A groundbreaking study from the United Kingdom has shed new light on a lesser-known variant of Alzheimer’s disease that primarily affects vision rather than memory. The variant, known as posterior cortical atrophy (PCA), can cause patients to experience significant visual difficulties even before any noticeable memory loss occurs.
While the classic form of Alzheimer’s disease is known for progressive memory deterioration, PCA presents a different and often misunderstood set of symptoms. It typically begins between the ages of 50 and 60, targeting the posterior regions of the brain responsible for visual processing. Patients with PCA often struggle to understand what they see, misinterpreting distances, losing their place while reading, or having difficulty recognizing familiar faces or places.
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Researchers at the Queen Square Institute of Neurology at University College London (UCL), led by Dr. Zeinab Abdi, examined the brains of patients diagnosed with PCA and compared them with individuals affected by typical Alzheimer’s disease. The findings, published in the journal Neuropathology and Applied Neurobiology, highlight crucial differences in how two key proteins associated with Alzheimer’s—tau and amyloid—accumulate in different regions of the brain.
In PCA cases, tau and amyloid proteins were predominantly found in the parietal lobe, which is integral to visual processing. In contrast, in typical Alzheimer’s patients, these proteins accumulated primarily in the temporal lobe—an area linked with memory. These insights help explain why patients with PCA suffer from vision-related symptoms first, while others develop memory issues.
Tau proteins, when abnormally clustered, can form tangles that impair neuronal function. Amyloid proteins, on the other hand, form plaques that interfere with communication between brain cells. In PCA, these proteins build up in regions involved in interpreting sensory input, causing disruptions in how the brain processes what the eyes see.
The research also explored the role of microglia—immune cells in the brain responsible for responding to inflammation. Increased microglial activity was observed in the parietal regions of PCA patients, suggesting that neuroinflammation could be contributing to the degeneration of vision-related brain areas. In contrast, microglial activity was lower in memory-related areas in typical Alzheimer’s patients, although tau build-up was more significant in those regions.
According to Dr. Abdi, these findings emphasize the importance of personalized approaches to Alzheimer’s treatment. “As we move toward disease-modifying therapies, understanding the unique pathological signatures of each form of Alzheimer’s becomes critical,” she said. “The hope is to develop more targeted treatments that address each patient’s specific symptoms—whether they’re memory-related or visual.”
The study further underscores the need for early and accurate diagnosis. Identifying which areas of the brain are affected early on could allow doctors to tailor interventions and delay symptom progression. For example, visual training therapies or anti-inflammatory treatments targeting specific brain areas may be more effective for PCA patients than general Alzheimer’s therapies.
Additionally, these results support a growing consensus that Alzheimer’s is not a one-size-fits-all disease. Instead, it comprises various subtypes, each with distinct symptoms, biological markers, and treatment needs.
Looking ahead, the researchers aim to investigate why different areas of the brain are more vulnerable to certain proteins. This could lead to a deeper understanding of Alzheimer’s subtypes and, ultimately, better outcomes for patients.
In summary, this UK study offers vital clues into how the distribution of harmful proteins and inflammation in the brain shapes the symptoms of Alzheimer’s disease. It paves the way for more precise diagnoses and individualized therapies that go beyond treating memory loss—ushering in a new era of targeted Alzheimer’s care.
This article is originally published on infobae.
