Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Sunday, November 2, 2025

Bridging Social Isolation, Loneliness, and Brain Aging: A Narrative Review of Mechanisms and Translational Interventions

You competent? doctor will prevent social isolation by having EXACT 100% RECOVERY PROCOVERY PROTOCOLS!  Hasn't done that, your doctor, hospital and board of directors are totally fucking incompetent! They have all known of the shitshow of stroke rehab ever since medical school. DOING NOTHING is your precise definition of incompetence! There are NO excuses!

Bridging Social Isolation, Loneliness, and Brain Aging: A Narrative Review of Mechanisms and Translational Interventions


https://doi.org/10.1016/j.neubiorev.2025.106451Get rights and content

Highlights

  • SIL contributes to cognitive decline and increased dementia risk in aging
  • Cross-species studies reveal neural and behavioral effects of SIL in aging
  • Novel intervention strategies may mitigate SIL-related brain health impairments
  • Enhancing cognitive control may help disrupt the SIL–cognitive impairment cycle
  • Social status may shape vulnerability and intervention outcomes in SIL

Abstract

Social isolation and loneliness (SIL) are increasingly recognized as potent determinants of cognitive decline in aging and Alzheimer’s disease–related dementias (ADRD). Yet, despite their prevalence, the neurobiological pathways through which SIL accelerates brain aging remain incompletely understood, and effective interventions are scarce. This narrative review synthesizes human and animal research to present a translational framework linking SIL to brain aging across cognitive-affective, socio-behavioral, physiological, and neural domains. Converging evidence indicates that SIL and cognitive impairment constitute a self-reinforcing loop: isolation amplifies age-related deficits in cognitive control, emotional regulation, and stress resilience, while these impairments heighten social threat sensitivity and blunt social reward, perpetuating isolation. Cross-species findings implicate interconnected neural networks, including the prefrontal and insular cortices, hippocampus, and associated reward and stress-regulatory systems, as critical hubs mediating this loop. Large-scale human neuroimaging consortia reveal convergent neural signatures of SIL within these networks, supported by mechanistic findings from animal models that identify shared molecular cascades involving neuroinflammation, glucocorticoid imbalance, myelin disruption, and dysregulated oxytocin and dopaminergic signaling. Importantly, evidence from animal resocialization paradigms and human multimodal interventions demonstrates that SIL-related neural and behavioral alterations are partially reversible, highlighting enduring plasticity in the aging brain. Together, these findings define SIL and cognitive decline as a dynamic, mutually reinforcing cycle that accelerates brain aging through convergent molecular and circuit mechanisms. Targeting these pathways, by enhancing cognitive control, modulating reward systems, reducing stress reactivity, and strengthening social connectedness, offers a promising translational route to preserve resilience and cognitive vitality across the lifespan.

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