Introduction
Memory loss, cognitive decline, and behavioral abnormalities are hallmarks of Alzheimer's disease, a progressive neurodegenerative illness. Millions of people worldwide are impacted by it, making it the most prevalent cause of dementia (Nicholas N., et al, 2022). The precise cause of the disease is still unknown despite much research, but it is strongly associated with pathological alterations in the brain, specifically the buildup of tau tangles and amyloid plaques (Selkoe,. et al, 2016). The pathophysiology, risk factors, diagnostic techniques, treatment plans, and current research initiatives of the disease are all examined in this article. As the world's population ages, the importance of comprehending Alzheimer's disease has increased, highlighting the necessity of early detection and successful interventions.
Pathophysiology and Causes
Alzheimer's disease is characterised by neurofibrillary tangles made of tau protein, which cause neuronal degeneration, and beta-amyloid plaques, which build up in the brain and impair cell function (Selkoe,. et al, 2016). A significant risk factor for late-onset Alzheimer's disease is the APOE 4 allele, whereas mutations in the APP, PSEN1, and PSEN2 genes are linked to early-onset Alzheimer's disease (Loy, C. T., 2014). A series of neurodegenerative processes that lead to cognitive impairment are triggered by these genetic factors, which also contribute to aberrant protein processing and accumulation in the brain. Environmental factors, such as head trauma and cardiovascular disease, may also raise the risk in addition to genetic factors (Corder, E. et al, 1993).
Figure 1 : Brain imaging showing Alzheimer’s-related atrophy. According to three visual rating scales—MCA (medial temporal atrophy), PA (posterior atrophy), and GCA-F (frontal atrophy)—different subtypes of Alzheimer's disease (AD) exhibit different patterns of brain atrophy. Widespread atrophy (abnormal MTA with PA and/or GCA-F) is characteristic of AD. Only MTA is impacted by limbo predominant. While MTA is normal, hippocampal sparing exhibits PA and/or GCA-F atrophy. On every scale, AD with minimal atrophy has normal scores. These patterns, which are frequently depicted alongside healthy controls, aid in differentiating between AD types.
Risk Factors
After age 65, Alzheimer’s disease is most strongly linked to getting older, as its rate of occurrence rises sharply with age (Livingston, 2020). People with the ε4 version of APOE and a family history of Alzheimer's have a significantly larger risk for the disease (Corder, E. et al, 1993). Things such as high blood pressure, diabetes and having too much cholesterol are added risks for heart disease (Kivipelto., et al, 2001). Experiencing head injuries, particularly repeatedly, appears to increase a person’s risk of dementia. Things related to a person’s lifestyle such as smoking, inactivity and a poor diet, can cause heart disease as well.
Lithium deficiency and the onset of Alzheimer’s disease
Research has shown that lithium levels in the brain may be linked to the development of Alzheimer’s disease. Studies comparing healthy individuals with those experiencing mild cognitive impairment (MCI) or Alzheimer’s found that lithium concentrations were significantly lower in the prefrontal cortex, a region strongly affected by the disease. However, no major changes were observed in the cerebellum or in blood lithium levels, suggesting that the deficiency is localised to brain tissue. This pattern indicates that disruptions in lithium balance within the brain could contribute to the onset and progression of Alzheimer’s disease (Aron, L, 2025).
Symptoms and Progression
Alzheimer’s usually takes three steps: early, middle and late. Early symptoms of Alzheimer’s disease are problems with language and mild memory problems. The middle stage is when people often have more noticeable struggles with thinking, communicating and recognising things. People who suffer from a stroke may have personality changes and difficulties remembering where they are. At this stage of the disease, patients require 24/7 care since they can’t talk, identify anyone or manage themselves (Cummings, J., 2021).
Diagnosis
Early discoveries help control symptoms and prepare plans. Expert doctors assess patients’ cognitive functions using MMSE and MoCA and also talk to people who care for them (Kivipelto., et al, 2001). Scans such as MRI and PET are often used to find out about Alzheimer’s changes in the brain. The use of amyloid-beta ratios in blood is being considered to diagnose Alzheimer’s disease earlier (Schindler, S. E, 2019).
Treatment Options
There is no cure, but medicine can control symptoms. Donepezil is taken in cholinesterase inhibitor form and improves brain activity, while memantine is given for mild to severe symptoms (Cummings, J., 2021). In 2021, aducanumab which works on beta-amyloid issues, was approved by the FDA although some scientists are not convinced it is helpful. Activities such as mental stimulation and physical exercise improve patients’ daily lives (Morris, M, 2015).
Prevention and Brain Health
Changes in lifestyle lower risk, but they cannot completely prevent it. Alzheimer's risk is reduced by regular exercise, a nutritious diet (such as a Mediterranean diet), and cognitively stimulating activities like reading (Morris, M, 2015). It's also crucial to control diabetes, cholesterol, and blood pressure (Kivipelto., et al, 2001). Protective factors include mental stimulation and social interaction.
Caregiving and Support
Lots of carers face burnout and extreme stress (Brodaty, H., & Donkin, M, 2009) Offering community programs, gatherings for support and respite services is very important. Technology such as reminder tools and tracking gadgets is helpful to those who look after patients (Schindler, S. E, 2019).
Research and Future Directions
Research continues into therapies like monoclonal antibodies targeting beta-amyloid (Cummings, J., 2021). Gene therapy, stem cell approaches, and neuroinflammation inhibitors are being studied. AI and digital biomarkers are improving early detection and personalised treatments (Schindler, S. E, 2019).
