{"id":312,"date":"2025-11-12T15:19:00","date_gmt":"2025-11-12T09:49:00","guid":{"rendered":"https:\/\/www.najao.com\/learn\/?p=312"},"modified":"2026-01-26T03:23:34","modified_gmt":"2026-01-25T21:53:34","slug":"alzheimers-disease","status":"publish","type":"post","link":"https:\/\/www.najao.com\/learn\/alzheimers-disease\/","title":{"rendered":"Alzheimer&#8217;s Disease: Unraveling the Enigma of Memory Loss"},"content":{"rendered":"\n<p class=\"wp-block-paragraph\">Alzheimer\u2019s disease remains, to this day, one of the greatest medical and social problems of our time<strong><sup>1<\/sup><\/strong>. It is a progressive, irreversible <a href=\"https:\/\/www.najao.com\/learn\/neurodegeneration\/\" target=\"_blank\" rel=\"noreferrer noopener\">neurodegenerative disorder<\/a> that corrodes memory, cognition, and autonomy, making it the most common cause of dementia among older people. Since Alois Alzheimer first describing the illness back in 1906, our understanding of its biology has advanced, yet no therapy to prevent or treat it has been identified so far<strong><sup>2<\/sup><\/strong>. With rapidly aging populations, the number of individuals affected worldwide is expected to increase dramatically, reaching a staggering <a href=\"https:\/\/www.alzint.org\/about\/dementia-facts-figures\/dementia-statistics\/\" target=\"_blank\" rel=\"noreferrer noopener\">139 million<\/a> in 2050. This is sure to put tremendous pressure on our healthcare systems, caregivers, and society at large. Understanding the mechanisms of this disease and developing effective therapies are the biggest challenges of contemporary medicine.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Pathophysiology: the hallmarks of the Alzheimer\u2019s brain<\/h2>\n\n\n\n<p class=\"wp-block-paragraph\">The Alzheimer\u2019s brain is characterized by overlapping processes that progressively damage networks of neurons and cause a decline of function.<\/p>\n\n\n\n<h3 class=\"wp-block-heading\">Amyloid-beta plaques<\/h3>\n\n\n\n<p class=\"wp-block-paragraph\">One of the earliest events is the accumulation of amyloid-beta (A\u03b2) peptides, produced when the amyloid precursor protein is abnormally cleaved<strong><sup>1<\/sup><\/strong>. A particularly toxic variant, A\u03b242, clumps outside neurons into dense plaques that block signaling and trigger downstream damage<strong><sup>1<\/sup><\/strong>. This forms the basis of what is known as the \u201camyloid cascade hypothesis\u201d<strong><sup>3<\/sup><\/strong>.<\/p>\n\n\n\n<h3 class=\"wp-block-heading\">Neurofibrillary tangles<\/h3>\n\n\n\n<p class=\"wp-block-paragraph\">Inside neurons, abnormal phosphorylation of the tau protein destabilizes microtubules that carry signals and nutrients<strong><sup>4<\/sup><\/strong>. The tau proteins thus freed undergo <a href=\"https:\/\/www.najao.com\/learn\/protein-misfolding\/\" target=\"_blank\" rel=\"noreferrer noopener\">misfolding<\/a> and aggregate into insoluble tangles that eventually lead to dysfunction and cell death.<\/p>\n\n\n\n<h3 class=\"wp-block-heading\">Neuroinflammation<\/h3>\n\n\n\n<p class=\"wp-block-paragraph\">The brain\u2019s immune and support cells, microglia and astrocytes, get activated in response to plaque and tangle build-up<strong><sup>5<\/sup><\/strong>. While they attempt clearance, prolonged activation fuels release of inflammatory molecules that accelerate degeneration.<\/p>\n\n\n\n<h3 class=\"wp-block-heading\">Neuronal loss and synaptic dysfunction<\/h3>\n\n\n\n<p class=\"wp-block-paragraph\">Combined effects of these lead to massive cell death, especially in the hippocampus and cortex areas, disrupting memory, reasoning, and language<strong><sup>6<\/sup><\/strong>. Neurotransmitter balance is severely disrupted, with acetylcholine deficiency playing a central role in cognitive decline<strong><sup>7<\/sup><\/strong>.