Description: <b>Shankhpushpi</b> (Convolvulus pluricaulis) is a traditional Ayurvedic herb renowned for its nootropic (cognitive-enhancing), anxiolytic, and adaptogenic properties. <br>
-5 druglike phytochemicals from CP constituents: scopoletin, 4-hydroxycinnamic acid, kaempferol, quercetin, and ayapanin.
<p><b>Shankhpushpi</b> — Ayurvedic nootropic “brain tonic” herbal drug; most commonly standardized/treated as <i>Convolvulus prostratus</i> Forssk. (syn. <i>Convolvulus pluricaulis</i> Choisy), but the name “Shankhpushpi” is also used for other botanicals in different regions (major source-of-variation risk). <br><br>
<b>Primary mechanisms (conceptual rank)</b><br>
1) Cholinergic support (AChE inhibition / pro-cholinergic nootropic profile)<br>
2) Antioxidant / redox buffering (ROS↓, lipid peroxidation↓; antioxidant enzymes↑) <br>
3) Anti-inflammatory neuroprotection (glial/inflammatory signaling dampening; model-dependent) <br>
4) Proteinopathy-related neuroprotection (tau-associated neurotoxicity mitigation; model-dependent) }<br><br>
<b>Bioavailability / pharmacokinetics relevance</b><br>
Human PK for defined Shankhpushpi extracts is not well-established in the clinical literature; composition varies by species, plant part, extraction solvent, and polyherbal formulations. <br><br>
<b>In-vitro vs systemic exposure</b><br>
Many mechanistic studies use extracts/fractions at concentrations not directly translatable to achievable systemic exposure; translational relevance hinges on standardized extract chemistry and demonstrated CNS delivery (often not reported). <br><br>
<b>Clinical evidence status</b><br>
Predominantly preclinical + traditional use; human evidence exists mostly in small/heterogeneous studies and often in polyherbal products rather than single-extract RCT-grade data.</p>
<br>
-Acetylcholinesterase (AChE) inhibition <br>
-Antioxidant activity Scavenges ROS<br>
-Memory enhancement<br>
<br>
Cancer:<br>
-Antioxidant/anti-inflammatory May reduce chronic inflammation, a driver of tumor progression.<br>
<h3>Shankhpushpi — AD/Neuro axis table</h3>
<table>
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Neural / Glial Systems</th>
<th>TSF</th>
<th>Primary Effect</th>
<th>Notes / Interpretation</th>
</tr>
<tr>
<td>1</td>
<td>Cholinergic axis (AChE)</td>
<td>↓ (model-dependent)</td>
<td>R→G</td>
<td>Memory/cognition support</td>
<td>Frequently presented as a nootropic mechanism; evidence base varies by extract and assay type. :contentReference[oaicite:22]{index=22}</td>
</tr>
<tr>
<td>2</td>
<td>ROS / antioxidant defense</td>
<td>↓ (often primary)</td>
<td>P→R→G</td>
<td>Oxidative stress reduction</td>
<td>Reports include decreased lipid peroxidation markers and increased antioxidant defense metrics in cognitive impairment paradigms. :contentReference[oaicite:23]{index=23}</td>
</tr>
<tr>
<td>3</td>
<td>Neuroinflammation (broad cytokine/glial tone)</td>
<td>↓ (model-dependent)</td>
<td>R→G</td>
<td>Neuroprotection / slower degeneration pressure</td>
<td>Often included in dementia-herb reviews as part of multi-target neuroprotection; direct causal evidence depends on study design. :contentReference[oaicite:24]{index=24}</td>
</tr>
<tr>
<td>4</td>
<td>Proteinopathy stress (tau-associated toxicity)</td>
<td>↓ (protective; model-dependent)</td>
<td>R→G</td>
<td>Protection from tau-driven neuronal injury</td>
<td>Aqueous extract reported to mitigate hMAPτ-induced neurotoxicity (cell-based). :contentReference[oaicite:25]{index=25}</td>
</tr>
<tr>
<td>5</td>
<td>Ca²⁺ signaling (excitotoxicity / ER-mito coupling)</td>
<td>↔/↓ (secondary; context-dependent)</td>
<td>R</td>
<td>Stress-amplification modulation</td>
<td>Mechanistically relevant when excitotoxic/mitochondrial stress endpoints are present; often not directly quantified in Shankhpushpi experiments.</td>
</tr>
<tr>
<td>6</td>
<td>NRF2 antioxidant response</td>
<td>↑ (adaptive/protective; context-dependent)</td>
<td>R→G</td>
<td>Transcriptional antioxidant program</td>
<td>Frequently inferred from antioxidant enzyme changes and redox outcomes rather than directly measured NRF2 pathway activation in many studies. :contentReference[oaicite:26]{index=26}</td>
</tr>
<tr>
<td>7</td>
<td><i>Clinical Translation Constraint</i></td>
<td>↔</td>
<td>—</td>
<td>Standardization + PK/BBB uncertainty</td>
<td>Multiple botanicals sold as “Shankhpushpi,” variable extraction/chemistry, and limited human PK/CNS delivery data constrain translation to AD claims. :contentReference[oaicite:27]{index=27}</td>
</tr>
</table>
<p><b>TSF legend:</b> P: 0–30 min | R: 30 min–3 hr | G: >3 hr</p>