Delving into the Latest Updates on Roskamp Institute with Synapse

概览

疾病领域	数量

神经系统疾病	1

排名前五的药物类型	数量

小分子化药	1

排名前五的靶点	数量

AChR x APP x GSK-3β x NF-κB x STAT3	1

关联

2

项与 Roskamp Institute 相关的药物

Anatabine citrate

靶点

AChR x APP x GSK-3β x NF-κB x STAT3

作用机制

AChR 激动剂 [+4]

在研机构

Roskamp Institute

原研机构

Rock Creek Pharmaceuticals, Inc.

在研适应症

阿尔茨海默症

非在研适应症

脑损伤 [+8]

最高研发阶段临床2期

首次获批国家/地区-

首次获批日期-

DIA-10-D

靶点

BACE x α-secretase

作用机制

BACE抑制剂 [+1]

在研机构-

原研机构

Arizona State University

在研适应症-

非在研适应症

阿尔茨海默症

最高研发阶段无进展

首次获批国家/地区-

首次获批日期-

1

项与 Roskamp Institute 相关的临床试验

EUCTR2005-002744-25-IE

/ Not yet recruitingN/A

An open label evaluation of the safety and efficacy of nilvadipine in mild to moderate Alzheimer's Disease - St. James's Hospital Nivadil Trial

开始日期2006-06-29

申办/合作机构

Roskamp Institute

100 项与 Roskamp Institute 相关的临床结果

登录后查看更多信息

0 项与 Roskamp Institute 相关的专利（医药）

登录后查看更多信息

300

项与 Roskamp Institute 相关的文献（医药）

2025-01-01·Environmental Toxicology and Pharmacology

The impact of APOE4 on neurological symptoms after exposure to K. brevis neurotoxin

Article

作者: Nkiliza, Aurore ; Crawford, Fiona ; Aldrich, Gregory J ; Niedospial, Daniel ; Paris, Daniel ; Kirkpatrick, Barbara ; Ferguson, Scott ; Abdullah, Laila ; Keegan, Andrew P ; Mullan, Michael ; Helgager, Dakota

INTRODUCTIONThe harmful alga Karenia brevis (K. brevis) releases brevetoxins (PbTx) that cause respiratory and neurological symptoms. The apolipoprotein E (APOE) ε4 allele has been linked to poor neurological outcomes after exposure to environmental toxicants. This study explores the influence of the ε4 allele on the relationship between K. brevis in coastal waters and neurological symptoms reported by Southwest Florida residents.METHODSA Surrogate Brevetoxin Exposure (SBE_air) index was developed to estimate aerosolized PbTx exposure. Data on past medical history and symptoms and blood for analyzing APOE genotypes were collected from 244 participants.RESULTSCompared to non-carriers, ε4 carriers more frequently reported experiencing memory problems and fatigue during red tide blooms, independent of conditions like dementia and chronic fatigue syndrome.CONCLUSIONThis study suggests that the ε4 allele may exacerbate neurological symptoms from aerosolized PbTx, highlighting the need for strategies to better understand the impact of PbTx on the brain.

2024-12-01·Neural Regeneration Research

Contribution of astrocytes to the neurovascular elimination of tau

Article

作者: Eisenbaum, Maxwell ; Bachmeier, Corbin

2024-12-01·Alzheimer's & Dementia

Inhibition of thrombin signaling after traumatic brain injury improves neurobehavioral dysfunction in 5xFAD mice

Article

作者: Shapiro, Lee A. ; Arismendi, Victoria ; Bandopadhyay, Shreya ; Grammas, Paula ; Iannucci, Jaclyn

AbstractBackgroundTraumatic brain injury (TBI) is a serious societal concern and is considered a major risk factor for the development of Alzheimer’s disease (AD) and related dementias. Identifying shared pathological mediators that contribute to the progression of AD following TBI may allow therapeutic targeting to reduce the likelihood of developing AD following TBI. Cerebrovascular dysfunction is present in both AD and TBI, and thrombin has been implicated as a mediator of cerebrovascular dysfunction and inflammation. Elevated thrombin levels and thrombin signaling following TBI have been associated with cognitive impairment. Thrombin has similarly been implicated as a pathological mediator in AD. Many of thrombin’s detrimental cellular effects have been linked to thrombin activation of protease activated receptors (PARs), including PAR‐1, which are expressed on a number of cell types in the brain and periphery, including endothelial cells, astrocytes, microglia, and neurons. Therefore, inhibiting thrombin activation of PAR‐1 may be a treatment strategy for AD pathogenesis after TBI. We hypothesize that targeting PAR‐1 activation will mitigate the TBI‐induced increase in AD pathogenesis.Methods8‐week‐old male 5xFAD mice received either our lateral fluid percussion injury (FPI) model of TBI or sham surgery. This was followed 3 hours later by inhibition of PAR‐1 activation via treatment with a selective PAR‐1 inhibitor (SCH‐79797; 25µg/kg, i.p.) or vehicle control (DMSO). Behavioral measures included digigait assessment of acute motor deficits, depression‐associated behaviors, including social interaction and burrowing, and cognitive behaviors. Mice were subsequently sacrificed and tissue was collected for analysis of AD‐associated pathology as well as cerebrovascular dysfunction.ResultsFPI causes chronic cerebrovascular alterations in 5xFAD mice. FPI was also found to induce deficits in depression‐associated behaviors in 5xFAD mice, most notably social interaction. FPI also induced hippocampal‐associated cognitive impairment in both the Y‐maze and Barnes maze. The impaired affective and cognitive behaviors were improved by SCH‐79797 treatment.ConclusionsThese findings indicate that there is chronic cerebrovascular dysfunction in 5xFAD mice that can be exacerbated by FPI and highlight the potential for targeting thrombin and related signaling processes for mitigating these effects after injury.

100 项与 Roskamp Institute 相关的药物交易

登录后查看更多信息

100 项与 Roskamp Institute 相关的转化医学

登录后查看更多信息

组织架构

使用我们的机构树数据加速您的研究。

登录

或

查看完整样例数据

管线布局

2025年01月31日管线快照

管线布局中药物为当前组织机构及其子机构作为药物机构进行统计，早期临床1期并入临床1期，临床1/2期并入临床2期，临床2/3期并入临床3期

临床2期

1

其他

登录后查看更多信息

当前项目

药物(靶点)	适应症	全球最高研发状态

Anatabine citrate ( AChR x APP x GSK-3β x NF-κB x STAT3 )	阿尔茨海默症更多	临床2期
DIA-10-D ( BACE x α-secretase )	阿尔茨海默症更多	无进展