽  
Artery Occlusion ◽  
Stroke Outcomes ◽  
Post Stroke ◽  
Sagittal Sinus ◽  
The Central Nervous System ◽  
Vessel Development ◽  
The Impact

The discovery of meningeal lymphatic vessels (LVs) has sparked interest in identifying their role in diseases of the central nervous system. Similar to peripheral LVs, meningeal LVs depend on vascular endothelial growth factor receptor-3 (VEGFR3) signaling for development. Here we characterize the effect of stroke on meningeal LVs, and the impact of meningeal lymphatic hypoplasia on post-stroke outcomes. We show that photothrombosis (PT), but not transient middle cerebral artery occlusion (tMCAo), induces meningeal lymphangiogenesis in young male C57Bl/J6 mice. We also show that Vegfr3wt/mut mice develop significantly fewer meningeal LVs than Vegfr3wt/wt mice. Again, meningeal lymphangiogenesis occurs in the alymphatic zone lateral to the sagittal sinus only after PT-induced stroke in Vegfr3wt/wt mice. Interestingly, Vegfr3wt/mut mice develop larger stroke volumes than Vegfr3wt/wt mice after tMCAo, but not after PT. Our results reveal differences between PT and tMCAo models of stroke and underscore the need to consider method of stroke induction when investigating the role of meningeal lymphatics. Taken together, our data indicate that ischemic injury can induce the growth of meningeal LVs and that the absence of these LVs can impact post-stroke outcomes.

Abstract 3133: Impact of Post-stroke Isolation on Stroke Outcome

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Venugopal R Venna ◽  
Yan Xu ◽  
Jun Li ◽  
Fudong Liu ◽  
Louise D McCullough
Keyword(s):  
Infarct Size ◽  
Functional Recovery ◽  
Forced Swim Test ◽  
Statistical Significance ◽  
Experimental Studies ◽  
Stroke Recovery ◽  
Stroke Outcome ◽  
Post Stroke ◽  
The Impact

Background: Psychosocial factors are increasingly accepted as critical factors in post-stroke recovery, mortality and morbidity. Although, emerging data from clinical and population based studies support the role of social support in improved functional recovery and reducing the risk of mortality, to date no experimental studies have investigated such effects in post-stroke animal models. The aim of this study is to investigate for the impact of post stroke housing and the effects of long-term social isolation and pair housing with either a healthy or a stroked partner, and explored for the mechanisms. Methods: Male mice (20-25g; C57BL/6N, Charles River Labs), all initially pair housed, were subjected to right middle cerebral artery occlusion (MCAO - 60min) and then randomly assigned to a specific housing condition - isolated, paired with a stroke partner or paired with a healthy partner. Infarct size was quantified with TTC 72h after stroke (n=8/grp). We then investigated the effects of housing on long-term functional recovery using corner test, cylinder test, forced swim test (FST) and tail suspension test (TST). We further explored the mechanisms underlying the improved behavioral recovery by injecting BrDU 150mg/kg/day i.p. for 5 days starting from day 3 post-stroke (n=8/grp), and assessing changes in BDNF levels by western-blot analysis (n=4/grp). Data were expressed as mean±sem. Two-way ANOVA was performed and P value < .05 was set for statistical significance. Results: Post-stroke housing conditions can significantly impact infarct size; we observed that mice isolated after stroke had increased infarct volume compared to pair housed mice in all three brain regions (Cortex: 63.2±2.5 vs 40.0±6.2; p<0.01); (Striatum: 86.6±2.2 vs 67.7±2.9; p<0.01); (Total: 60.9±1.3 vs 32.6±4.3; p<0.01). Although post-stroke housing with healthy vs a stroked partner did not influenced infarct size (p>0.05), animals pair housed with healthy partner showed a significantly improved functional recovery by as early as day 15 in the cylinder and corner tests (p<0.05). Increased mobility was observed in FST and TST in PH mice compared to SI mice at day 90 (p<0.05). Consistently, housing with a healthy partner increased BrDU positive cells (p<0.05) and enhanced BDNF expression compared to other cohorts (SI 1±0.1; PH with stroke partner 1.9±0.2; PH with healthy partner 2.6±0.1; n=4/grp), no changes were seen in sham mice. Conclusions: Post-stroke housing has an important impact on stroke outcome; isolation has a detrimental effect on infarct size compared to pair housed cohorts. Interestingly, independent of infarct size, housing with a healthy partner hastened recovery compared to those stroke mice housed with partner that had also been subjected to stroke. Molecular analysis indicates the involvement of BDNF and neurogenesis may be important regulators of post-stroke housing induced functional recovery.

Prolonged release of VEGF and Ang1 from intralesionally implanted hydrogel promotes perilesional vascularization and functional recovery after experimental ischemic stroke

2022 ◽  
pp. 0271678X2110699
Author(s):  
Pavel Yanev ◽  
Geralda AF van Tilborg ◽  
Annette van der Toorn ◽  
Xiangmei Kong ◽  
Ann M Stowe ◽  
...  
Keyword(s):  
Functional Recovery ◽  
Release Kinetics ◽  
Chronic Phase ◽  
Stroke Recovery ◽  
Intralesional Injection ◽  
Prolonged Release ◽  
Post Stroke ◽  
In Situ Forming

Injectable hydrogels can generate and support pro-repair environments in injured tissue. Here we used a slow-releasing drug carrying in situ-forming hydrogel to promote post-stroke recovery in a rat model. Release kinetics were measured in vitro and in vivo with MRI, using gadolinium-labeled albumin (Galbumin), which demonstrated prolonged release over multiple weeks. Subsequently, this hydrogel was used for long-term delivery of vascular endothelial growth factor (VEGF) and angiopoietin-1 (Ang1) (Gel VEGF + Ang1, n = 14), in a photothrombotically induced cortical stroke lesion in rats. Control stroke animals were intralesionally injected with saline (Saline, n = 10), non-loaded gel (Gel, n = 10), or a single bolus of VEGF + Ang1 in saline (Saline VEGF + Ang1, n = 10). MRI was executed to guide hydrogel injection. Functional recovery was assessed with sensorimotor function tests, while tissue status and vascularization were monitored by serial in vivo MRI. Significant recovery from sensorimotor deficits from day 28 onwards was only measured in the Gel VEGF + Ang1 group. This was accompanied by significantly increased vascularization in the perilesional cortex. Histology confirmed (re)vascularization and neuronal sparing in perilesional areas. In conclusion, intralesional injection of in situ-forming hydrogel loaded with pro-angiogenic factors can support prolonged brain tissue regeneration and promote functional recovery in the chronic phase post-stroke.

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