July 16, 24:06

New autopsy suggests Alzheimer's medications fail due to uneven action in the brain

An unprecedented analysis conducted on a human brain after death suggested that aducanumab, an experimental drug intended for the treatment of Alzheimer's disease, failed to exert its function homogeneously across all brain areas.

Study and Methodology

The research, published last Sunday (12) in the journal JAMA, was based on the post-mortem examination of an individual who received the treatment for a period of 4.5 years. Scientists from the University of Pennsylvania, located in the United States, conducted the study by comparing brain images and analyses before and after therapy, using the case of a patient with mild cognitive impairment who participated in a clinical trial.

The findings revealed that certain brain regions showed a decrease in beta-amyloid plaques and a reduction in tau protein accumulation, while other areas maintained signs associated with the progression of Alzheimer's disease. This finding helps explain the inconsistency of results observed in patients treated with drugs targeting these structures.

The studied case was notable for allowing the observation, within the same brain, of areas that responded to the drug and others that did not show the same effect. This disparity provided researchers with an unusual opportunity to evaluate how the elimination of beta-amyloid protein correlates with other modifications related to the pathology. The patient received 30 doses of aducanumab over four and a half years. After his death, four years after the last application, his family authorized the donation of the brain for scientific purposes, which was then compared with brains of people with dementia who did not receive the medication.

Observed Brain Patterns

The evaluation performed after death demonstrated that the outermost layers of the brain had fewer beta-amyloid plaques, while more internal regions of the cortex still contained a significant amount of this material. For the researchers, this pattern indicates that the drug may not have reached all necessary locations to generate a comprehensive effect. According to the responsible scientists, the areas with lower concentrations of beta-amyloid also exhibited fewer tau tangles and less brain tissue loss, strengthening the idea that plaque removal can influence the advancement of other neuronal degenerative processes.

Edward Lee, a neuropathologist at the University of Pennsylvania and one of the researchers, commented that the case represented a rare situation where some regions eliminated amyloid and others did not, allowing for a direct comparison of what occurred in adjacent areas and improving the understanding of the link between amyloid, tau, and neurodegeneration. David Wolk, a neurologist and director of the University of Pennsylvania's Alzheimer's Disease Research Center, stated that the simultaneous visualization of these different patterns in the same brain provided crucial evidence about the impact of anti-beta-amyloid therapies. Wolk declared that the findings offer some of the clearest human evidence to date that anti-amyloid therapies can restrict tau accumulation and delay brain changes that lead to memory loss and cognitive decline.

Limitations and Treatment Context

Despite the positive signs in this specific case, the researchers themselves warn that it is only one patient. They emphasize that Alzheimer's shows great variation among individuals, and a single autopsy is not sufficient to define the overall efficacy of any therapeutic strategy. Aducanumab had already generated controversy before this analysis; in 2021, the U.S. drug regulatory agency approved the treatment on an accelerated basis, a decision criticized for being based on considered limited results. Later, in 2024, the manufacturer Biogen suspended the production of the drug to focus resources on other Alzheimer's-related initiatives.

The discussion about the role of beta-amyloid plaques remains polarized among experts. While some argue that eliminating this protein in early stages can reduce future damage, others maintain that it may only be a consequence of the disease, not the primary cause of cognitive decline. A review that included 17 clinical trials and over 20,000 participants, cited in the study, indicated that anti-beta-amyloid drugs showed no clinically relevant benefits in people with mild cognitive impairment or mild Alzheimer's dementia.

Christopher Brown, a neurologist and lead author of the research, did not rule out the possibility of beta-amyloid remaining a relevant target. The hypothesis raised by the study is that the timing of treatment initiation may be decisive, given that this protein can appear in the brain many years before symptoms appear. Brown assessed that this case suggests that removing amyloid early can help limit changes that harm brain cells. Future studies will need to confirm whether interventions initiated before the onset of symptoms can generate more pronounced effects, while this patient's brain analysis remains important data for understanding why certain treatments affect some brain regions and fail in others.

noticiasaominuto.comJuly 15, 21:19

Study strengthens link between Epstein-Barr virus and multiple sclerosis

A new study deepens the understanding of the immunological mechanisms underlying the link between the Epstein-Barr virus (EBV) and multiple sclerosis, providing critically important data for the development of future vaccines.

