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06:02
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Neuroplasticity and Alzheimer's Disease.
Ashkan Asgari Gashtrodkhani1, Samaneh Ghorbani Shirkouhi2, Seyed Sepehr Khatami3
1School of Medicine, Guilan University of Medical Sciences, 41937-13111 Rasht, Iran.
Journal of Integrative Neuroscience
|January 29, 2026
Summary
Alzheimer's disease impairs brain neuroplasticity, leading to cognitive decline. Enhancing neuroplasticity through various methods offers potential for preventing and treating Alzheimer's disease.
Area of Science:
- Neuroscience
- Pathophysiology
- Neurodegenerative Diseases
Background:
- Alzheimer's disease (AD) is a progressive neurodegenerative disorder causing cognitive decline, particularly memory loss.
- AD is characterized by neuronal loss, impaired synaptic connectivity, and disrupted neuroplasticity.
- Current treatments cannot halt AD progression, highlighting the need for novel therapeutic strategies.
Purpose of the Study:
- To review the pathophysiological mechanisms underlying neuroplasticity impairment in Alzheimer's disease pathogenesis.
- To explore neuromodulation approaches that promote neuroplasticity for AD prevention and treatment.
Main Methods:
- This narrative review synthesizes existing research on Alzheimer's disease and neuroplasticity.
- It examines pathophysiological explanations for neuroplasticity deficits in AD.
- It discusses various interventions aimed at enhancing neuroplasticity.
Main Results:
- Impaired neuroplasticity and synaptic dysfunction are key contributors to cognitive decline in AD.
- Enhancing neuroplasticity has shown potential in improving cognition and memory.
- Several neuromodulation strategies show promise for AD management.
Conclusions:
- Understanding neuroplasticity's role is crucial for developing effective Alzheimer's disease treatments.
- Neuromodulation techniques like exercise, diet, and light therapy may offer therapeutic benefits.
- Further research into promoting neuroplasticity could lead to interventions that prevent or slow AD progression.
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01:35Long-term Potentiation
Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
01:25Long-term Potentiation
Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
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Hebbian LTP
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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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01:01Neuroplasticity
Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.
01:29Alzheimer Disease l: Introduction
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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