Estimated reading time: 19 minutes


If you are reading this blog post, it may be because you already suspect or have a diagnosis of mild cognitive impairment (MCI). Some cases of mild cognitive impairment (MCI) will stop in progression and not move towards impaired functioning at a level to meet the criteria for Dementia.

What is Mild Cognitive Impairment (MCI)? Start here:

But the majority of Mild Cognitive Impairment (MCI) cases will develop into dementias. And even if your neurodegenerative progression stops at Mild Cognitive Impairment (MCI), those symptoms affect the quality of your life and your functioning. Unfortunately, there are not particularly stellar treatments for this type of general cognitive decline found in mainstream medicine, there actually are in fact, treatments with excellent research found to improve functioning.

So whether you want your brain back from early cognitive decline in the form of recurrent or chronic brain fog and/or Mild Cognitive Impairment (MCI) symptoms, or you are wanting to stop the neurodegenerative progression into Alzheimer’s or some other form of dementia, this is the blog post for you. You may be reading this blog post not because you are suffering from symptoms of cognitive decline, but researching how to help someone you love. And if that is the case, this is still the blog post for you.

There can be a lot of factors that contribute to cognitive decline. But don’t let that overwhelm you. There is a first place to start that will improve symptoms and set the stage for any other testing and improvements that need to be made. There are a lot of things that go wrong in brains with cognitive symptoms. In this post we will discuss two theories about what is going wrong with what I consider to be very compelling evidence. Then we will talk about an excellent first step to begin addressing it and then what I see to be effective in my work as a licensed mental health counselor using nutritional and functional psychiatry principles in my work with clients. Many of them suffer from cognitive symptoms, with and without identifying as mood disorders, at a variety of ages.

The Network Hypothesis of Alzheimer’s Disease

This hypothesis has some excellent evidence to support it and uses data from functional MRI. What they notice is that there is a problem in how different brain structures speak to one another and that it happens very early in the disease process. In fact, people who have a predisposition to develop Alzheimer’s disease (e.g., APOE-ε4 carriers) can begin to see the dysfunctional connectivity happening before any symptoms. It tends to begin in the posterior default mode network (DMN) and once it begins to travel to the dorsal attention network (DAN) researchers begin to see symptoms emerge of mild cognitive impairment (MCI). This part of the brain does just what its title would suggest. It allows you to pay attention. If you cannot pay attention, you cannot take in information well and episodic memory becomes impaired.

ep·i·sod·ic mem·o·ry - noun (Oxford Languages via Google)

a type of long-term memory that involves conscious recollection of previous experiences together with their context in terms of time, place, associated emotions, etc.
"those results suggest that participants were using episodic memory to recall the presented words in all conditions"

a conscious memory of a previous experience.
"the hippocampus is critically involved in forming episodic memories" 

As researchers watch the decrease in functional connectivity progress, they can observe and even predict decreased performance in attentional tasks that include being alert, orienting toward what needs their attention and holding attention. There is also decreased functional connectivity in the salience network and includes important brain structures of the anterior cingulate and ventral anterior insular cortices, which also include important nodes of communication in the amygdala, ventral striatum, brainstem, thalamus and hypothalamus. Different people will experience connectivity issues in different parts of the brain, and so you may see problems with a person’s ability to evaluate their own functioning or visual disturbances as disease progression continues.

Not Enough Brain Energy

If you are having neurodegenerative disorder symptoms (brain fog, MCI, dementia), you are having glucose energy metabolism problems in your brain. What does that mean? It means there are parts of your brain that are taking up less glucose and producing less energy. And it’s happening most likely in your medial temporal lobe regions that include the hippocampus, entorhinal cortex, and the posterior cingulate cortex we just discussed that is part of the posterior DMN. This is a problem because these are areas that researchers know are involved when episodic memory becomes impaired. But this decrease in fuel in these parts of the brain is about a lot more than just memory function. It is important to understand that the brain takes enormous amounts of energy to upkeep neurons and once there is a deficit of energy your brain cells cannot do basic functions to ensure the health and functioning of the cells:

  • upkeeping membranes
  • creation and function of cell batteries (mitochondria)
  • storing nutrients needed to create neurotransmitters and enzymes
  • having nice strong pulses of action potential to signal between neurons

I could go on and on about all the ways just not having enough energy in the brain creates a neurodegenerative cascade that is the equivalent of a runaway train of cognitive doom.