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Risk factors for Alzheimer\u2019s disease<\/h2>\n\n\n\n<p class=\"wp-block-paragraph\">The causes of Alzheimer\u2019s are multifactorial, influenced by both non-modifiable and preventable risks.<\/p>\n\n\n\n<h3 class=\"wp-block-heading\">Non-modifiable risks<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Age&nbsp;is the single greatest factor, with prevalence doubling every five years after 65<strong><sup>8<\/sup><\/strong>.<\/li>\n\n\n\n<li>Genetics:&nbsp;The <em>APOE4<\/em> allele significantly increases the risk<strong><sup>9<\/sup><\/strong>. Mutations in <em>APP<\/em>, <em>PSEN1<\/em>, and <em>PSEN2<\/em> cause rare familial Alzheimer\u2019s before 65<strong><sup>10<\/sup><\/strong>. Other small-effect genes identified in population studies, such as <em>TREM2<\/em> and <em>CD33<\/em>, contribute to further vulnerability<strong><sup>11<\/sup><\/strong>.<\/li>\n\n\n\n<li>Having a family history&nbsp;raises risk<strong><sup>9<\/sup><\/strong>. Additionally,&nbsp;females are associated with a higher prevalence of Alzheimer\u2019s, influenced by longevity and possible hormonal factors<strong><sup>12<\/sup><\/strong>.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Modifiable risks<\/h3>\n\n\n\n<p class=\"wp-block-paragraph\">Lifestyle and environment strongly shape risk:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Cardiovascular factors like hypertension, diabetes, obesity, smoking, and hypercholesterolemia damage brain vessels<strong><sup>13<\/sup><\/strong>.<\/li>\n\n\n\n<li>Sedentary behavior, poor diet, and excessive alcohol consumption worsen vulnerability<strong><sup>14-16<\/sup><\/strong>.<\/li>\n\n\n\n<li>Severe head injury leaves lasting risk<strong><sup>17<\/sup><\/strong>.<\/li>\n\n\n\n<li>Poor quality of sleep, including sleep apnea, could slow down clearance of toxic proteins<strong><sup>18<\/sup><\/strong>.<\/li>\n\n\n\n<li>Limited mental activity and education reduce \u201ccognitive reserve\u201d<strong><sup>19<\/sup><\/strong>.<\/li>\n\n\n\n<li>Social isolation and exposure to pollution are emerging contributors<strong><sup>20, 21<\/sup><\/strong>.<\/li>\n<\/ul>\n\n\n\n<h2 class=\"wp-block-heading\">Stages and symptoms of Alzheimer\u2019s disease<\/h2>\n\n\n\n<p class=\"wp-block-paragraph\">Alzheimer\u2019s progresses gradually, passing through distinct stages.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">1. The preclinical stage occurs decades before the symptoms even start to appear, marked by silent amyloid accumulation<strong><sup>22<\/sup><\/strong>. This is detectable only through advanced biomarkers such as positron emission tomography (PET) imaging or cerebrospinal fluid (CSF) assays.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">2. This may progress to mild cognitive impairment (MCI), in which individuals experience subtle declines\u2014frequent forgetfulness, difficulty with complex tasks, and impaired judgment<strong><sup>22<\/sup><\/strong>. While not all MCI cases become dementia, Alzheimer\u2019s -related MCI carries a high conversion rate.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">3. In mild dementia, memory lapses begin to disrupt daily life<strong><sup>23<\/sup><\/strong>. Orientation starts to fail, language declines, and mood shifts arise. Independence is reduced but not entirely lost.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">4. Moderate dementia, often the longest stage, is marked by profound disorientation, hallucinations, disturbed sleep, inability to recognize close family, and behavioral problems such as agitation or wandering<strong><sup>24<\/sup><\/strong>. Patients in this stage require regular functional assistance.