From the Guidelines
There are no supplements or medications definitively proven to remove amyloid beta, tau, asynuclein, or TDP-43 proteins from the brain, and current treatments for Alzheimer's disease, such as Aducanumab and Lecanemab, have limited clinical benefits and only target amyloid plaques. These proteins are associated with neurodegenerative diseases like Alzheimer's, Parkinson's, and ALS. While some medications like Aducanumab (Aduhelm) and Lecanemab (Leqembi) have been approved by the FDA for treating Alzheimer's disease and can reduce amyloid plaques, their clinical benefits remain limited and controversial, as noted in a recent study published in Alzheimer's and Dementia 1. These medications are administered via intravenous infusion and carry risks including brain swelling and bleeding. They don't address tau, alpha-synuclein, or TDP-43 accumulation.
Some key points to consider:
- Research is ongoing for therapies targeting these proteins, but currently available supplements claiming to remove these proteins lack scientific validation, as highlighted in a study published in Nature Reviews Neurology 1.
- Management of neurodegenerative diseases typically involves symptomatic treatment rather than protein removal.
- Lifestyle factors like regular exercise, cognitive stimulation, Mediterranean diet, quality sleep, and stress management may help maintain brain health, though they don't directly remove these protein aggregates.
- The use of blood biomarker tests for the detection of AD pathology has become more widespread, and these tests are more acceptable and accessible than amyloid PET and CSF tests, as noted in a recent consensus statement 1.
- However, the performance of these tests varies widely, and minimum standards for clinically used blood biomarker tests are needed, as recommended by The Global CEO Initiative (CEOi) on Alzheimer’s Disease BBM Workgroup 1.
From the Research
Supplements/Medications for Removing Amyloid B, Tau, Alpha-Synuclein, and TDP-43
There are several studies that have investigated the role of supplements and medications in removing or reducing the levels of Amyloid B, Tau, Alpha-Synuclein, and TDP-43. Some of the key findings include:
- Apomorphine infusion has been shown to promote the degradation of Amyloid B in rodent models 2
- There is evidence that soluble forms of Amyloid B and Tau work together to drive healthy neurons into the diseased state, and that hallmark toxic properties of Amyloid B require Tau 3
- Alpha-Synuclein containing Lewy bodies and dystrophic Lewy neurites are found in Parkinson's disease and dementia with Lewy bodies, and there is a synergistic interplay among Amyloid B, Tau, and Alpha-Synuclein in several neurodegenerative diseases 4
- TDP-43 and total Tau protein play roles in frontotemporal dementia pathology, and plasma biomarkers such as Amyloid B 1-40, Aβ1-42, T-Tau, Alpha-Synuclein, and TDP-43 can be used to assess the presence of these pathologies 5
Potential Therapeutic Targets
Some potential therapeutic targets for removing or reducing the levels of Amyloid B, Tau, Alpha-Synuclein, and TDP-43 include:
- Inhibiting the aggregation of these proteins
- Promoting their degradation
- Reducing their production
- Blocking their toxic effects on neurons
- Using immunotherapies to target these proteins 4, 3
Current Research and Future Directions
Current research is focused on understanding the complex interactions between Amyloid B, Tau, Alpha-Synuclein, and TDP-43, and how they contribute to the development of neurodegenerative diseases. Future directions include: