About Alzheimer's Disease
Currently, there are no significant prevention or cure for Alzheimer's Disease.
Hallmarks of Alzheimer's Disease
1. Aggregation of amyloid plaques
2. Neurofibrillary tangles
3. Neuro-inflammation
4. Cognitive decline
Prevalence
1 1 | 2 2 | 3 3 | 4 4 | 5 5 | 6 6 | |
|---|---|---|---|---|---|---|
Region | Asia | Europe | Northern America | Latin America & Caribbean | Africa | Oceania |
| Estimated Cases in 2022 | 64.5 M | 8.9 M | 4.9 M | 3.9 M | 3.1 M | 0.3 M |
| Estimated Cases in 2025 | 71.9 M | 9.4 M | 5.3 M | 4.4 M | 3.5 M | 0.3 M |
| Increased rate (2022-2025) | +11.5% | +5.4% | +8.5% | +11.7% | +11.2% | +9.4% |
Unmet Needs
Despite the progress in understanding the pathophysiology of Alzheimer's Disease, there is currently no cure for Alzheimer's Disease, and existing treatments are limited in their efficacy.
Anti-dementia drugs only help to temporarily slow the decline of symptoms and do not address the underlying cause or progression of the disease. Moreover, these medications are often associated with unpleasant side effects, such as nausea, vomiting, and dizziness.
GBC is developing a novel and oral intake compound that has the potential to address the unmet medical needs of Alzheimer's Disease. This innovative therapy will lead to a more comprehensive approach to treating the condition.
Antroquinonol – proposed model
1. Antroquinonol reduces amyloid plaque accumulation
2. Antroquinonol enhances Nrf2 , and inhibits Tau and IL-1β
3. Antroquinonol restores cognitive function and memory
Nrf2 – A Promising Target to treat Alzheimer's Disease
- Relationship between Nrf2 & Aβ:
Nrf2/ARE pathway negatively regulates BACE1 expression & ameliorates cognitive deficits in mouse Alzheimer's models.
- Relationship between Nrf2 & Tau:
A significant increase is also observed in the insoluble p-Tau and Aβ levels in Nrf2-deficient mice.
- Relationship between Nrf2 & Pro-inflammatory cytokines:
Nrf2 negatively controls the NF-KB signaling pathway. NF-KB induces the expression of pro-inflammatory cytokines (IL-1, IL-6, TNF-α).
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