Scholarlink

<p>Alzheimer’s disease (AD) is the most common form of dementia, characterized by progressive cognitive decline driven by a complex interplay of genetic, environmental, and lifestyle factors. Increasing evidence highlights impaired synaptic plasticity as a major contributor to early cognitive deficits, often preceding neuronal loss. In particular, disruption of long-term potentiation (LTP) within the hippocampus, a region essential for learning and memory, plays a central role. Accumulation of amyloid β (Aβ) plaques and hyperphosphorylated tau proteins compromises synaptic integrity, leading to reduced synaptic density and altered protein expression critical for excitatory signaling. Additional mechanisms, including microglial activation and mitochondrial dysfunction, further aggravate synaptic impairment through inflammation and oxidative stress. Understanding these interconnected molecular and cellular disruptions offers crucial insight into the pathways underlying synaptic dysfunction in AD. By elucidating these mechanisms, future research can inform novel therapeutic strategies aimed at preserving synaptic function and slowing disease progression.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Impaired Synaptic Plasticity Mechanisms in Alzheimer’s Disease

  • 期刊论文

  • 发表日期：

    2025年9月29日

查看全文
  • Rasoul Ebrahimi,
  • Zahra Golzari,
  • Mahsa Heidari-Foroozan,
  • Abolfazl Khosravi,
  • Samin Ghaheri Sharghi,
  • Mobina Saleh,
  • Shakiba Salarvandian,
  • Khadijeh Esmaeilpour

摘要

Alzheimer’s disease (AD) is the most common form of dementia, characterized by progressive cognitive decline driven by a complex interplay of genetic, environmental, and lifestyle factors. Increasing evidence highlights impaired synaptic plasticity as a major contributor to early cognitive deficits, often preceding neuronal loss. In particular, disruption of long-term potentiation (LTP) within the hippocampus, a region essential for learning and memory, plays a central role. Accumulation of amyloid β (Aβ) plaques and hyperphosphorylated tau proteins compromises synaptic integrity, leading to reduced synaptic density and altered protein expression critical for excitatory signaling. Additional mechanisms, including microglial activation and mitochondrial dysfunction, further aggravate synaptic impairment through inflammation and oxidative stress. Understanding these interconnected molecular and cellular disruptions offers crucial insight into the pathways underlying synaptic dysfunction in AD. By elucidating these mechanisms, future research can inform novel therapeutic strategies aimed at preserving synaptic function and slowing disease progression.