Economic and Social Impact
Alzheimer’s disease costs society a lot of money in addition to affecting patients and their families. Owing to population aging, the world's overall cost of dementia, including that of Alzheimer’s disease, is projected to double from $1.3 trillion in 2019 to $2.6 trillion in 2030 (Wimo, A., et al, 2017). Long-term care must be planned, including support from family members without pay and payment for direct medical services. Most often, informal carers are members of the family, leading to losses in income, various challenges to mental wellbeing and stress on their bodies. Around 18 billion unpaid hours of care for people with Alzheimer’s was given by more than 11 million US citizens in 2022 (Adelman r., et al, 2023). Because of this, increased support for health measures, help for caregivers and funding in therapy are all important to tackle illness better.
Conclusion
Alzheimer’s disease is still a major health issue around the world. Currently, there is no a cure, but finding the disease earlier, treating it well and changing lifestyle habits can help people live better. Researchers believe that additional studies may help stop or reverse how the disease develops (Selkoe,. et al, 2016).
References
Adelman, R. D., Tmanova, L. L., Delgado, D., Dion, S., & Lachs, M. S. (2014). Caregiver burden: A clinical review. JAMA, 311(10), 1052–1060. https://doi.org/10.1001/jama.2014.304
Alzheimer’s Association. (2022). 2022 Alzheimer’s disease facts and figures. Alzheimer’s & Dementia, 19(1), 1–98. https://doi.org/10.1002/alz.12694
Aron, L., Ngian, Z. K., Qiu, C., Choi, J., Liang, M., Drake, D. M., Hamplova, S. E., Lacey, E. K., Roche, P., Yuan, M., Hazaveh, S. S., Lee, E. A., Bennett, D. A., & Yankner, B. A. (2025). Lithium deficiency and the onset of Alzheimer’s disease. Nature. Advance online publication. https://doi.org/10.1038/s41586-025-07411-5
Brodaty, H., & Donkin, M. (2009). Family caregivers of people with dementia. Dialogues in Clinical Neuroscience, 11(2), 217–228. https://doi.org/10.31887/DCNS.2009.11.2/hbrodaty
Corder, E. H., Saunders, A. M., Strittmatter, W. J., Schmechel, D. E., Gaskell, P. C., Small, G. W., Roses, A. D., Haines, J. L., & Pericak-Vance, M. A. (1993). Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer’s disease in late-onset families. Science, 261(5123), 921–923. https://doi.org/10.1126/science.8346443
Cummings, J., Lee, G., Zhong, K., Fonseca, J., & Taghva, K. (2021). Alzheimer’s disease drug development pipeline: 2021. Alzheimer’s & Dementia: Translational Research & Clinical Interventions, 7(1), e12179. https://doi.org/10.1002/trc2.12179
Kivipelto, M., Helkala, E. L., Laakso, M. P., Hänninen, T., Hallikainen, M., Alhainen, K., Soininen, H., Tuomilehto, J., & Nissinen, A. (2001). Midlife vascular risk factors and Alzheimer’s disease in later life: Longitudinal, population-based study. BMJ, 322(7300), 1447–1451. https://doi.org/10.1136/bmj.322.7300.1447
Livingston, G., Huntley, J., Sommerlad, A., Ames, D., Ballard, C., Banerjee, S., Brayne, C., Burns, A., Cohen-Mansfield, J., Cooper, C., Costafreda, S. G., Dias, A., Fox, N., Gitlin, L. N., Howard, R., Kales, H. C., Kivimäki, M., Larson, E. B., Ogunniyi, A., … & Mukadam, N. (2020). Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. The Lancet, 396(10248), 413–446. https://doi.org/10.1016/S0140-6736(20)30367-6
Loy, C. T., & Schofield, P. R. (2014). Genetics of dementia. The Lancet, 383(9919), 828–840. https://doi.org/10.1016/S0140-6736(13)60630-3
Morris, M. C., Tangney, C. C., Wang, Y., Sacks, F. M., Bennett, D. A., & Aggarwal, N. T. (2015). MIND diet associated with reduced incidence of Alzheimer’s disease. Alzheimer’s & Dementia, 11(9), 1007–1014. https://doi.org/10.1016/j.jalz.2014.11.009
Schindler, S. E., Bollinger, J. G., Ovod, V., Mawuenyega, K. G., Li, Y., Gordon, B. A., Holtzman, D. M., Morris, J. C., Benzinger, T. L. S., Xiong, C., Fagan, A. M., & Bateman, R. J. (2019). High-precision plasma β-amyloid 42/40 predicts current and future brain amyloidosis. JAMA Neurology, 76(9), 1060–1069. https://doi.org/10.1001/jamaneurol.2019.1633
Selkoe, D. J., & Hardy, J. (2016). The amyloid hypothesis of Alzheimer’s disease at 25 years. EMBO Molecular Medicine, 8(6), 595–608. https://doi.org/10.15252/emmm.201606210
Wimo, A., Guerchet, M., Ali, G. C., Wu, Y. T., Prina, A. M., Winblad, B., Jönsson, L., Liu, Z., & Prince, M. (2017). The worldwide costs of dementia 2015 and comparisons with 2010. Alzheimer’s & Dementia, 13(1), 1–7. https://doi.org/10.1016/j.jalz.2016.07.150