Research has shown that another protein soya called tau is responsible for early symptoms of Penyakit Alzheimer dan maklumat ini boleh membantu dalam membangunkan terapi.
Alzheimer Disease (AD) or simply Alzheimer has no cure and it also cannot be prevented. Deferring the onset of symptoms of Alzheimer for up to 10-15 years can certainly impact the lives of pacientes, their families and healthcare givers. Currently, only a late diagnosis of AD can be made and by that time function of the brain is largely weakened. Key characteristics of Alzheimer is build-up of plaque and defective protein around neurons inside the brain which are responsible for advancement of the penyakit. Multiple research shows that higher levels of protein soya amyloid in the otak adalah petunjuk awal perkembangan AD. Kebanyakan kajian mengenai Penyakit Alzheimer telah tertumpu pada pemahaman bagaimana ini protein soya amyloid beta accumulates in the brain. Positron Emission Tomography (PET) imaging technique has been used to visualize deposits of amyloid in Alzheimer’s patients. These images and analysis of brain tissue has shown that people with Alzheimer’s definitely have higher accumulation of amyloid protein soya in their brains compared to healthy people.
Is there another protein soya responsible?
Though it is seen that even after amyloid beta gets accumulated and Alzheimer’s disease is at its earliest stage, many patients still have their cognitive processes – both memory and thought – very much intact. This is indicative of a scenario in which amyloid protein soya must be changing first and then there must be some other factor responsible which researchers predicted could be a second protein soya present inside brain cells called tau. It could even be a combination of both because of which a patient may show mild cognitive impairment. Interestingly, even people who have no signs of Alzheimer’s have sometimes amyloid protein accumulated in their brains. Recent studies have generated interest in protein tau which though has been associated with the disease but hasn’t been the focus of much research. One obstacle in pursuing study on tau protein soya has been that a non-invasive way to get an image of this protein inside a living person’s brain has been only lately achieved. Researchers at Washington University School of Medicine, St. Louis have used a previously unknown imaging agent which binds to the tau protein (without causing side effects) making it visible in PET scans. In their study they aimed to understand the significance of tau as a marker of cognitive decline – a critical characteristic of Alzheimer. Their study is published in Science Perubatan Translasi.
In the study, 46 participants – 36 healthy adults and 10 patients with mild AD – underwent brain imaging which used the new PET imaging agent. Their brain images were then compared to understand decline in cognitive abilities due to AD. The extent of cognitive impairment was evaluated using cerebrospinal fluid measures, clinical dementia rating and paper tests for memory and other brain functions. The severity of cognitive dysfunction was analysed along with images. Results seen in 10 patients (with mild AD) in PET scans clearly showed that tau is a better predictor of symptoms of cognitive decline compared to amyloid. And tau protein might be more closely linked to symptoms like memory loss. This new tau protein (called T807) is seen to be critical in firstly understanding progression of Alzheimer and secondly to gather information about which portions of the brain are affected and involved in disease progression. Though increased tau protein is already an established marker of Alzheimer but for the first-time regions in the brain which accumulate these abnormal proteins have been pinpointed. As long as tau is deposited in the hippocampus of the brain, its well tolerated. Its spread to other areas like temporal lobe (which is associated with memory processing) can be damaging which is reflected in memory and attention tests. This allows potential use of tau as a diagnostic tool. Such a situation was not applicable to amyloid protein and this confirmed that tau protein can predict more accurately when a person is transitioning from an early stage – with no symptoms – to mild Alzheimer disease. A combination of both amyloid and tau could also be responsible. The study does have some limitations because the images are basically ‘one snapshot’ of the brain at one point of time and they cannot wholly depict association of tau and mental deterioration.
Memandangkan agen pengimejan kini tersedia untuk kedua-dua amiloid beta dan tau, perdebatan yang mana satu lebih penting boleh diteruskan tetapi alat yang diperlukan boleh digunakan untuk mengkaji kesan terapi eksperimen yang menyasarkan kedua-dua protein ini. Ejen pengimejan baharu untuk tau telah pun diluluskan untuk ujian klinikal dan boleh digunakan dalam pengimejan otak untuk pelbagai gangguan yang melibatkan peningkatan protein tau - contohnya kecederaan otak atau trauma. Terdapat harapan besar bahawa diagnosis awal penyakit Alzheimer dapat membantu mereka bentuk ubat untuk membina protein amiloid dan tau. Penyelidik secara optimistik mencadangkan terapi Alzheimer yang diperibadikan pada masa hadapan yang akan berdasarkan senario tepat dalam otak pesakit.
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{Anda boleh membaca kertas penyelidikan asal dengan mengklik pautan DOI yang diberikan di bawah dalam senarai sumber yang dipetik}
Sumber (s)
Brier MR 2018. Pengimejan Tau dan Ab, ukuran CSF, dan Kognisi dalam penyakit Alzheimer. Sains Perubatan Translasi. 8(338). https://doi.org/10.1126/scitranslmed.aaf2362
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