Introducing Alzheimer’s
Alzheimer’s disease (AD) is a degenerative brain disease and the most common form of dementia - approximately 60-70% of dementia incidence (1). Dementia is a syndrome (a cluster of symptoms) which is characterised by difficulties in cognitive faculties like memory, language, and problem-solving, that impact performance of every day activities (2). These symptoms arise due to neuron (nerve cell) destruction in the brain. In Alzheimer’s, neurons are also destroyed in parts of the brain that govern basic bodily functions, like walking and swallowing, as well as cognitive functions. In the early stages of neuronal damage, the brain is able to compensate and no symptoms are seen. However, eventually there is a tipping point and disease begins to manifest. The neuropathological hallmarks of AD include extracellular (outside the cell) accumulation of amyloid-beta (AB) plaques, intracellular (inside the cell) neurofibrillary tangles (NFTs), inflammation, synaptic impairment, and neuronal loss, ultimately leading to atrophy or brain shrinkage (3).
A Growing Concern
This decline in cognition is on the rise around the world. In 2020 there were an estimated 400,000-450,000 Australians living with dementia, 70% of which was Alzheimer’s (4). This is projected to increase to 590,000 by 2030. Another study projected that from 2005 to 2050, Alzheimer’s incidence in Australia and China will increase three- and five-fold respectively (5). In the United States, it is expected that there will be 16 million people living with AD by 2050 (1). Globally, 2050 expects to see 140 million Alzheimer’s cases that will cost a staggering $US20 trillion in medical care and lost productivity (1). Over half of aged-care residents in Australia likely have dementia, and in 2016, the annual cost in Australia of those suffering dementia in residential care was $88,000 per person. Due to the incapacitating nature of the disease, especially in its later stages, the direct and indirect costs are immense, and it is by far the most expensive chronic disease.
The Personal Costs
Almost half of the family and unpaid caregivers providing care to those suffering with health complications are caring for an older adult with dementia (6). In 2020, nearly US$257 billion was provided by friends and family in unpaid care (2). The majority of dementia sufferers in Australia and China are reliant on family caregivers, and there are major concerns for recipients’ care and caregivers’ health. In fact, a 2010 American study found that spouses of AD sufferers are 600% more likely to develop Alzheimer’s themselves compared to matched controls without a spouse with AD (7). This is likely due to shared risk factors of AD between spouses as well as the significant toll of being a primary care giver - it’s difficult to take care of yourself when you are so depended upon by someone else.
Just Bad Genes?
While the risk of Alzheimer’s exponentially increases past the age of 65, evidence suggests the pathology of Alzheimer’s begins decades before symptoms arise (8). This includes accumulation of amyloid and tau proteins in the brain, and highlights the importance of prevention. There are twenty five genes associated with AD risk and they are mostly involved in the formation and removal of amyloid plaques (9). While there is a genetic component to Alzheimer’s disease, those who have a very strong genetic predisposition (as is the case for those born with Down syndrome) do not always develop clinical dementia (10). In 95% of cases, AD is “sporadic”, occurring without an obvious familial aggregation (11, 3). This highlights the importance of our environment on our risk for developing this disease, and puts the power of our health trajectory back in our hands.
Risk Factors
Advanced age is a clear risk factor for AD, however, it is accumulation of other risk factors overtime that leads to disease rather than age itself (12). Other risk factors include vascular issues like hypertension, high cholesterol, stroke, and atherosclerosis (plaque build up in arteries), as well as metabolic issues like type-2 diabetes, hyperinsulinaemia and obesity (3). In fact, some people are referring to AD as “type 3 diabetes” due to the connection to glucose dysregulation and insulin resistance has been found to occur in the brain itself. Other risk factors include traumatic brain injury, depression, smoking, and heavy alcohol consumption. These risk factors propel the mechanisms that are responsible for the development of AD, which lead to disease manifestation in concordance with genetic predispositions that further aggravate these drivers (1).
The Drivers
There are four mechanisms leading to AD. They are:
Glucose/energy dysregulation: Alzheimer’s disease has also been termed “Type 3 Diabetes” due to the link between the brain insulin resistance and Alzheimer’s pathology (13).
Lipid dysregulation: high cholesterol and an unfavourable fatty acid profile contribute to disease processes, while also moderating Alzheimer’s related genes like APOE4, which most highly correlates with disease risk (14).
Inflammation: chronic and destructive immune response in the brain, increasing neurodegeneration, vascular impairment, and toxin production (15).
Oxidative stress: the brain is particularly vulnerable to oxidative stress due to its high energy consumption and lack of an effective antioxidant system. Its high lipid content also makes it vulnerable to lipid “peroxidation” which damages tissue (16).
A Lifestyle Disease
These drivers of Alzheimer’s are all impacted by our lifestyles: what we eat, how we move, how we deal with stress, our sleep quality, and how we use and challenge our brains. This means that this devastating disease can very much be prevented - and the science clearly shows this. The next five blogs will unravel the science of preventing Alzheimer’s through nutrition, exercise, unwinding, restorative sleep, and optimising brain function. This method is the NEURO method, and was introduced by the amazing husband and wife neurologist powerhouse Drs Dean and Ayesha Sherzai.
