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Updated: Feb 26, 2026

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APOE-ε4遺伝子型と西洋食は、D-セリンの破壊を介してアルツハイマー病におけるシナプス機能障害を相乗的に悪化させる

M Matos1, A Oliveira2, I Matias2

  • 1Univ. Bordeaux, INSERM, Neurocentre Magendie, U1215, Bordeaux, F-33000, France. marco.ledbetter@gmail.com.

Alzheimer's research & therapy
|February 24, 2026
PubMed
まとめ

No abstract available in PubMed .

キーワード:
D-セリンAPOE-ε4APP/PS1マウスアルツハイマー病遺伝子-環境相互作用海馬NMDARシナプス可塑性西洋食

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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'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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