Description: <b>Sesame</b> (particularly sesame seeds and sesame oil) has been studied for its potential neuroprotective effects, including relevance to Alzheimer’s disease (AD)<br>
<p><b>Sesame (seeds/oil) — AD relevance:</b> Preclinical literature (sesamin/sesamolin/sesamol and sesame oil) supports neuroprotection via antioxidant + anti-inflammatory mechanisms, with reported effects on amyloid toxicity/aggregation in models. Human AD-specific clinical evidence is limited.</p>
<p><b>Primary mechanisms (conceptual rank):</b><br>
1) ↓ Oxidative stress (ROS ↓; lipid peroxidation ↓)<br>
2) ↓ Neuroinflammation (NF-κB ↓; p38MAPK tone ↓; microglial activation ↓)<br>
3) ↑ Neurotrophic/synaptic support (BDNF ↑ in some models; network resilience)<br>
4) Aβ toxicity/aggregation ↓ (preclinical; model-dependent)</p>
<p><b>Bioavailability / PK relevance:</b> Effects are typically chronic (weeks) and metabolite/remodeling driven.</p>
<p><b>Clinical evidence status:</b> Predominantly preclinical for AD mechanisms; not established as disease-modifying in humans.</p>
-Sesame seeds are rich in sesamin, sesamol, and sesaminol, lignans with strong antioxidant properties.<br>
-Sesamol has been shown to inhibit pro-inflammatory cytokines like TNF-α, IL-1β, and IL-6, and suppress NF-κB signaling<br>
-may inhibit acetylcholinesterase (AChE)<br>
-Sesamol may help inhibit Aβ aggregation<br>
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Mechanism Effect
↓ ROS (Oxidative stress) Protects neurons from oxidative damage
↓ NF-κB Reduces neuroinflammation
↓ AChE Increases acetylcholine levels
↓ Aβ aggregation Limits amyloid plaque formation
↑ BDNF Supports neurogenesis
Nutritional Richness
-Healthy fats: High in monounsaturated and polyunsaturated fats (especially omega-6)
-Protein: A good plant-based protein source
-Minerals: Rich in calcium, magnesium, iron, zinc, selenium, and copper
-Vitamins: Contains B vitamins (especially B1, B3, B6), vitamin E
-High in calories and fats—consume in moderation
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<h3>Sesame Seeds / Sesame Oil — AD / Neurodegeneration Pathway Map</h3>
<table border="1" cellpadding="4" cellspacing="0">
<tr>
<th>Rank</th><th>Pathway / Axis</th><th>Cells</th><th>TSF</th><th>Primary Effect</th><th>Notes / Interpretation</th>
</tr>
<tr>
<td>1</td><td>ROS / lipid peroxidation</td>
<td>↓</td><td>P/R</td>
<td>Reduced oxidative burden</td>
<td>Core neuroprotective mechanism across sesamin/sesamol studies (oxidative injury models).</td>
</tr>
<tr>
<td>2</td><td>Neuroinflammation (NF-κB; microglial activation)</td>
<td>↓</td><td>R/G</td>
<td>Lower inflammatory stress</td>
<td>Microglial inhibition and reduced inflammatory signaling reported in neurodegeneration models.</td>
</tr>
<tr>
<td>3</td><td>p38MAPK stress signaling</td>
<td>↓ (model-dependent)</td><td>R/G</td>
<td>Reduced stress-activated damage signaling</td>
<td>Highlighted in sesame-oil AD rodent work as part of NF-κB/p38 coupling.</td>
</tr>
<tr>
<td>4</td><td>BDNF / synaptic support</td>
<td>↑ (model-dependent)</td><td>G</td>
<td>Plasticity / resilience support</td>
<td>Often presented as downstream of reduced inflammation/oxidative stress; typically requires sustained exposure.</td>
</tr>
<tr>
<td>5</td><td>Aβ toxicity / aggregation</td>
<td>↓ (preclinical)</td><td>G</td>
<td>Reduced amyloid-associated injury</td>
<td>Sesamin has reported anti-Aβ aggregation/toxicity effects in models; human biomarker confirmation limited.</td>
</tr>
<tr>
<td>6</td><td>NRF2 axis</td>
<td>↔ / ↑ (context-dependent)</td><td>R/G</td>
<td>Stress-defense regulation</td>
<td>Often inferred/secondary to antioxidant enzyme induction; not always directly measured.</td>
</tr>
<tr>
<td>7</td><td>Ca²⁺ homeostasis / excitotoxic vulnerability</td>
<td>↔ / stabilized (indirect)</td><td>P/R</td>
<td>Excitotoxic buffering (supportive)</td>
<td>Secondary to mitochondrial/redox support; treat as secondary unless explicit Ca²⁺ endpoints exist.</td>
</tr>
<tr>
<td>8</td><td>Clinical Translation Constraint</td>
<td>↓ (constraint)</td><td>—</td>
<td>Preclinical-dominant evidence</td>
<td>AD evidence is largely animal/cell-model based; dosing forms (oil vs isolated lignans) and human endpoints remain insufficient for disease-modifying claims.</td>
</tr>
</table>
<p><b>TSF legend:</b> P: 0–30 min; R: 30 min–3 hr; G: >3 hr</p>