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Related Concept Videos

Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

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Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
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Dementia01:30

Dementia

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Dementia is a collective term for cognitive disorders primarily affecting memory, thinking, and reasoning. It is not a specific disease but a syndrome, with Alzheimer's disease being the most common cause, accounting for approximately 60-80% of cases. Other types include vascular dementia, Lewy body dementia, and frontotemporal dementia. Dementia affects millions worldwide, particularly older adults, though it is not a normal part of aging.
The progression of dementia is generally gradual....
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Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

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Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
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Clot Retraction and Fibrinolysis01:16

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After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
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Related Experiment Video

Updated: Jul 12, 2025

Analysis of β-Amyloid-induced Abnormalities on Fibrin Clot Structure by Spectroscopy and Scanning Electron Microscopy
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Fibrin-Targeting Immunotherapy for Dementia.

A B Kantor1, K Akassoglou, J B Stavenhagen

  • 1Jeffrey Stavenhagen, PhD, Therini Bio, Inc, Sacramento, CA, USA,

The Journal of Prevention of Alzheimer'S Disease
|October 24, 2023
PubMed
Summary
This summary is machine-generated.

Blood-brain barrier disruption allows fibrinogen to enter the brain, triggering inflammation and neurodegeneration. Targeting the fibrin P2 epitope with antibodies like THN391 shows promise for treating Alzheimer's disease and other neurological disorders.

Keywords:
Alzheimer’s diseaseFibrinogenfibrinmicroglianeurodegenerationneuroinflammation

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Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Blood-brain barrier (BBB) disruption is an early event in Alzheimer's disease pathogenesis.
  • Leaked fibrinogen converts to fibrin, exposing a P2 epitope that activates innate immune cells and causes neuroinflammation.
  • This fibrin-mediated inflammation is toxic to neurons and implicated in neurodegenerative diseases.

Purpose of the Study:

  • To investigate the role of fibrin P2 epitope in neuroinflammation and neurodegeneration.
  • To evaluate the therapeutic potential of targeting the fibrin P2 epitope with monoclonal antibodies.

Main Methods:

  • Utilized mouse monoclonal antibody 5B8 targeting the fibrin P2 epitope.
  • Assessed the efficacy of 5B8 in reducing neurodegeneration and neuroinflammation in animal models.
  • Developed THN391, a humanized antibody with enhanced affinity for fibrin P2.

Main Results:

  • Antibody 5B8 demonstrated reduced neurodegeneration and neuroinflammation in Alzheimer's and multiple sclerosis models.
  • THN391 exhibits 100-fold higher affinity for fibrin P2 and improved properties over 5B8.
  • THN391 is currently undergoing Phase 1 clinical trials.

Conclusions:

  • Targeting the fibrin P2 epitope is a viable therapeutic strategy for neurodegenerative diseases.
  • Monoclonal antibodies like THN391 offer a promising approach for treating conditions associated with BBB disruption and neuroinflammation.
  • Further clinical investigation of THN391 is warranted.