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Related Concept Videos

Alzheimer's Disease: Treatment01:22

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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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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.
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Alzheimer Disease ll: Pathophysiology01:23

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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...
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Alzheimer Disease l: Introduction01:29

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Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
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Dementia l: Introduction01:22

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Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
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Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists01:30

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Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function.
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Neurodegeneration in an Animal Model of Chronic Amyloid-beta Oligomer Infusion Is Counteracted by Antibody Treatment Infused with Osmotic Pumps
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Intranasal deferoxamine engages multiple pathways to decrease memory loss in the APP/PS1 model of amyloid

Jared M Fine1, Daniel B Renner1, Anna C Forsberg1

  • 1Health Partners Institute for Education and Research, Center for Memory and Aging, Regions Hospital, 640 Jackson St., Saint Paul, MN, USA.

Neuroscience Letters
|December 3, 2014
PubMed
Summary
This summary is machine-generated.

Intranasal deferoxamine (DFO) improved memory and reduced Alzheimer's disease pathology in mice. This treatment targets multiple disease pathways, showing promise for Alzheimer's therapy.

Keywords:
Alzheimer’s diseaseGlycogen synthase kinaseIntranasalMalondialdehydeOxidative stressRadial arm water maze

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Alzheimer's disease (AD) involves amyloid plaques, tau tangles, inflammation, oxidative stress, and metal dysregulation.
  • Metal chelators are an emerging therapeutic strategy for AD.
  • Deferoxamine (DFO), a metal chelator, is being developed for intranasal (IN) delivery.

Purpose of the Study:

  • To investigate the efficacy of chronic, low-dose intranasal deferoxamine (IN DFO) in an APP/PS1 mouse model of Alzheimer's disease.
  • To examine the effects of IN DFO on cognitive function, AD neuropathology, and key molecular pathways.

Main Methods:

  • APP/PS1 mice received 0.24 C IN DFO 3x/week for 18 weeks.
  • Cognitive function was assessed using Morris water maze and radial arm water maze tests.
  • Brain tissues were analyzed for amyloid-beta (Aβ) levels, oxidative stress markers, and GSK3β activity.

Main Results:

  • IN DFO treatment significantly improved both working and reference memory.
  • A significant reduction in soluble Aβ40 and Aβ42 levels was observed in the cortex and hippocampus.
  • DFO treatment decreased GSK3β activity and reduced oxidative stress markers.

Conclusions:

  • Low-dose IN DFO effectively ameliorates cognitive deficits and key neuropathological hallmarks in an AD mouse model.
  • IN DFO modulates multiple pathways implicated in Alzheimer's disease pathogenesis.
  • Intranasal deferoxamine is a promising therapeutic candidate for Alzheimer's disease.