TRFT has three “disease-modifying” mechanisms of action that target many diseases of aging, and normal aging itself, to likely increase human longevity.

• TRFT re-balances the body and brain’s immune system

• TRFT disaggregates and removes toxic proteins from the brain

• TRFT Increases energy production in the brain

Question: What do all of the below diseases of aging have in common?

• Alzheimer’s Disease
• Brain Cancer
• Multiple Sclerosis
• Chronic Kidney Disease
• Arterial Hypertension
• Parkinson’s Disease

• Cardiovascular Disease
• Bacterial/Viral Infections
• FTL Dementia
• Body Cancers (e.g., lung)
• Amyotophic Lat Sclerosis
• IBD

• Diabetes
• Rheumatoid Arthritis
• Lymphomas
• Peripheral Neuropathy
• Chronic Pain
• LATE Dementia

Answer: An imbalanced immune system in later years, also known as “Inflamm-aging”. This imbalance is due to over-activation of the immune system’s pro-inflammatory component over its anti-inflammatory component, as indexed by the immune system’s effectors — “cytokines”.

Another Question: Aside from possible genetic advantages, what is it about Centenarians that provides for their extreme longevity?

Answer: They maintain a balanced immune system.

Although neuritic plaques and neurofibrillary tangles in the brain have long been thought to be the cause of AD, this is no longer the case in view of compelling newer evidence that toxic protein aggregates (oligomers) inside neurons are the real culprits [Arendash 2016; Arendash et al., 2022]. More specifically, small toxic oligomers of two proteins (Aβ and p-Tau) increase in neurons during aging and much more so in AD (see below figure, left). In AD, these oligomers cause neurons to dysfunction (e.g., mitochondrial and microtubule dysfunction), which ultimately leads to their death. Drugs have thus far failed to prevent, stop, or reverse AD in large part because they have great difficulty getting inside neurons and because they do not specifically target Aβ and p-Tau oligomers.

In sharp contrast, TRFT disaggregates BOTH of these toxic oligomers inside neurons into single (monomeric) proteins that are non-toxic (see above figure, right). This results in a substantial decrease in these two toxic oligomers and ensuing reversal of the damage they cause, including reversal of cognitive impairment in AD subjects [Arendash et al., 2019].

Evidence for TRFT-induced disaggregation of Aβ oligomers has been attained from homogenized brains from AD subjects [NIH grant R43NS090653-01A1, Arendash/NeuroEM Therapeutics], wherein a sharp decrease in oligomeric Aβ in frontal cortex is seen within a few days of TRFT. In these same human brain homogenates, (oligomerized) p-Tau is decreased substantially within a few days of TRFT. Additional evidence for TRFT’s ability to disaggregate p-Tau oligomers is clinically present in living AD subjects (see “TRFT Clinical Studies” tab).

In a recently published study [Arendash et al., 2024], TRFT was also shown to increase the drainage/removal of these toxins from the brain, thus providing both toxin disaggregation in the brain and their subsequent removal from the brain. Collectively, the published body of TRFT clinical studies in AD subjects are noteworthy because they are the first to: 1) report effects of an intervention on soluble brain toxin levels (e.g., Aβ, tau), and 2) provide blood biomarker evidence of increased brain cleansing by a therapeutic intervention.

In addition to Alzheimer’s Disease, there are a host of age-related neurologic conditions whose pathogenesis involves toxic protein oligomers (Aβ, p-Tau, α-synuclein, and others) that are targeted by TRFT (see below listing) − this, because they all have the same basic structure that is vulnerable to disaggregation by specific radiofrequency waves [Arendash et al., 2019; 2022]:

Initial indications that TRFT is a mitochondrial/metabolic enhancer to increase the brain’s energy production were attained from our pre-clinical studies wherein both “aged” AD transgenic mice and normal mice were given one month of daily RF wave treatment [Dragicevic et al., 2011]. In aged AD mice, RF wave treatment enhanced brain mitochondrial function by 50-150%, especially in cognitively-important brain areas. Even normal “aged” mice showed an increase in mitochondrial function. Moreover, some human AD subjects given 2 months of daily TRFT showed a substantial increase in cerebral metabolic rate, as indicated by FDG-PET scans taken before and after 2 months of treatment (see figure) [Arendash et al., 2019]. Therefore, TRFT appears to be a brain metabolic/energy enhancer in humans.