Correction: Fu et al. C16 Peptide and Ang-1 Improve Functional Disability and Pathological Changes in an Alzheimer's Disease Model Associated with Vascular Dysfunction. Pharmaceuticals 2022, 15, 471
Related Experiment Video
Updated: Sep 10, 2026

08:01
Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
Published on: March 16, 2016
Xiaoxiao Fu1, Jing Wang2, Huaying Cai2
1Institute of Anatomy, Medical College, Zhejiang University, Hangzhou 310058, China.
Pharmaceuticals (Basel, Switzerland)
|July 30, 2025
Abstract:
In the original publication [...].
More Related Videos
Related Concept Videos
Alzheimer's Disease: Treatment
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...
Alzheimer Disease ll: Pathophysiology
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...