Now, enough of this talk about what is going wrong. Let’s begin the discussion of how to fix it.

Enter Ketones

Ketones provide an alternative fuel for areas of the brain that are energy-starved. Remember our discussion about some areas of the brain not being able to use glucose for fuel as well? Ketones bypass those faulty mechanisms and upregulate energy metabolism. Ketones are signaling molecules, andhave a lot of other wonderful functions other than as an alternative fuel.  

Ketogenic interventions are now a promising neurotherapeutic strategy to restore cognitive functions in MCI and AD

Roy, M., Edde, M., Fortier, M., Croteau, E., Castellano, C. A., St-Pierre, V., … & Descoteaux, M. (2022). A ketogenic intervention improves dorsal attention network functional and structural connectivity in mild cognitive impairment. Neurobiology of Aging.

The most obvious benefit ketones provide is fuel for starving areas of the brain. But they do so much more. Ketones are structurally important for brain cell maintenance and healing. For example, they are building blocks for myelin sheaths that protect nerves from the electrical firing of action potentials and are in constant need of repair. In their role as signaling bodies, they turn on anti-inflammatory pathways, although I would argue that if relying on exogenous ketone supplements alone without changing an inflammatory diet these benefits would be under-realized for a person working to heal their brain. Ketones reduce oxidative stress and improve connectivity between brain structures, even within the deep white matter areas in the brain. They upregulate the production of Brain-Derived Neurotrophic Factor (BDNF) which contributes to that improved connectivity and neuronal repair, and this substance plays an intimate role in memory and the hippocampus.

Ketones also improve the integrity of the blood-brain barrier, which has an important job to protect the brain from toxins or other substances that would cause inflammatory processes that could increase damage to the brain. They upregulate the production of glutathione, which is the body’s own antioxidant system designed to help combat oxidative stress (yes, especially in the brain).

Ketones provide a multi-level intervention to not only rescue cognitive function but to heal brains and slow or possibly even stop, neurodegenerative processes.

Ketogenic Therapies

As you do your research on how to improve cognitive function, you will encounter studies about ketones and the different ways that ketones can be supplied. There are exogenous ketones that a person can drink or add to food in the form of MCT oil, for example. Or there are ketones that are made from a person breaking down dietary fats or their own body fat into ketone bodies. And there is of course the combination of the two. Most studies are looking at MCT oil. MCT oil is excellent fuel for the brain, and I highly recommend it. But it can cause a lot of digestive distress and so it should be worked up in dose very slowly. However, because it has distinct digestive drawbacks (diarrhea) for many people, it can be difficult or sometimes even impossible to work up to a dose that relieves symptoms.

From just a practical standpoint, if you ask anyone to take MCT oil, they will tell you even a tablespoon (15mL) can cause issues. In one study I looked at participants had to begin with 50mL (about 3 TBSP) and work up to 250mL (about 17 TBSP). The participants had to be worked up to such a large dose over 6 months, and the pre-proof version of the study (at the time I write this blog post) did not specify how often participants were needing to dose themselves. (See Roy, et al., 2022 in references).

Why just taking a lot of MCT oil is not the answer

Your state of insulin resistance also matters in neurodegenerative disease progression. It’s great to increase your brain fuel with MCT oil that will help provide ketones to do all the things that heal your brain. But focusing on only increasing ketones does not address that a brain awash in glucose is not a happy brain. If you have developed insulin resistance, you will need to change your diet significantly in order to improve or reverse this disease state.

