Research has shown that another protini called tau is responsible for early symptoms of Ugonjwa wa Alzheimer na habari hii inaweza kusaidia katika kuendeleza matibabu.
Alzheimers Disease (AD) or simply Alzheimers has no cure and it also cannot be prevented. Deferring the onset of symptoms of Alzheimers for up to 10-15 years can certainly impact the lives of wagonjwa, 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 Alzheimers is build-up of plaque and defective protini around neurons inside the brain which are responsible for advancement of the ugonjwa. Multiple research shows that higher levels of protini amyloid in the ubongo ni viashiria vya mapema sana vya kukuza AD. Wengi wa utafiti juu ya Ugonjwa wa Alzheimer imekuwa ikilenga kuelewa jinsi hii protini 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 protini in their brains compared to healthy people.
Is there another protini 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 protini must be changing first and then there must be some other factor responsible which researchers predicted could be a second protini 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 protini accumulated in their brains. Recent studies have generated interest in protini 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 protini 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 Alzheimers. Their study is published in Science Dawa ya Kutafsiri.
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 Alzheimers 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 Alzheimers 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 Alzheimers 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.
Kwa kuwa vielelezo vya kupiga picha sasa vinapatikana kwa beta ya amiloidi na tau, mjadala ambao ni muhimu zaidi unaweza kuendelea lakini zana muhimu zinaweza kutumika kuchunguza athari za matibabu ya majaribio yanayolenga protini hizi zote mbili. Wakala mpya wa tau wa kupiga picha tayari umeidhinishwa kwa majaribio ya kimatibabu na inaweza kutumika katika kupiga picha ya ubongo kwa matatizo mbalimbali yanayohusisha kiwango cha juu cha protini ya tau - mfano jeraha la ubongo au kiwewe. Kuna matumaini makubwa kwamba utambuzi wa mapema wa ugonjwa wa Alzeima unaweza kusaidia kuunda dawa za mkusanyiko wa protini za amiloidi na tau. Watafiti wanapendekeza kwa matumaini matibabu ya Alzheimer ya kibinafsi katika siku zijazo ambayo yatatokana na hali halisi katika ubongo wa mgonjwa.
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{Unaweza kusoma karatasi asili ya utafiti kwa kubofya kiungo cha DOI kilichotolewa hapa chini katika orodha ya (vyanzo) vilivyotajwa}
Chanzo (s)
Brier MR 2018. Upigaji picha wa Tau na Ab, vipimo vya CSF, na Utambuzi katika ugonjwa wa Alzeima. Sayansi Translational Madawa. 8 (338). https://doi.org/10.1126/scitranslmed.aaf2362
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