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Marginal vitamin A deficiency facilitates Alzheimer's pathogenesis
Jiaying Zeng1,2,3, Li Chen1,2, Zhe Wang3
1Children's Nutrition Research Center, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base for Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Acta Neuropathologica
|January 29, 2017
Summary
Marginal vitamin A deficiency (MVAD) exacerbates Alzheimer's disease (AD) by promoting amyloid-beta plaque formation. Supplementing with vitamin A (VA) improved cognitive deficits in AD mice, suggesting VA supplementation as a potential AD treatment.
Area of Science:
- Neuroscience
- Nutritional Science
- Pathology
Background:
- Alzheimer's disease (AD) is characterized by amyloid-beta (Aβ) plaque deposition.
- Vitamin A deficiency (VAD) impacts cognitive function, with marginal VAD (MVAD) being a widespread issue.
- The link between MVAD and AD pathogenesis is not well understood.
Purpose of the Study:
- To investigate the role of marginal vitamin A deficiency (MVAD) in Alzheimer's disease (AD) pathogenesis.
- To determine if MVAD affects amyloid-beta (Aβ) production and cognitive decline in AD models.
- To evaluate the therapeutic potential of vitamin A (VA) supplementation in mitigating MVAD-induced AD symptoms.
Main Methods:
- Assessed MVAD prevalence in the elderly and correlated it with cognitive decline.
- Utilized AD model mice to study the effects of prenatal MVAD on Aβ production and plaque formation.
- Examined the impact of beta-site APP cleaving enzyme 1 (BACE1) activity in MVAD-exposed mice.
- Administered therapeutic doses of VA to MVAD-affected AD mice to assess rescue of cognitive deficits.
Main Results:
- MVAD is more prevalent than VAD in the elderly, correlating with increased cognitive decline.
- Prenatal MVAD significantly enhanced BACE1-mediated Aβ production and neuritic plaque formation in AD mice.
- MVAD exacerbated memory deficits in AD model mice.
- Vitamin A supplementation effectively rescued MVAD-induced memory impairments.
Conclusions:
- Marginal vitamin A deficiency (MVAD) promotes Alzheimer's disease (AD) pathogenesis by increasing amyloid-beta (Aβ) production and deposition.
- Vitamin A (VA) supplementation demonstrates therapeutic potential for improving cognitive deficits associated with MVAD in AD.
- VA supplementation may represent a viable strategy for AD prevention and treatment.
Keywords:
Alzheimer’s diseaseAmyloid β proteinMarginal vitamin A deficiencyMemory deficitsVitamin A supplementMore Related Videos
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