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">5. The final, severe stage is one of complete dependence<strong><sup>25<\/sup><\/strong>. Patients lose communication skills, mobility, and the ability to swallow, and thus become bedridden and often highly vulnerable to fatal infections<strong><sup>26<\/sup><\/strong>.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Diagnosis of Alzheimer\u2019s disease<\/h2>\n\n\n\n<p class=\"wp-block-paragraph\">Diagnosis requires the integration of clinical expertise with technological tools.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">It is initially assessed via a comprehensive assessment of medical history, reports from family, and neurological and cognitive tests such as the MMSE or MoCA<strong><sup>27<\/sup><\/strong>.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">Biomarker advances also offer strong confirmation. Cerebrospinal fluid analysis shows characteristic changes in amyloid and tau<strong><sup>22<\/sup><\/strong>. Amyloid and tau PET scans visualize pathology directly<strong><sup>22<\/sup><\/strong>. Blood biomarkers\u2014especially assays detecting phosphorylated tau\u2014are emerging as non-invasive, scalable tools, which have the potential to transform early detection<strong><sup>28<\/sup><\/strong>.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">Structural imaging with MRI or CT further supports diagnosis by ruling out mimicking conditions and revealing atrophy, particularly in the hippocampus region<strong><sup>29<\/sup><\/strong>.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Current treatment approaches<\/h2>\n\n\n\n<p class=\"wp-block-paragraph\">While there is no cure, several approaches aim to relieve symptoms or alter disease course.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">Symptomatic treatments focus on neurotransmitter systems. Cholinesterase inhibitors, like Donepezil, Rivastigmine, and Galantamine, boost acetylcholine, and thus provide modest cognitive benefits in mild to moderate disease<strong><sup>30<\/sup><\/strong>. Memantine, an NMDA receptor antagonist, regulates glutamate signaling to support cognition and behavior in more advanced stages<strong><sup>30<\/sup><\/strong>.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">More recently, disease-modifying monoclonal antibodies, such as Aducanumab, Lecanemab, and Donanemab, have been approved in some settings<strong><sup>31<\/sup><\/strong>. These drugs clear amyloid and slightly slow decline in early patients. However, their benefits remain limited; and risks, such as amyloid-related brain swelling, require close monitoring.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">Non-drug strategies are equally important.<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Regular exercise, cognitive stimulation, and brain-healthy diets are crucial to build resilience<strong><sup>32<\/sup><\/strong>.<\/li>\n\n\n\n<li>Structured behavioral interventions are important for easing agitation and sleep disruption<strong><sup>33<\/sup><\/strong>.<\/li>\n\n\n\n<li>Caregiver support is vital, given the heavy emotional and physical toll that comes with prolonged care<strong><sup>34<\/sup><\/strong>.<\/li>\n<\/ul>\n\n\n\n<h2 class=\"wp-block-heading\">Challenges in research and treatment<\/h2>\n\n\n\n<p class=\"wp-block-paragraph\">Despite major advances, Alzheimer\u2019s poses a formidable challenge to our healthcare system.