Pasindu Hansana Singhaarachchi , Peter Antal , Frédéric Calon , Carsten Culmsee , Jean-Christophe Delpech , Martin Feldotto , Jorine Geertsema , Emmy E. Hoeksema , Aniko Korosi , Sophie Layé , Jonathan McQualter , Susanne R. de Rooij , Christoph Rummel , Mary Slayo , Luba Sominsky , Sarah J. Spencer
{"title":"阿尔茨海默病的啮齿动物模型:对当前假设和未来研究途径的批判性分析","authors":"Pasindu Hansana Singhaarachchi , Peter Antal , Frédéric Calon , Carsten Culmsee , Jean-Christophe Delpech , Martin Feldotto , Jorine Geertsema , Emmy E. Hoeksema , Aniko Korosi , Sophie Layé , Jonathan McQualter , Susanne R. de Rooij , Christoph Rummel , Mary Slayo , Luba Sominsky , Sarah J. Spencer","doi":"10.1016/j.pneurobio.2025.102821","DOIUrl":null,"url":null,"abstract":"<div><div>Alzheimer’s disease (AD) was first described over a century ago. However, the mechanisms underlying the disease are not well understood to this day. This has negatively impacted our ability to create animal models to design and test targeted reliable treatments for the disease. Amyloid β plaque accumulation, aggregation of neurofibrillary tangles, neuroinflammation, neurodegeneration, and, of course, cognitive decline, are few of the many observed pathological features associated with AD. However, there is a concern that the animal models of AD that are based on these frameworks may not be accurately representing AD in people. As such, the results from preclinical trials have not historically translated well to the clinic. In this article, we review the current major hypotheses to describe AD; we outline the major strengths and weaknesses of the commonly used rodent models used to replicate features of these hypotheses; and we provide a strategy for the field for future research.</div></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"252 ","pages":"Article 102821"},"PeriodicalIF":6.1000,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Rodent models of Alzheimer's disease: Critical analysis of current hypotheses and pathways for future research\",\"authors\":\"Pasindu Hansana Singhaarachchi , Peter Antal , Frédéric Calon , Carsten Culmsee , Jean-Christophe Delpech , Martin Feldotto , Jorine Geertsema , Emmy E. Hoeksema , Aniko Korosi , Sophie Layé , Jonathan McQualter , Susanne R. de Rooij , Christoph Rummel , Mary Slayo , Luba Sominsky , Sarah J. Spencer\",\"doi\":\"10.1016/j.pneurobio.2025.102821\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Alzheimer’s disease (AD) was first described over a century ago. However, the mechanisms underlying the disease are not well understood to this day. This has negatively impacted our ability to create animal models to design and test targeted reliable treatments for the disease. Amyloid β plaque accumulation, aggregation of neurofibrillary tangles, neuroinflammation, neurodegeneration, and, of course, cognitive decline, are few of the many observed pathological features associated with AD. However, there is a concern that the animal models of AD that are based on these frameworks may not be accurately representing AD in people. As such, the results from preclinical trials have not historically translated well to the clinic. In this article, we review the current major hypotheses to describe AD; we outline the major strengths and weaknesses of the commonly used rodent models used to replicate features of these hypotheses; and we provide a strategy for the field for future research.</div></div>\",\"PeriodicalId\":20851,\"journal\":{\"name\":\"Progress in Neurobiology\",\"volume\":\"252 \",\"pages\":\"Article 102821\"},\"PeriodicalIF\":6.1000,\"publicationDate\":\"2025-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Progress in Neurobiology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0301008225001121\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Progress in Neurobiology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0301008225001121","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
Rodent models of Alzheimer's disease: Critical analysis of current hypotheses and pathways for future research
Alzheimer’s disease (AD) was first described over a century ago. However, the mechanisms underlying the disease are not well understood to this day. This has negatively impacted our ability to create animal models to design and test targeted reliable treatments for the disease. Amyloid β plaque accumulation, aggregation of neurofibrillary tangles, neuroinflammation, neurodegeneration, and, of course, cognitive decline, are few of the many observed pathological features associated with AD. However, there is a concern that the animal models of AD that are based on these frameworks may not be accurately representing AD in people. As such, the results from preclinical trials have not historically translated well to the clinic. In this article, we review the current major hypotheses to describe AD; we outline the major strengths and weaknesses of the commonly used rodent models used to replicate features of these hypotheses; and we provide a strategy for the field for future research.
期刊介绍:
Progress in Neurobiology is an international journal that publishes groundbreaking original research, comprehensive review articles and opinion pieces written by leading researchers. The journal welcomes contributions from the broad field of neuroscience that apply neurophysiological, biochemical, pharmacological, molecular biological, anatomical, computational and behavioral analyses to problems of molecular, cellular, developmental, systems, and clinical neuroscience.