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Alzheimer's Disease: Treatment01:22

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...
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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 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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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...
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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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Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease
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Growth factors decrease in subjects with mild to moderate Alzheimer's disease (AD): potential correction with

C Luppi1, M Fioravanti, B Bertolini

  • 1Department of Internal Medicine, School of Geriatrics, University of Pavia, Pavia, Italy.

Archives of Gerontology and Geriatrics
|October 20, 2009
PubMed
Summary

Dehydroepiandrosterone sulfate (DHEAS) supplementation normalized reduced neuroprotective growth factors in Alzheimer's disease (AD) patients. This suggests DHEAS may offer a novel therapeutic strategy for dementia by enhancing brain aging defenses.

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Area of Science:

  • Neuroscience
  • Endocrinology
  • Immunology

Background:

  • Neuroprotection is crucial for preventing cognitive disorders and Alzheimer's disease (AD).
  • Dehydroepiandrosterone sulfate (DHEAS) may delay brain aging by improving neuroprotective growth factors.
  • Reduced growth factor secretion is observed in AD patients.

Purpose of the Study:

  • To investigate the impact of DHEAS on neuroprotective growth factors in AD.
  • To compare growth factor secretion in healthy individuals and AD patients.
  • To explore DHEAS as a potential therapeutic agent for AD.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) was used to measure insulin-like growth factor-1 (IGF-1), vascular endothelial growth factor (VEGF), and transforming growth factor-beta1 (TGF-beta1).
  • Peripheral blood mononuclear cells (PBMC) and natural killer (NK) cells were cultured from healthy subjects and age-matched AD patients.
  • Cells were stimulated with growth hormone (GH), lipopolysaccharide (LPS), or glucose, and co-incubated with DHEAS.

Main Results:

  • AD patients showed significantly reduced baseline levels of IGF-1, VEGF, and TGF-beta1 compared to healthy controls.
  • Significant positive correlations were found between IGF-1 and VEGF concentrations in both groups.
  • DHEAS treatment increased IGF-1, VEGF, and TGF-beta1 production in AD patients, restoring levels to those seen in healthy individuals.

Conclusions:

  • DHEAS enhances the immunoendocrine production of neuroprotective growth factors, which are diminished in AD.
  • DHEAS supplementation shows promise as a novel therapeutic approach for dementia.
  • Restoring growth factor levels with DHEAS may mitigate cognitive decline associated with AD.