<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Complexity of disease<\/strong>:&nbsp;Alzheimer\u2019s stems from multiple interacting mechanisms\u2014amyloid, tau, vascular dysfunction, and inflammation\u2014which makes a single-drug cure unlikely. Studies are increasingly shifting the focus towards combination therapies<strong><sup>35<\/sup><\/strong>. Addressing this complexity requires systems-level strategies like <a href=\"https:\/\/www.najao.com\/learn\/network-pharmacology\/\" target=\"_blank\" rel=\"noreferrer noopener\">network pharmacology<\/a>, which uses <a href=\"https:\/\/www.najao.com\/learn\/multi-omics\/\" target=\"_blank\" rel=\"noreferrer noopener\">multi-omics data<\/a> and computational modeling to analyze the entire disease network and predict synergistic multi-target drug combinations for optimal intervention.<\/li>\n\n\n\n<li><strong>Delayed diagnosis<\/strong>:&nbsp;Symptoms typically appear after the brain has undergone irreparable changes. To counter this, researchers are developing sensitive blood-based biomarkers and AI-driven risk models to detect the disease in earlier stages<strong><sup>36<\/sup><\/strong>.<\/li>\n\n\n\n<li><strong>Blood-brain barrier<\/strong>: <a href=\"https:\/\/www.najao.com\/learn\/blood-brain-barrier\/\" target=\"_blank\" rel=\"noreferrer noopener\">Blood-brain barrier<\/a> excludes most drugs from reaching their targets. Scientists are exploring novel strategies, such as nanoparticles, <a href=\"https:\/\/www.najao.com\/learn\/drug-delivery\/\" target=\"_blank\" rel=\"noreferrer noopener\">intranasal delivery<\/a>, and ultrasound-assisted openings<strong><sup>37<\/sup><\/strong>.<\/li>\n\n\n\n<li><strong>Disease variability<\/strong>:&nbsp;The rate and pattern of progression vary in each patient. <a href=\"https:\/\/www.najao.com\/learn\/precision-medicine\/\" target=\"_blank\" rel=\"noreferrer noopener\">Precision medicine<\/a> approaches using genetic and biomarker profiles are being developed to personalize treatment<strong><sup>38<\/sup><\/strong>.<\/li>\n\n\n\n<li><strong>Incomplete biomarkers<\/strong>:&nbsp;Current PET and CSF tests are expensive and invasive. However, global efforts are ongoing to make blood assays affordable to ensure that Alzheimer\u2019s screening is accessible to everyone.<\/li>\n\n\n\n<li><strong>Clinical trial hurdles<\/strong>:&nbsp;Slow disease progression makes trials long and costly<strong><sup>39<\/sup><\/strong>. Adaptive trial frameworks, biomarker-guided patient selection, and digital monitoring tools are being introduced to improve efficiency.<\/li>\n\n\n\n<li><strong>Side effects of new drugs<\/strong>:&nbsp;Anti-amyloid antibodies carry risks of swelling and bleeding in the brain<strong><sup>40<\/sup><\/strong>. Adjusted dosing protocols and careful monitoring are being adopted to minimize these risks.<\/li>\n<\/ul>\n\n\n\n<h2 class=\"wp-block-heading\">Emerging research and future directions<\/h2>\n\n\n\n<p class=\"wp-block-paragraph\">A number of ongoing research avenues are offering hope. Experimental anti-tau and neuroinflammation-modulating drugs are being tested alongside compounds that enhance synaptic plasticity<strong><sup>41<\/sup><\/strong>. Efforts to improve vascular health and investigate the gut-brain axis are underway which can provide fresh perspectives<strong><sup>42, 43<\/sup><\/strong>.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">There has been rapid progress in diagnostics, especially blood biomarkers and <a href=\"https:\/\/www.najao.com\/learn\/artificial-intelligence-applications-in-healthcare\/\" target=\"_blank\" rel=\"noreferrer noopener\">artificial intelligence<\/a> analyses of imaging and genomic data<strong><sup>28, 44<\/sup><\/strong>. This could enable early personalized interventions.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">Advances in therapies such as gene editing, <a href=\"https:\/\/www.najao.com\/learn\/crispr-cas-systems\/\" target=\"_blank\" rel=\"noreferrer noopener\">CRISPR<\/a>-based tools, and stem cells are still at an experimental stage, but they nonetheless reflect the overall momentum of this field<strong><sup>45, 46<\/sup><\/strong>.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">Researchers are increasingly thinking of future treatments as a combination of drugs that can target several of Alzheimer&#8217;s pathological pathways at once<strong><sup>35<\/sup><\/strong>.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Socio-economic impact and caregiver burden<\/h2>\n\n\n\n<p class=\"wp-block-paragraph\">Alzheimer\u2019s disease imposes numerous social and economic strains. Medical costs for care and long-term support are huge, and indirect costs from lost productivity magnify the challenge<strong><sup>47<\/sup><\/strong>. The illness strips away a patient&#8217;s autonomy, dignity, and personal identity, while placing an overwhelming toll on caregivers and family, which can result in stress, depression, and financial hardship<strong><sup>48<\/sup><\/strong>. Sustained policy action and community support are therefore equally essential alongside scientific progress<strong><sup>49, 50<\/sup><\/strong>.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Conclusion<\/h2>\n\n\n\n<p class=\"wp-block-paragraph\">Alzheimer\u2019s disease continues to be a debilitating condition of aging, defined by complex pathology and immense human and societal costs. While a cure remains elusive, advances in early detection, disease-modifying therapies, and supportive care are bringing hope. The future lies in integrating scientific innovation with compassionate care, which ensures that progress at the laboratory bench translates to improved ways of life for patients and their families.<\/p>\n\n\n\n<!--nextpage-->\n\n\n\n<h2 class=\"wp-block-heading\">FAQs<\/h2>\n\n\n\n<h4 class=\"wp-block-heading\">1. How is Alzheimer\u2019s different from normal aging?<\/h4>\n\n\n\n<p class=\"wp-block-paragraph\">Normal aging may cause minor changes like forgetting names or misplacing objects, but people remain independent. In contrast, Alzheimer&#8217;s involves more severe memory loss that interferes with daily life and progressively worsens. This is accompanied by broader issues like language problems, confusion, poor judgment, and difficulty with complex tasks.<\/p>\n\n\n\n<h4 class=\"wp-block-heading\">2. What role does diet play in Alzheimer\u2019s risk?<\/h4>\n\n\n\n<p class=\"wp-block-paragraph\">While diet alone cannot prevent Alzheimer\u2019s, it is one of the most modifiable risk factors. Diets like the Mediterranean or MIND diet emphasize leafy greens, berries, whole grains, fish, olive oil, and nuts, which may lower risk by reducing inflammation and supporting vascular health. In contrast, diets high in processed foods, sugar, and saturated fats are associated with increased risk.<\/p>\n\n\n\n<h4 class=\"wp-block-heading\">3. Are there gender differences in Alzheimer\u2019s disease?<\/h4>\n\n\n\n<p class=\"wp-block-paragraph\">Yes. Women are disproportionately affected, with about two-thirds of Alzheimer\u2019s patients being female. This is partly because women generally live longer, but biological factors likely also play a role. Hormonal changes after menopause, genetic differences, and brain structural variations may contribute to women\u2019s higher vulnerability.<\/p>\n\n\n\n<h4 class=\"wp-block-heading\">4. Is there a link between Alzheimer\u2019s and other diseases?<\/h4>\n\n\n\n<p class=\"wp-block-paragraph\">Yes, many vascular and metabolic conditions increase Alzheimer\u2019s risk. Diabetes, hypertension, obesity, and stroke damage blood vessels and weaken brain health. Depression and chronic stress are linked to faster cognitive decline. This overlap suggests that preventive care for cardiovascular and mental health may lower dementia risk.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Reference<\/h2>\n\n\n\n<p class=\"wp-block-paragraph\">1. Scheltens, P., De Strooper, B., Kivipelto, M., <em>et al<\/em>. (2021). Alzheimer&#8217;s disease.