Written by Jessica Zabow
Clinical Nutritionist (BHSc)
& Yoga Teacher (RYT500)
References:
Sherzai, D., & Sherzai, A. (2019). Preventing Alzheimer’s: Our most urgent health care priority. American Journal of Lifestyle Medicine, 13(5), 451-461. https://doi.org/10.1177/1559827619843465
Alzheimer's Association. (2017). Alzheimer's Disease Facts and Figures. Retrieved from https://www.alz.org/media/images/2017-facts-and-figures.pdf
Edwards III, G.A., Gamez, N., Escobedo Jr, G., Calderon, O., & Moreno-Gonzalez, I. (2019). Modifiable risk factors for Alzheimer’s disease. Frontiers in Aging Neuroscience, 11(146), 1-18. https://doi.org/10.3389/fnagi.2019.00146
Australian Institute of Health and Welfare. (2020). Dementia. Retrieved from https://www.aihw.gov.au/reports/australias-health/dementia
Xiao, L.D., Wang, J., He, G., De Bellis, A., Verbeeck, J., & Kyriazopoulos, H. (2014). Family care giver challenges in dementia care in Australia and China: A critical perspective. BMC Geriatrics, 14(6), 1-13. https://doi.org/10.1186/1471-2318-14-6
Wolff, J.L., Spillman, B.C., Freedman, V.A., & Kasper, J.D. (2016). A national profile of family and unpaid caregivers who assist older adults with health care activities. Journal of the American Medical Association, 176(3), 372-379. https://doi.org/10.1001/jamainternmed.2015.7664
Norton, M.C., Smith, K.R., Ostbye, T., Tschanz, J.T., Corcoran, C., Schwartz, S., Piercy, K.W., Rabins, P.V., Steffens, D.C., Skoog, I., Breitner, J.C.S., & Welsh-Böhmer, K.A. (2010). Increased risk of dementia when spouse has dementia? The Cache County Study. Journal of American Geriatric Society, 58(5), 895-900. https://doi.org/10.1111/j.1532-5415.2010.02806.x
Beason-Held, L.L., Goh, J.O., An, Y., Kraut, M.A., O’Brien, R.J., Ferrucci, L., & Resnick, S.M. (2013). Changes in brain function occurs years before the onset of cognitive impairment. The Journal of Neuroscience, 33(46), 18008-18014. https://doi.org/10.1523/JNEUROSCI.1402-13.2013
Karch, C.M., & Grate, A.M. (2015). Alzheimer’s disease risk genes and mechanisms of disease pathogenesis. Biological Psychiatry, 77(1), 43-51. https://doi.org/10.1016/j.biopsych.2014.05.006
Head, E., Powell, D., Gold, B.T., & Schmitt, F.A. (2012). Alzheimer’s disease in Down syndrome. European Journal of Neurodegenerative Disease, 1(3), 353-364. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4184282/
Bellenguez, C., Grenier-Boley, B., & Lambert, J-C. (2020). Genetics of Alzheimer’s disease: Where we are, and where we are going. Current Opinion in Neurobiology, 61(1), 40-48. https://doi.org/10.1016/j.conb.2019.11.024
Nicolia, V., Lucarelli, M., & Fuso, A. (2014). Environment, epigeneti and neurodegeneration: Focus on nutrition in Alzheimer's disease. Experimental Gerontology, 68(1), 8-12. https://doi.org/10.1016/j.exger.2014.10.006
Ferreira, L.S.S., Fernandes, C.S., Vieira, M.N.N., & De Felice, F.G. (2018). Insulin resistance in Alzheimer’s disease. Frontiers in Neuroscience, 12(830), 1-11. https://doi.org/10.3389/fnins.2018.00830
Chew, H., Solomon, V.A., & Fonteh, A.N. (2020). Involvement of lipids in Alzheimer’s disease pathology and potential therapies. Frontiers in Physiology, 11(598), 1-28. https://doi.org/10.3389/fphys.2020.00598
Govindpani, K., McNamara, L.G., Smith, N.R., Vinnakota, C., Waldvogel, H.J., Fall, R.L.M., & Kwakowsky, A. (2019). Vascular dysfunction in Alzheimer’s disease: A prelude to the pathological process or a consequence of it? Journal of Clinical Medicine, 8(5), 1-57. https://doi.org/10.3390/jcm8050651
Cutler, R.G., Kelly, J., Storie, K., Pedersen, W.A., Tammara, A., Hatanpaa, K., Troncoso, J.C., & Mattson, M.P. (2004). Involvement of oxidative stress-induced abnormalities in ceramics and cholesterol metabolism in brain aging and Alzheimer’s disease. PNAS, 101(7), 2070-2075. https://doi.org/10.1073/pnas.0305799101