Specifically, while individuals with increasing fasting glucose did not yet show cognitive decline, they did have regional atrophy in the hippocampus and inferior parietal cortex, and increased amyloid accumulation in the precuneus cortex.

Honea, R. A., John, C. S., Green, Z. D., Kueck, P. J., Taylor, M. K., Lepping, R. J., … & Morris, J. K. (2022). Relationship of fasting glucose and longitudinal Alzheimer’s disease imaging markers. Alzheimer’s & Dementia: Translational Research & Clinical Interventions8(1), e12239.

Also, as you age the likelihood that you have developed insulin resistance increases, and improving your insulin sensitivity can help stave off diseases of aging. People with high insulin resistance are at a higher risk of many disease processes, either directly in a causative manner or at the very least in a highly associational and suspect manner. What are some of the diseases found to have roots in untreated insulin resistance? Or at the very least a very high association? They include the following:

  • Cardiovascular – Hypertension, Atherosclerosis, Cardiomyopathy, Hyperlipidemia profiles
  • Neurological – Alzheimer’s Disease, Parkinson’s Disease, Vascular Dementia, Migraine Headaches, Neuropathy
  • Cancer – Breast, Prostate, and Colorectal
  • Musculoskeletal – Sarcopenia, Osteoporosis, Osteoarthritis
  • Digestive – Gout, Reflux Esophagitis (GERD), Problems passing stool (Gastroparesis)
  • Liver Disease – Hyperlipidemia (indicative of a problem with the liver, not the cardiovascular system), Nonalcoholic Fatty Liver Disease,
  • Gallbladder and Kidney Disease – Gallstones, Kidney Stones, Kidney Failure

These disease processes will steal your vitality and quality of life just as severely as untreated cognitive symptoms and Alzheimer’s disease or another dementia would. But besides that fact, these chronic disease processes also affect your brain indirectly.

Just providing the brain with an alternative fuel source is not a sufficient intervention for mild cognitive impairment or early Alzheimer’s disease. Not if we care about the entire body and your future quality of life. For example, if you give yourself lots of MCT oil, and feel better in your brain, but do not change your diet to help reverse insulin resistance (which ketogenic diets do), then as your atherosclerosis progresses you will begin to have cardiovascular disease.

As your cardiovascular disease progresses you are going to start to have problems with oxygen and nutrients being pumped to your brain and the rest of your body. And that is just one of many mechanisms that become impaired in cardiovascular disease that can influence the health of the brain. A failing cardiovascular system will most certainly affect your brain. I don’t care how much MCT oil you take.


I see much better clinical outcomes when we implement a ketogenic diet for the treatment of cognitive impairment, whether it is slightly more severe run-of-the-mill brain fog that many people experience, formally diagnosed Mild Cognitive Impairment (MCI), or even early dementia. MCT oil and other exogenous ketone supplements are used to build upon an already ketogenic base of brain fuel that happens with therapeutic carbohydrate restriction. MCT oil is an enhancement. It is not the intervention that saves your brain. MCT oil by itself is an attempted band-aid for neurodegenerative processes. Without the reduction in carbohydrates that treats hyperglycemia and insulin resistance, you are not adequately addressing the neurodegenerative processes that will continue to happen in the background. Whether these are directly happening in the brain (which I guarantee they are) or by a secondary chronic disease process, such as those we already read about.

I don’t tell you the shortfalls of MCT oil in treating neurodegenerative processes to make you despair. I know the possibility of having to change your diet to slow down, stop or even reverse your disease process is hard, and you may not be sure what that would even look like. You may find these blog posts helpful.

I write this because if you or a loved one is suffering from cognitive symptoms, I do not want you to dose MCT oil, not see improvements, and then give up believing that ketones can help you. MCT oil alone is not the same level of intervention that a well-formulated ketogenic diet is, and it is not the same intervention you would experience if you combined the two. I have had many clients who felt no difference when supplementing MCT oil but felt their brains heal and improve function using a ketogenic diet.