&nbsp;<em>The Lancet<\/em>,&nbsp;<em>397<\/em>(10284), 1577-1590.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">2. Hippius, H., &amp; Neund\u00f6rfer, G. (2003). The discovery of Alzheimer&#8217;s disease. <em>Dialogues in clinical neuroscience<\/em>, <em>5<\/em>(1), 101-108.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">3. Reitz, C. (2012). Alzheimer\u2032 s disease and the amyloid cascade hypothesis: a critical review.&nbsp;<em>International journal of Alzheimer\u2019s disease<\/em>,&nbsp;<em>2012<\/em>(1), 369808.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">4. Sepulveda-Diaz, J. E., Naini, S. M. A., Huynh, M. B., <em>et al<\/em>. (2015). HS3ST2 expression is critical for the abnormal phosphorylation of tau in Alzheimer\u2019s disease-related tau pathology.&nbsp;<em>Brain<\/em>,&nbsp;<em>138<\/em>(5), 1339.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">5. Fakhoury, M. (2018). Microglia and astrocytes in Alzheimer&#8217;s disease: implications for therapy.&nbsp;<em>Current neuropharmacology<\/em>,&nbsp;<em>16<\/em>(5), 508-518.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">6. Bayer, T. A., &amp; Wirths, O. (2010). Intracellular accumulation of amyloid-Beta-a predictor for synaptic dysfunction and neuron loss in Alzheimer&#8217;s disease.&nbsp;<em>Frontiers in aging neuroscience<\/em>,&nbsp;<em>2<\/em>, 1359.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">7. Sun, Q., Zhang, J., Li, A., <em>et al<\/em>. (2022). Acetylcholine deficiency disrupts extratelencephalic projection neurons in the prefrontal cortex in a mouse model of Alzheimer\u2019s disease.&nbsp;<em>Nature communications<\/em>,&nbsp;<em>13<\/em>(1), 998.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">8. Guerreiro, R., &amp; Bras, J. (2015). The age factor in Alzheimer\u2019s disease.&nbsp;<em>Genome medicine<\/em>,&nbsp;<em>7<\/em>(1), 106.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">9. Donix, M., Small, G. W., &amp; Bookheimer, S. Y. (2012). Family history and APOE-4 genetic risk in Alzheimer\u2019s disease.&nbsp;<em>Neuropsychology review<\/em>,&nbsp;<em>22<\/em>(3), 298-309.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">10. Cruchaga, C., Chakraverty, S., Mayo, K., <em>et al<\/em>. (2012). Rare variants in APP, PSEN1 and PSEN2 increase risk for AD in late-onset Alzheimer&#8217;s disease families.&nbsp;<em>PloS one<\/em>,&nbsp;<em>7<\/em>(2), e31039.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">11. Griciuc, A., Patel, S., Federico, A. N., <em>et al<\/em>. (2019). TREM2 acts downstream of CD33 in modulating microglial pathology in Alzheimer\u2019s disease.&nbsp;<em>Neuron<\/em>,&nbsp;<em>103<\/em>(5), 820-835.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">12. Andrew, M. K., &amp; Tierney, M. C. (2018). The puzzle of sex, gender and Alzheimer\u2019s disease: Why are women more often affected than men?.&nbsp;<em>Women&#8217;s Health<\/em>,&nbsp;<em>14<\/em>, 1745506518817995.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">13. de Bruijn, R. F., &amp; Ikram, M. A. (2014). Cardiovascular risk factors and future risk of Alzheimer\u2019s disease.&nbsp;<em>BMC medicine<\/em>,&nbsp;<em>12<\/em>(1), 130.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">14. Lu, Z., Harris, T. B., Shiroma, E. J., <em>et al<\/em>. (2018). Patterns of physical activity and sedentary behavior for older adults with Alzheimer\u2019s disease, mild cognitive impairment, and cognitively normal in Hong Kong.&nbsp;<em>Journal of Alzheimer\u2019s Disease<\/em>,&nbsp;<em>66<\/em>(4), 1453-1462.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">15. Vasefi, M., Hudson, M., &amp; Ghaboolian-Zare, E. (2019). Diet associated with inflammation and Alzheimer\u2019s disease.