Post-viral myocarditis evolves from direct viral damage to autoimmune-driven fibrosis, with imaging revealing lasting heart injury and guiding prognosis.| David Lingenfelter, PhD
SARS-CoV-2 leaves lasting epigenetic changes in lung cells, impairing repair and surfactant function—driving chronic inflammation, fibrosis, and long-term vulnerability.| David Lingenfelter, PhD
Long COVID stems from persistent SARS-CoV-2 reservoirs causing chronic T-cell exhaustion and dysfunction, leading to inflammation, autoimmunity, fatigue, & impaired immunity, driving diverse symptoms.| davidlingenfelter.substack.com
Long COVID is driven by neuroinflammation, autoimmunity, viral persistence, and vascular injury—requiring stratified, multi-modal, and precision-targeted therapies for effective treatment.| davidlingenfelter.substack.com
This is a guide for researchers on how to partner with an AI assistant, shifting their role from data gatherer to strategic analyst.| David Lingenfelter, PhD
Post-COVID cognitive deficits—especially in executive function and processing speed—can persist or worsen, driven by neuroinflammation and brain network damage, raising dementia risk.| davidlingenfelter.substack.com
Neuro-PASC arises from genetic and environmental vulnerabilities, triggered by COVID-19, leading to blood-brain barrier disruption and chronic immune dysregulation.| davidlingenfelter.substack.com
SARS-CoV-2 may trigger or accelerate neurodegeneration via inflammation, protein misfolding, and persistent viral antigens—suggesting a “slow burn” pathology akin to Alzheimer’s and Parkinson’s.| David Lingenfelter, PhD
Long COVID brain fog arises from two synergistic pathologies: a leaky blood-brain barrier and persistent microthrombosis, causing chronic inflammation and cerebral hypoperfusion.| davidlingenfelter.substack.com
COVID-19 is a systemic disease driven by ACE2 disruption, cytokine storms, and endotheliitis—causing multi-organ damage and laying the groundwork for Long COVID.| David Lingenfelter, PhD
Long COVID causes lasting glial dysfunction via chronic neuroinflammation and epigenetic reprogramming, disrupting brain support systems and impairing cognition, mood, and neural repair.| David Lingenfelter, PhD
Long COVID’s neurological symptoms stem from systemic inflammation, BBB disruption, glial activation, and microvascular damage—often diverging into cognitive or autoimmune motor phenotypes.| David Lingenfelter, PhD
Controlled opposition preserves power by simulating dissent, managing narratives, and infiltrating movements. Recognizing its tactics is vital to resist manipulation and protect authentic civic engage| David Lingenfelter, PhD
Prior COVID-19 infection increases risk of musculoskeletal injuries via inflammation, muscle loss, bone fragility, neurological deficits, and prolonged inactivity.| David Lingenfelter, PhD
SARS-CoV-2 triggers chronic inflammation and fibrosis, degrading muscle biomechanics and increasing injury risk—demanding cautious, tissue-aware rehab protocols.| David Lingenfelter, PhD
Acute IL-6 and TNF-α surges in COVID-19 reprogram muscle, bone, and joint cells, triggering chronic inflammation, fibrosis, and impaired repair—driving long-term musculoskeletal decline.| David Lingenfelter, PhD
SARS-CoV-2 causes lasting musculoskeletal damage mainly via systemic inflammation, not direct infection—triggering muscle atrophy, bone loss, and connective tissue fibrosis.| David Lingenfelter, PhD
Long COVID myopathy stems from SARS-CoV-2-induced mitochondrial dysfunction, causing fatigue, poor muscle recovery, and injury risk—demanding a shift in clinical understanding and treatment.| David Lingenfelter, PhD
MKULTRA failed to achieve mind control but left a legacy of torture, ethical collapse, and public distrust—proof of the dangers of unchecked state power.| David Lingenfelter, PhD
Operation Gladio exposed NATO’s covert stay-behind armies, revealing state-sponsored terror and deep-state manipulation to suppress leftist movements and erode democratic trust.| David Lingenfelter, PhD
SARS-CoV-2 has a unique S1/S2 furin site, but also shares a conserved S2' site with bat and pangolin viruses—key for infectivity and a target for broad-spectrum vaccines.| davidlingenfelter.substack.com
Click to read David Lingenfelter, PhD, a Substack publication with hundreds of subscribers.| davidlingenfelter.substack.com
SARS-CoV-2 leaves lasting epigenetic changes that may dysregulate immunity, increasing reinfection and long COVID risk, though effects vary and IL-6 blockade may offer protection.| davidlingenfelter.substack.com