Association between single moderate to severe traumatic brain injury and long-term tauopathy in humans and preclinical animal models: a systematic narrative review of the literature.
Association between single moderate to severe traumatic brain injury and long-term tauopathy in humans and preclinical animal models: a systematic narrative review of the literature.
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人类和临床前动物模型中单一中度至重度创伤性脑损伤与长期tau蛋白病之间的关联：文献的系统性叙述性综述
DOI：
10.1186/s40478-022-01311-0
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发表时间：
2022-01-31
影响因子：
7.1
通讯作者：
DeKosky ST
中科院分区：
文献类型：
--
作者：
Walker A;Chapin B;Abisambra J;DeKosky ST
创伤性脑损伤（TBI）中tau扩散的起始、解剖模式和程度，以及TBI导致长期tau病理学的机制仍然存在争议。一些研究表明，中度至重度TBI足以促进tau病理学;然而，其他研究表明，这仅仅是衰老的结果。因此，我们对文献进行了系统的叙述性综述，以解决单一中度至重度头部损伤是否会导致人类和动物模型中tau蛋白病的长期发展。考虑纳入本综述的研究评估了单一中度至重度TBI，评估了损伤后长期时间点的tau病理学，包括实验性或观察性研究，并进行了同行评审并以英文发表。检索的数据库包括：PUBMED、NCBI-PMC、EMBASE、Web of Science、Academic Search Premiere和阿帕Psychnet。将检索结果上传至Covidence®，删除重复文献，并对文献进行摘要和全文筛选。然后提取数据并评估文章的偏倚风险。在筛选的4，150项研究中，26项符合纳入条件，其中17项为人体研究，8项为临床前动物研究，1项包括人体和临床前动物研究。大多数研究具有低至中度偏倚风险。大多数人类和动物研究（分别为n = 12和9）表明，与无头部损伤史相比，单次中度至重度TBI导致长期tau蛋白病的发展更大。然而，由于以下几个限制，应谨慎解释该结论：样本量小;控制可能影响tau病理学的混杂因素（例如，痴呆或神经系统疾病的家族史、载脂蛋白E基因型等），包括大多数男性，以及报告伤害参数的变化。结果表明，与没有头部损伤史相比，单一中度至重度TBI导致tau蛋白病的更大慢性发展。这意味着诱导的tau病理可能不是短暂的，而是可以在人类和动物模型中随时间逐渐发展。应进一步探索针对这些tau蛋白变化进行治疗干预，以阐明疾病进展是否可以逆转或缓解。在线版本包含补充材料，可通过10.1186/s40478-022-01311-0获取。
The initiation, anatomic pattern, and extent of tau spread in traumatic brain injury (TBI), and the mechanism by which TBI leads to long-term tau pathology, remain controversial. Some studies suggest that moderate to severe TBI is sufficient to promote tau pathology; however, others suggest that it is simply a consequence of aging. We therefore conducted a systematic narrative review of the literature addressing whether a single moderate to severe head injury leads to long-term development of tauopathy in both humans and animal models. Studies considered for inclusion in this review assessed a single moderate to severe TBI, assessed tau pathology at long-term timepoints post-injury, comprised experimental or observational studies, and were peer-reviewed and published in English. Databases searched included: PUBMED, NCBI-PMC, EMBASE, Web of Science, Academic Search Premiere, and APA Psychnet. Search results were uploaded to Covidence®, duplicates were removed, and articles underwent an abstract and full-text screening process. Data were then extracted and articles assessed for risk of bias. Of 4,150 studies screened, 26 were eligible for inclusion, of which 17 were human studies, 8 were preclinical animal studies, and 1 included both human and preclinical animal studies. Most studies had low to moderate risk of bias. Most human and animal studies (n = 12 and 9, respectively) suggested that a single moderate to severe TBI resulted in greater development of long-term tauopathy compared to no history of head injury. This conclusion should be interpreted with caution, however, due to several limitations: small sample sizes; inconsistencies in controlling for confounding factors that may have affected tau pathology (e.g., family history of dementia or neurological illnesses, apolipoprotein E genotype, etc.), inclusion of mostly males, and variation in reporting injury parameters. Results indicate that a single moderate to severe TBI leads to greater chronic development of tauopathy compared to no history of head injury. This implies that tau pathology induced may not be transient, but can progressively develop over time in both humans and animal models. Targeting these tau changes for therapeutic intervention should be further explored to elucidate if disease progression can be reversed or mitigated. The online version contains supplementary material available at 10.1186/s40478-022-01311-0.
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影响因子：
5.3
作者：
Dollé JP;Jaye A;Anderson SA;Ahmadzadeh H;Shenoy VB;Smith DH
通讯作者：
Smith DH
影响因子：
17.1
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影响因子：
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影响因子：
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影响因子：
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作者：
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通讯作者：
Deisenhammer, F