&nbsp;<em>Journal of Alzheimer&#8217;s disease reports<\/em>,&nbsp;<em>3<\/em>(1), 299-309.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">16. Heymann, D., Stern, Y., Cosentino, S., <em>et al<\/em>. (2016). The association between alcohol use and the progression of Alzheimer\u2019s disease.&nbsp;<em>Current Alzheimer Research<\/em>,&nbsp;<em>13<\/em>(12), 1356-1362.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">17. Li, Y., Li, Y., Li, X., <em>et al<\/em>. (2017). Head injury as a risk factor for dementia and Alzheimer\u2019s disease: a systematic review and meta-analysis of 32 observational studies.&nbsp;<em>PloS one<\/em>,&nbsp;<em>12<\/em>(1), e0169650.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">18. Andrade, A. G., Bubu, O. M., Varga, A. W., <em>et al<\/em>. (2018). The relationship between obstructive sleep apnea and Alzheimer\u2019s disease.&nbsp;<em>Journal of Alzheimer\u2019s Disease<\/em>,&nbsp;<em>64<\/em>(s1), S255-S270.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">19. Stern, Y. (2012). Cognitive reserve in ageing and Alzheimer&#8217;s disease.&nbsp;<em>The Lancet Neurology<\/em>,&nbsp;<em>11<\/em>(11), 1006-1012.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">20. Drinkwater, E., Davies, C., &amp; Spires\u2010Jones, T. L. (2022). Potential neurobiological links between social isolation and Alzheimer&#8217;s disease risk.&nbsp;<em>European Journal of Neuroscience<\/em>,&nbsp;<em>56<\/em>(9), 5397-5412.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">21. Moulton, P. V., &amp; Yang, W. (2012). Air pollution, oxidative stress, and Alzheimer\u2032 s disease.&nbsp;<em>Journal of environmental and public health<\/em>,&nbsp;<em>2012<\/em>(1), 472751.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">22. Caselli, R. J., &amp; Reiman, E. M. (2012). Characterizing the preclinical stages of Alzheimer&#8217;s disease and the prospect of presymptomatic intervention.&nbsp;<em>Journal of Alzheimer\u2019s Disease<\/em>,&nbsp;<em>33<\/em>(s1), S405-S416.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">23. Knopman, D. S., &amp; Petersen, R. C. (2014, October). Mild Cognitive Impairment and Mild Dementia: A Clinical Perspective. In&nbsp;<em>Mayo Clinic proceedings<\/em>&nbsp;(Vol. 89, No. 10, p. 1452).<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">24. Cerejeira, J., Lagarto, L., &amp; Mukaetova-Ladinska, E. B. (2012). Behavioral and psychological symptoms of dementia.&nbsp;<em>Frontiers in neurology<\/em>,&nbsp;<em>3<\/em>, 73.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">25. Brucki, S. M. D., Aprahamian, I., Borelli, W. V., <em>et al<\/em>. (2022). Management in severe dementia: recommendations of the Scientific Department of Cognitive Neurology and Aging of the Brazilian Academy of Neurology.&nbsp;<em>Dementia &amp; Neuropsychologia<\/em>,&nbsp;<em>16<\/em>(3 Suppl 1), 101.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">26. Shen, H. N., Lu, C. L., &amp; Li, C. Y. (2012). Dementia increases the risks of acute organ dysfunction, severe sepsis and mortality in hospitalized older patients: a national population-based study, <em>7<\/em>(8), e42751.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">27. Jia, X., Wang, Z., Huang, F., <em>et al<\/em>. (2021). A comparison of the Mini-Mental State Examination (MMSE) with the Montreal Cognitive Assessment (MoCA) for mild cognitive impairment screening in Chinese middle-aged and older population: a cross-sectional study.&nbsp;<em>BMC psychiatry<\/em>,&nbsp;<em>21<\/em>(1), 485.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">28. Hansson, O., Blennow, K., Zetterberg, H., <em>et al<\/em>. (2023). Blood biomarkers for Alzheimer\u2019s disease in clinical practice and trials.