So if MCT oil does not reduce your symptoms, please do not give up hope.

Providing ketones, whether through a well-formulated ketogenic diet or with increased MCT ingestion are the first step in rescuing cognitive function. Secondary steps can be nutrigenomic analysis to ensure adequate micronutrient intake, and additional testing to rule out other factors in the disease process, often done with functional medicine testing. But first thing first, we must rescue brain energy.

Ketones do that.

But whatever you decide, do not waste time. Time is of the essence in the treatment of neurodegenerative disorders.

If you are a woman who is suffering from cognitive symptoms, in the form of brain fog, difficulty focusing or remembering things, or paying attention, please sign up for my program research. I am creating a program to help bring these steps of healing and transformation to women in a way that marries nutritional and functional psychiatry with group support and coaching to ensure success.

You can learn more about it here:

If you would like to sign up for the mailing list to learn about upcoming programs, courses, and learning opportunities you may do so here:

Because you have the right to know all of the ways that you can feel better.


Achanta, L. B., & Rae, C. D. (2017). β-Hydroxybutyrate in the Brain: One Molecule, Multiple Mechanisms. Neurochemical Research, 42(1), 35–49.

An, Y., Varma, V. R., Varma, S., Casanova, R., Dammer, E., Pletnikova, O., Chia, C. W., Egan, J. M., Ferrucci, L., Troncoso, J., Levey, A. I., Lah, J., Seyfried, N. T., Legido-Quigley, C., O’Brien, R., & Thambisetty, M. (2018). Evidence for brain glucose dysregulation in Alzheimer’s disease. Alzheimer’s & Dementia, 14(3), 318–329.

Avgerinos, K. I., Egan, J. M., Mattson, M. P., & Kapogiannis, D. (2020). Medium Chain Triglycerides induce mild ketosis and may improve cognition in Alzheimer’s disease. A systematic review and meta-analysis of human studies. Ageing Research Reviews, 58, 101001.

Balthazar, M. L. F., de Campos, B. M., Franco, A. R., Damasceno, B. P., & Cendes, F. (2014). Whole cortical and default mode network mean functional connectivity as potential biomarkers for mild Alzheimer’s disease. Psychiatry Research: Neuroimaging, 221(1), 37–42.

Banjara, M., & Janigro, D. (n.d.). Effects of the Ketogenic Diet on the Blood-Brain Barrier. In Ketogenic Diet and Metabolic Therapies. Oxford University Press. Retrieved January 8, 2022, from

Bernard, C., Dilharreguy, B., Helmer, C., Chanraud, S., Amieva, H., Dartigues, J.-F., Allard, M., & Catheline, G. (2015). PCC characteristics at rest in 10-year memory decliners. Neurobiology of Aging, 36(10), 2812–2820.

Bickman, B. (2020). Why we get sick: The hidden epidemic at the root of most chronic disease—And how to fight it. BenBella Books, Inc.

Carneiro, L., & Pellerin, L. (2021). Nutritional Impact on Metabolic Homeostasis and Brain Health. Frontiers in Neuroscience, 15.

Croteau, E., Castellano, C. A., Fortier, M., Bocti, C., Fulop, T., Paquet, N., & Cunnane, S. C. (2018). A cross-sectional comparison of brain glucose and ketone metabolism in cognitively healthy older adults, mild cognitive impairment and early Alzheimer’s disease. Experimental Gerontology, 107, 18–26.

Cunnane, S. C., Trushina, E., Morland, C., Prigione, A., Casadesus, G., Andrews, Z. B., Beal, M. F., Bergersen, L. H., Brinton, R. D., de la Monte, S., Eckert, A., Harvey, J., Jeggo, R., Jhamandas, J. H., Kann, O., la Cour, C. M., Martin, W. F., Mithieux, G., Moreira, P. I., … Millan, M. J. (2020). Brain energy rescue: An emerging therapeutic concept for neurodegenerative disorders of ageing. Nature Reviews Drug Discovery, 19(9), 609–633.

