German Study Finds That Just SARS-CoV-2 Spike Protein Alone Can Trigger Brain Damage Similar to Parkinsons
Nikhil Prasad Fact checked by:Thailand Medical News Team May 25, 2025 1 month, 2 weeks, 4 days, 20 hours, 40 minutes ago
Medical News: A shocking new study by German scientists from the University of Veterinary Medicine Hannover and the Center for Systems Neuroscience Hannover has revealed that the spike protein of SARS-CoV-2, the virus that causes COVID-19, may directly cause brain inflammation and trigger pathological changes in brain regions commonly affected by Parkinson’s disease—even in the absence of actual viral infection.
German Study Finds That Just SARS-CoV-2 Spike Protein Alone Can Trigger Brain Damage Similar to Parkinsons
The research, led by Dr. Cara Sophie Schreiber, Lucas Navarro Ramil, Juliette Bieligk, Robert Meineke, Dr. Christopher Käufer, and Dr. Franziska Richter, examined how the spike protein’s S1 subunit affects the brain when introduced into the body through different routes—intranasally (via the nose), intravenously (into the bloodstream), or directly into the brain (intracerebral injection). This
Medical News report reveals the alarming extent to which the spike protein alone, detached from the whole virus, can wreak havoc on the central nervous system.
Spike Protein Triggers Parkinsons-Like Brain Changes
The team injected mice with purified S1 spike protein and studied its effects over a two-week period. They focused on brain areas involved in emotion, cognition, memory, and motor control—regions that are often damaged in Parkinson’s disease and Long COVID sufferers. Remarkably, the spike protein alone was enough to increase inflammation in the brain and disrupt crucial proteins like alpha-synuclein (aSyn), a key player in Parkinson’s pathology.
One of the most alarming findings was that intravenous injection of the spike protein caused a significant increase in alpha-synuclein accumulation in regions such as the caudate putamen and hippocampus. This protein, when it clumps abnormally, is the hallmark of Parkinson’s disease. Researchers also found elevated levels of the phosphorylated form of alpha-synuclein (pS129), which is a toxic variant associated with neurodegenerative diseases. These changes occurred without the virus itself ever entering the brain.
Inflammation and Brain Circuit Disruption Without Infection
Besides protein aggregation, the study documented significant neuroinflammation. Both microglia (immune cells of the brain) and astrocytes (supportive brain cells) became hyperactivated, especially after intravenous administration. The team noted sex-dependent differences in response—female mice often exhibited more pronounced changes in certain brain regions like the hippocampus and substantia nigra, while males showed a greater increase in pS129 levels, especially after direct brain exposure.
Importantly, the spike protein also disrupted inhibitory neuronal circuits, particularly in parvalbumin-positive interneurons, which are crucial for balancing brain activity. These disruptions were route- and sex-dependent and could explain cognitive and emotional disturbances observed in Long COVID patients.
Alterations in Key Receptors and Blood Cytokines
The researchers also measured changes in the brain's expression of ACE2 and Neuropilin-1 receptors—both used by the virus to enter cells. They found significant sex- and route-dependent differences in receptor levels, potentially affecting how the brain responds to future viral exposure or even mRNA-based vaccines.
Furthermore, the study uncovered shifts in blood cytokine levels—molecules that mediate immune responses—highlighting systemic inflammation that may link to the central nervous system's pathology. For example, IL-10 (an anti-inflammatory cytokine) was increased while IP-10 (an interferon-induced chemokine) decreased in certain groups, supporting the idea that the spike protein can drive immune imbalance.
Conclusions and Implications
This study demonstrates, for the first time with this level of detail, that the spike protein alone—absent of full viral particles—can cause long-lasting and region-specific brain damage in mice. The effects mimic early features of Parkinson’s disease and Long COVID, including inflammation, altered brain circuits, and abnormal protein accumulation. This supports the hypothesis that viral proteins persisting in tissue may contribute to the long-term neurological symptoms reported in many COVID-19 survivors.
These findings also raise serious questions about spike protein exposure through infection and possibly vaccination, although the study dose used in mice was significantly higher than post-vaccination levels in humans. Still, the results underscore the need for further research into long-term neurological risks tied to spike protein presence in the body.
The study findings were published in the peer reviewed journal: Brain Behavior and Immunity.
https://www.sciencedirect.com/science/article/pii/S0889159125001977
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https://www.thailandmedical.news/news/alarming-rise-in-brain-degeneration-risks-after-covid-19-infection-sparks-global-medical-alert
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https://www.thailandmedical.news/news/covid-19-virus-found-to-disrupt-key-brain-protein-tdp-43-in-a-manner-similarly-seen-in-alzheimer-and-als-like-diseases
https://www.thailandmedical.news/articles/coronavirus
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