GreenSaxo

Recurrent mild SARS-CoV-2 infection affects the lung-brain axis in wild type and Alzheimer’s mice 🚨New mouse study: two mild COVID infections (ancestral then Omicron) quietly damage hippocampal synapses and worsen amyloid plaques in Alzheimer’s models, no brain virus, no microglial activation. Lung–brain axis in action! 🚨Interesting BELGIUM study, that sparked broad MSM coverage, and that’s unique!🤔 ➡️“Even mild corona infections can leave traces in the brain: Ghent researchers discover possible link with Alzheimer's" ➡️Let’s dig into the study: - Mice received sequential mild intranasal infections: ancestral SARS-CoV-2 (10 PFU) followed 14 days later by Omicron BA.1 (7000 PFU), - Lungs showed detectable virus after each exposure, no viral RNA was found in brain (cortex/hippocampus) at the final time point (day 28), - Disease remained sublethal with low systemic/brain cytokine responses, - Two weeks after the second infection, microglia (IBA1) and astrocytes (GFAP) showed no significant changes in number, density, or reactivity in hippocampus or cortex of either genotype, - Hippocampal synaptic integrity was reduced (lower SYP+ presynaptic and SYP/PSD-95 colocalized puncta), most clearly in the Alzheimer’s disease model mice(AD mice), no neuronal loss (NeuN) was observed, - In AD mice only, repeated infection increased hippocampal Aβ plaque number (with area trend) and cortical insoluble Aβ1-40/1-42 levels. Soluble Aβ and microglial plaque association/phagocytosis were largely unchanged, - Effects appear mediated indirectly via the lung–brain axis rather than direct CNS infection. ➡️Attention: THIS STUDY IS EXPLICITLY A REINFECTION MODEL! ‼️So, even mild, repeated SARS-CoV-2 infections leave a measurable footprint on the brain, eroding hippocampal synapses and accelerating amyloid pathology in susceptible hosts, without triggering detectable neuroinflammation. And indeed, this study adds further experimental support to the idea that repeated SARSCOV2 exposures can produce lasting, subtle CNS effects relevant to longC0VID “brain fog,” cognitive complaints, and possible accelerated neurodegenerative risk. The absence of overt gliosis suggests the damage can be stealthy and cumulative rather than driven by classic neuroinflammation. For people with genetic or early Alzheimer’s risk, or those experiencing successive infections, the findings underscore the value of monitoring cognitive trajectories and considering cumulative viral burden as a potential modifier of brain health. It does not yet prove causation in humans but strengthens without any doubt the biological rationale for taking mild reinfections seriously! #AvoidSars2 #AvoidReinfections link.springer.com/article/10… hln.be/gent/zelfs-milde-coro…

Pulmonary vascular abnormalities in Long COVID: a radiological perspective 🚨Your CT is ‘normal,’ yet you’re still breathless months after COVID. New review shows hidden microvascular damage (perfusion defects, vessel pruning, gas-transfer defects) that standard scans miss, explaining LongC0VID symptoms that routine imaging miss! ➡️Interesting new narrative review from India shifts the focus of LongC0VID from parenchymal lung damage to a distinct pulmonary vascular phenotype! REMEMBER SARSCOV2 is basically a VASCULAR VIRUS! ➡️Core mechanisms: - SARSCoV2 enters endothelial cells via ACE2 receptors, triggering endotheliitis that creates a pro-coagulant environment and promotes the formation of in-situ microthrombi, - This is amplified by immunothrombosis (driven by neutrophil extracellular traps) and the generation of amyloid-like fibrin microclots that resist normal breakdown, - Over time, the vasculature undergoes maladaptive remodelling, including intussusceptive angiogenesis and progressive “pruning” of small vessels, which reduces the available surface area for gas exchange, ➡️Conventional CT pulmonary/angiography frequently appears normal or near-normal and misses microvascular disease, ➡️Advanced imaging uncovers the pathology: 1. Dual-energy CT (DECT) detects persistent wedge-shaped perfusion defects in otherwise normal lung tissue, seen in 36–60% of symptomatic patients and still present in 36.3% at roughly 3 months, 2. Quantitative CT shows reduced small-vessel volume (PBV5), which correlates with lower DLCO and poorer exercise tolerance, 3. Hyperpolarized xenon-129 MRI reveals a hallmark gas-transfer defect, impaired alveolar-to-RBC gas exchange, even when standard CT and pulmonary function tests appear normal, 4. V/Q SPECT and PREFUL MRI demonstrate mottled perfusion patterns consistent with diffuse small-vessel disease, ➡️Findings correlate with ongoing dyspnoea, fatigue, and reduced exercise capacity, ➡️Higher (admission) D-dimer/CRP often predict later defects, ➡️2025 RSNA/STR/ESTI consensus guidelines recommend imaging at 3 months with paired inspiratory/expiratory protocols and the term “Post-COVID-19 Residual Lung Abnormality.” ‼️So, AGAIN, routine CT scans can look reassuring while the pulmonary microvasculature remains structurally and functionally damaged, directly accounting for persistent breathlessness and fatigue in a substantial subset of LongC0VID patients. ‼️The proposed framework matters clinically every day: many patients with ongoing dyspnoea or exercise intolerance after COVID have occult vascular injury that conventional imaging and basic Pulmonary Function Tests(PFTs) fail to detect. Recognizing the vascular phenotype guides use of functional/quantitative techniques (DECT, xenon MRI, etc.), supports standardized 3-month imaging protocols, and should shift management toward vascular rather than purely parenchymal explanations. It also helps differentiate vascular from airway-related causes of symptoms and UNDERSCORES the public-health scale of residual impairment in survivors! REMINDER AGAIN, COVID-19(SARSCOV2) is basically a VASCULAR INFECTION! #AvoidSars2 #AvoidReinfections #Mitigation link.springer.com/article/10…