Decreased hippocampal metabolism in high‐amyloid mild cognitive impairment—Hanseeuw—2016—Alzheimer’s & Dementia—Wiley Online Library. (n.d.). Retrieved April 16, 2022, from

Default Mode Network—An overview | ScienceDirect Topics. (n.d.). Retrieved April 16, 2022, from

Dewsbury, L. S., Lim, C. K., & Steiner, G. Z. (2021). The Efficacy of Ketogenic Therapies in the Clinical Management of People with Neurodegenerative Disease: A Systematic Review. Advances in Nutrition, 12(4), 1571–1593.

Dorsal Attention Network—An overview | ScienceDirect Topics. (n.d.). Retrieved April 16, 2022, from

Fascicle- and Glucose-Specific Deterioration in White Matter Energy Supply in Alzheimer’s Disease—IOS Press. (n.d.). Retrieved April 16, 2022, from

Field, R., Field, T., Pourkazemi, F., & Rooney, K. (2021). Ketogenic diets and the nervous system: A scoping review of neurological outcomes from nutritional ketosis in animal studies. Nutrition Research Reviews, 1–14.

Forsythe, C. E., Phinney, S. D., Fernandez, M. L., Quann, E. E., Wood, R. J., Bibus, D. M., Kraemer, W. J., Feinman, R. D., & Volek, J. S. (2008). Comparison of Low Fat and Low Carbohydrate Diets on Circulating Fatty Acid Composition and Markers of Inflammation. Lipids, 43(1), 65–77.

Gano, L. B., Patel, M., & Rho, J. M. (2014). Ketogenic diets, mitochondria, and neurological diseases. Journal of Lipid Research, 55(11), 2211–2228.

Gough, S. M., Casella, A., Ortega, K. J., & Hackam, A. S. (2021). Neuroprotection by the Ketogenic Diet: Evidence and Controversies. Frontiers in Nutrition, 8, 782657.

Grammatikopoulou, M. G., Goulis, D. G., Gkiouras, K., Theodoridis, X., Gkouskou, K. K., Evangeliou, A., Dardiotis, E., & Bogdanos, D. P. (2020). To Keto or Not to Keto? A Systematic Review of Randomized Controlled Trials Assessing the Effects of Ketogenic Therapy on Alzheimer Disease. Advances in Nutrition, 11(6), 1583–1602.

Hodgetts, C. J., Shine, J. P., Williams, H., Postans, M., Sims, R., Williams, J., Lawrence, A. D., & Graham, K. S. (2019). Increased posterior default mode network activity and structural connectivity in young adult APOE-ε4 carriers: A multimodal imaging investigation. Neurobiology of Aging, 73, 82–91.

Honea, R. A., John, C. S., Green, Z. D., Kueck, P. J., Taylor, M. K., Lepping, R. J., Townley, R., Vidoni, E. D., Burns, J. M., & Morris, J. K. (2022). Relationship of fasting glucose and longitudinal Alzheimer’s disease imaging markers. Alzheimer’s & Dementia: Translational Research & Clinical Interventions, 8(1), e12239.

Huang, J., Beach, P., Bozoki, A., & Zhu, D. C. (2021). Alzheimer’s Disease Progressively Reduces Visual Functional Network Connectivity. Journal of Alzheimer’s Disease Reports, 5(1), 549–562.

Jensen, N. J., Wodschow, H. Z., Nilsson, M., & Rungby, J. (2020). Effects of Ketone Bodies on Brain Metabolism and Function in Neurodegenerative Diseases. International Journal of Molecular Sciences, 21(22).

Jones, D. T., Graff-Radford, J., Lowe, V. J., Wiste, H. J., Gunter, J. L., Senjem, M. L., Botha, H., Kantarci, K., Boeve, B. F., Knopman, D. S., Petersen, R. C., & Jack, C. R. (2017). Tau, amyloid, and cascading network failure across the Alzheimer’s disease spectrum. Cortex, 97, 143–159.