Details of the New Study

The details of this study were published in the journal 'Science Translational Medicine'. The work was led by Kjetil Bjornvik from Harvard School of Public Health (USA), who also participated in the 2022 study previously published by the agency EFE.

Previous Findings and Current Challenges

The initial study, published in the same journal, established a correlation between EBV infection and an increased risk of developing multiple sclerosis. This early analysis was based on long-term observation of millions of US military participants over twenty years.

Despite the significance of these results, experts believe that the development of the disease is caused by a combination of genetic and environmental factors, rather than a single cause. Furthermore, scientists still face the complex task of understanding why only a small portion of the population develops multiple sclerosis, given that over 95% of the adult population is already infected with EBV.

Immune Response Mechanisms

This new research is one of the first to clarify potential immunological pathways linking the virus and multiple sclerosis, offering a fundamental basis for creating antiviral drugs and vaccines. Multiple sclerosis is defined as an inflammatory autoimmune disease of the central nervous system, which is the main cause of neurological disability in young adults.

Although later works, including the one from 2022, point to a 'consistent association' with EBV, present in almost all patients, other experiments highlight CD4+ T-cells (key immune white blood cells) as an important factor. However, scientists emphasize the need for further investigation to accurately determine the mechanisms before developing therapeutic agents.

Analysis of Cellular Reactions

As part of the new study, scientists conducted a comprehensive analysis of CD4+ T-cells in multiple sclerosis patients. They found that these cells were attracted by various components of target viral particles, specifically late lytic capsid antigens (structural proteins forming the protective shell of a virus such as Epstein-Barr) and glycoprotein (molecules consisting of protein chains linked to carbohydrates).

The reactions of these T-cells were twice as strong in patients with untreated multiple sclerosis compared to healthy controls, indicating a link to the biology of the disease. The team also found that therapy aimed at reducing B-cells using anti-CD20 antibodies decreased the mentioned viral T-cell responses by 2.5 times in two groups of patients (a total of 69 people) and almost completely eliminated viral spread in saliva.

Authors' Conclusion

The study authors conclude that by identifying a easily measurable and peripherally accessible immune response associated with the disease, this work lays the foundation for the rational design and monitoring of vaccines and antiviral agents aimed at combating the illness.

noticiasaominuto.comJuly 15, 21:14

Woman contracts corneal parasite infection after contact with soil while wearing contact lenses

Emma Marsden's life changed on February 28th due to an accident that occurred while working with horses. The 47-year-old woman fell headfirst into a trough containing a mixture of water and dirt. After this, she washed her face and hands to remove the grime, but left her contact lenses in.

Diagnosis of the vision problem

According to the British newspaper The Mirror, four days after the incident, Emma began experiencing severe pain in her right eye. She went to the hospital, where doctors initially suspected an ulcer, prescribed eye drops, and sent her home.

However, the problem and pain persisted until Emma lost vision in her right eye. During a subsequent appointment on March 7th, she was diagnosed with keratitis caused by Acanthamoeba—an infection triggered by a parasite that settled in the cornea.

Cause and consequences of the infection

Emma Marsden was told that the cause of this situation was washing her face while continuing to wear contact lenses. The parasite 'ate away' at the cornea, and the British woman's eye became gray and cloudy. There is a risk that Emma may permanently lose sight in her right eye, which The Mirror described as a 'heartbreaking' situation.

Doctors performed eyelid sutures on the affected eye to begin the recovery process. However, in the future, Marsden may face the need for a corneal transplant. Because of this, she appeals to all contact lens users to handle them carefully and properly.