What specific molecular pathways does Dr. Gupta target in Alzheimer’s compared to amyloid and tau therapies

1. Who is being talked about — Gupta’s role and what the sources actually report

Popular materials in the dataset reference Dr. Sanjay Gupta in the context of media and misinformation: a CNN podcast note and a debunking of ads that used a deepfake to claim he found a natural Alzheimer’s cure; these items do not describe Gupta as leading a molecular-therapy program or name pathways he targets ^[1]. The available sources do not mention Dr. Gupta as an investigator of specific molecular pathways in Alzheimer’s disease ^[1].

2. How mainstream 2024–25 drug efforts differ: amyloid and tau remain the headline targets

Clinical and review coverage in 2025 treats anti-amyloid immunotherapies as the major recently approved, disease-modifying approach—lecanemab and donanemab are explicitly cited as FDA-approved agents that reduce amyloid plaques for early-stage AD ^[2]. Tau is tracked via CSF and imaging biomarkers (total tau and phosphorylated tau) as core indicators of neuronal injury and tau pathology ^[7]. These remain the clearest, specific molecular foci in late-stage translational work ^{[2] [7]}.

3. Broader molecular web: what researchers are targeting beyond amyloid and tau

Contemporary research emphasizes a network of interacting pathways rather than single-molecule fixes. Large multi-omics and transcriptomic studies point to dysregulated signaling such as PI3K–Akt and Wnt, metabolic and oxidative phosphorylation changes in glia, calcium and cAMP signaling, and long-term potentiation/circadian pathways that can be modulated by combination treatments ^{[3] [4] [8]}. Reviews and proteomic atlases frame AD as a systems disease with immune, metabolic, synaptic-plasticity and protein-homeostasis nodes that are actionable in preclinical screens ^{[8] [9]}.

4. Cell-type and network strategies: why this matters for “what’s being targeted”

A 2025 Cell paper argues for cell-type-directed, network-correcting combination therapy: astrocytes, microglia and oligodendrocyte precursor cells show distinct pathway enrichments (gap junctions, oxidative phosphorylation), and combination (L + I) treatments were reported to perturb AD-associated pathways including long-term potentiation, circadian entrainment, cAMP and calcium signaling—shifting the therapeutic view from single-target amyloid/tau drugs to cell-type-specific pathway correction ^[4].

5. Peripheral and gut–brain angles: new pathways under investigation

Work on the microbiome–gut–brain axis highlights microglial modulation by microbial signals (LPS, neuroactive metabolites) and altered kynurenine-pathway metabolites in AD, suggesting targets in peripheral metabolism and immune signaling that are distinct from classical amyloid/tau interventions ^{[5] [6]}. These represent pragmatic alternative pathways researchers aim at for neuroinflammation and microglial phenotype control ^[6].

6. What the sources do not say about “Dr. Gupta’s pathways”

Available reporting in the provided set contains no description of Dr. Gupta leading laboratory-based molecular interventions or naming molecular pathways he targets in Alzheimer’s therapy; the sources either place him in media roles or in discussions refuting false cure claims ^[1]. There is no source here that attributes to him specific pathway-modulating drugs or mechanisms (not found in current reporting).

7. Takeaway for readers: separate media figures from lab programs, and map the real targets

If your question seeks the scientific contrast between “Dr. Gupta’s” approach and amyloid/tau drugs, the dataset cannot support claims that Gupta runs a distinct molecular program; instead, current scientific reporting shows a field expanding beyond amyloid and tau into PI3K–Akt, Wnt, calcium/cAMP, oxidative phosphorylation, microglial/immune pathways, and gut–brain metabolites—areas where combination, cell-type-specific and systems-biology strategies are actively being pursued ^{[2] [3] [4] [5] [6]}.