Jones, D. T., Knopman, D. S., Gunter, J. L., Graff-Radford, J., Vemuri, P., Boeve, B. F., Petersen, R. C., Weiner, M. W., Jack, C. R., Jr, & on behalf of the Alzheimer’s Disease Neuroimaging Initiative. (2016). Cascading network failure across the Alzheimer’s disease spectrum. Brain, 139(2), 547–562.

Juby, A. G., Blackburn, T. E., & Mager, D. R. (2022). Use of medium chain triglyceride (MCT) oil in subjects with Alzheimer’s disease: A randomized, double-blind, placebo-controlled, crossover study, with an open-label extension. Alzheimer’s & Dementia: Translational Research & Clinical Interventions, 8(1), e12259.

Kovacs, Z., D’Agostino, D. P., & Ari, C. (2022). Neuroprotective and behavioral benefits of exogenous ketones. In Ketogenic Diet and Metabolic Therapies: Expanded roles in health and disease (2nd ed., pp. 426–465). Oxford University Press. 10.1093/med/9780197501207.001.0001

Masino, S. A., & Rho, J. M. (2012). Mechanisms of Ketogenic Diet Action. In J. L. Noebels, M. Avoli, M. A. Rogawski, R. W. Olsen, & A. V. Delgado-Escueta (Eds.), Jasper’s Basic Mechanisms of the Epilepsies (4th ed.). National Center for Biotechnology Information (US).

Morris, A. a. M. (2005). Cerebral ketone body metabolism. Journal of Inherited Metabolic Disease, 28(2), 109–121.

Newman, J. C., & Verdin, E. (2017). β-Hydroxybutyrate: A Signaling Metabolite. Annual Review of Nutrition, 37, 51.

Ranganath, C., & Ritchey, M. (2012). Two cortical systems for memory-guided behaviour. Nature Reviews Neuroscience, 13(10), 713–726.

Roy, M., Edde, M., Fortier, M., Croteau, E., Castellano, C.-A., St-Pierre, V., Vandenberghe, C., Rheault, F., Dadar, M., Duchesne, S., Bocti, C., Fulop, T., Cunnane, S. C., & Descoteaux, M. (2022). A ketogenic intervention improves dorsal attention network functional and structural connectivity in mild cognitive impairment. Neurobiology of Aging.

Roy, M., Fortier, M., Rheault, F., Edde, M., Croteau, E., Castellano, C.-A., Langlois, F., St-Pierre, V., Cuenoud, B., Bocti, C., Fulop, T., Descoteaux, M., & Cunnane, S. C. (2021). A ketogenic supplement improves white matter energy supply and processing speed in mild cognitive impairment. Alzheimer’s & Dementia: Translational Research & Clinical Interventions, 7(1), e12217.

Saito, E. R., Miller, J. B., Harari, O., Cruchaga, C., Mihindukulasuriya, K. A., Kauwe, J. S. K., & Bikman, B. T. (2021). Alzheimer’s disease alters oligodendrocytic glycolytic and ketolytic gene expression. Alzheimer’s & Dementia, 17(9), 1474–1486.

Schultz, A. P., Buckley, R. F., Hampton, O. L., Scott, M. R., Properzi, M. J., Peña-Gómez, C., Pruzin, J. J., Yang, H.-S., Johnson, K. A., Sperling, R. A., & Chhatwal, J. P. (2020). Longitudinal degradation of the default/salience network axis in symptomatic individuals with elevated amyloid burden. NeuroImage: Clinical, 26, 102052.

Seeley, W. W. (2019). The Salience Network: A Neural System for Perceiving and Responding to Homeostatic Demands. Journal of Neuroscience, 39(50), 9878–9882.

Shimazu, T., Hirschey, M. D., Newman, J., He, W., Shirakawa, K., Le Moan, N., Grueter, C. A., Lim, H., Saunders, L. R., Stevens, R. D., Newgard, C. B., Farese, R. V., de Cabo, R., Ulrich, S., Akassoglou, K., & Verdin, E. (2013). Suppression of Oxidative Stress by β-Hydroxybutyrate, an Endogenous Histone Deacetylase Inhibitor. Science, 339(6116), 211–214.

Shippy, D. C., Wilhelm, C., Viharkumar, P. A., Raife, T. J., & Ulland, T. K. (2020). β-Hydroxybutyrate inhibits inflammasome activation to attenuate Alzheimer’s disease pathology. Journal of Neuroinflammation, 17(1), 280.

Staffaroni, A. M., Brown, J. A., Casaletto, K. B., Elahi, F. M., Deng, J., Neuhaus, J., Cobigo, Y., Mumford, P. S., Walters, S., Saloner, R., Karydas, A., Coppola, G., Rosen, H. J., Miller, B. L., Seeley, W. W., & Kramer, J. H. (2018). The Longitudinal Trajectory of Default Mode Network Connectivity in Healthy Older Adults Varies As a Function of Age and Is Associated with Changes in Episodic Memory and Processing Speed. The Journal of Neuroscience, 38(11), 2809–2817.

The Salience Network: A Neural System for Perceiving and Responding to Homeostatic Demands | Journal of Neuroscience. (n.d.). Retrieved April 16, 2022, from

Thomas, J. B., Brier, M. R., Bateman, R. J., Snyder, A. Z., Benzinger, T. L., Xiong, C., Raichle, M., Holtzman, D. M., Sperling, R. A., Mayeux, R., Ghetti, B., Ringman, J. M., Salloway, S., McDade, E., Rossor, M. N., Ourselin, S., Schofield, P. R., Masters, C. L., Martins, R. N., … Ances, B. M. (2014). Functional Connectivity in Autosomal Dominant and Late-Onset Alzheimer Disease. JAMA Neurology, 71(9), 1111–1122.

Valera-Bermejo, J. M., De Marco, M., & Venneri, A. (2022). Altered Interplay Among Large-Scale Brain Functional Networks Modulates Multi-Domain Anosognosia in Early Alzheimer’s Disease. Frontiers in Aging Neuroscience, 13, 781465.

van Niekerk, G., Davis, T., Patterton, H.-G., & Engelbrecht, A.-M. (2019). How Does Inflammation-Induced Hyperglycemia Cause Mitochondrial Dysfunction in Immune Cells? BioEssays: News and Reviews in Molecular, Cellular and Developmental Biology, 41(5), e1800260.

Vemuri, P., Jones, D. T., & Jack, C. R. (2012). Resting state functional MRI in Alzheimer’s Disease. Alzheimer’s Research & Therapy, 4(1), 2.

Very-low-carbohydrate diet enhances human T-cell immunity through immunometabolic reprogramming. (2021). EMBO Molecular Medicine, 13(8), e14323.

Vizuete, A. F., de Souza, D. F., Guerra, M. C., Batassini, C., Dutra, M. F., Bernardi, C., Costa, A. P., & Gonçalves, C.-A. (2013). Brain changes in BDNF and S100B induced by ketogenic diets in Wistar rats. Life Sciences, 92(17), 923–928.

Yamanashi, T., Iwata, M., Kamiya, N., Tsunetomi, K., Kajitani, N., Wada, N., Iitsuka, T., Yamauchi, T., Miura, A., Pu, S., Shirayama, Y., Watanabe, K., Duman, R. S., & Kaneko, K. (2017). Beta-hydroxybutyrate, an endogenic NLRP3 inflammasome inhibitor, attenuates stress-induced behavioral and inflammatory responses. Scientific Reports, 7(1), 7677.

Leave a Reply

This site uses Akismet to reduce spam. Learn how your comment data is processed.