&nbsp;<em>Nature aging<\/em>,&nbsp;<em>3<\/em>(5), 506-519.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">29. Cuttler, J. M., Moore, E. R., Hosfeld, V. D., <em>et al<\/em>. (2016). Treatment of Alzheimer disease with CT scans: a case report.&nbsp;<em>Dose-response<\/em>,&nbsp;<em>14<\/em>(2), 1559325816640073.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">30. Li, D. D., Zhang, Y. H., Zhang, W., <em>et al<\/em>. (2019). Meta-analysis of randomized controlled trials on the efficacy and safety of donepezil, galantamine, rivastigmine, and memantine for the treatment of Alzheimer\u2019s disease.&nbsp;<em>Frontiers in neuroscience<\/em>,&nbsp;<em>13<\/em>, 472.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">31. Ameen, T. B., Kashif, S. N., Abbas, S. M. I., <em>et al<\/em>. (2024). Unraveling Alzheimer\u2019s: the promise of aducanumab, lecanemab, and donanemab.&nbsp;<em>The Egyptian Journal of Neurology, Psychiatry and Neurosurgery<\/em>,&nbsp;<em>60<\/em>(1), 72.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">32. Mintzer, J., Donovan, K. A., Kindy, A. Z., <em>et al<\/em>. (2019). Lifestyle choices and brain health.&nbsp;<em>Frontiers in medicine<\/em>,&nbsp;<em>6<\/em>, 204.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">33. Gauthier, S., Cummings, J., Ballard, C., <em>et al<\/em>. (2010). Management of behavioral problems in Alzheimer&#8217;s disease.&nbsp;<em>International psychogeriatrics<\/em>,&nbsp;<em>22<\/em>(3), 346-372.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">34. Elif, K., Ta\u015fkapilio\u011flu, \u00d6., &amp; Bakar, M. (2017). Caregiver burden in different stages of Alzheimer\u2019s disease.&nbsp;<em>Archives of Neuropsychiatry<\/em>,&nbsp;<em>54<\/em>(1), 82.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">35. Cummings, J. L., Tong, G., &amp; Ballard, C. (2019). Treatment combinations for Alzheimer\u2019s disease: current and future pharmacotherapy options.&nbsp;<em>Journal of Alzheimer\u2019s Disease<\/em>,&nbsp;<em>67<\/em>(3), 779-794.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">36. Rasmussen, J., &amp; Langerman, H. (2019). Alzheimer\u2019s Disease\u2013Why We Need Early Diagnosis.&nbsp;<em>Degenerative Neurological and Neuromuscular Disease<\/em>,&nbsp;<em>9<\/em>, 123.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">37. Tsou, Y. H., Zhang, X. Q., Zhu, H., <em>et al<\/em>. (2017). Drug Delivery to the Brain across the Blood\u2013Brain Barrier Using Nanomaterials.&nbsp;<em>Small<\/em>, 1701921.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">38. Reitz, C. (2016). Toward precision medicine in Alzheimer\u2019s disease.&nbsp;<em>Annals of translational medicine<\/em>,&nbsp;<em>4<\/em>(6), 107.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">39. Oxford, A. E., Stewart, E. S., &amp; Rohn, T. T. (2020). Clinical trials in Alzheimer\u2019s disease: a hurdle in the path of remedy.&nbsp;<em>International Journal of Alzheimer\u2019s Disease<\/em>,&nbsp;<em>2020<\/em>(1), 5380346.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">40. Doran, S. J., &amp; Sawyer, R. P. (2024). Risk factors in developing amyloid related imaging abnormalities (ARIA) and clinical implications.&nbsp;<em>Frontiers in Neuroscience<\/em>,&nbsp;<em>18<\/em>, 1326784.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">41. Chen, Y., &amp; Yu, Y. (2023). Tau and neuroinflammation in Alzheimer\u2019s disease: interplay mechanisms and clinical translation.&nbsp;<em>Journal of neuroinflammation<\/em>,&nbsp;<em>20<\/em>(1), 165.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">42. Attems, J., &amp; Jellinger, K. A. (2014). The overlap between vascular disease and Alzheimer\u2019s disease-lessons from pathology.&nbsp;<em>BMC medicine<\/em>,&nbsp;<em>12<\/em>(1), 206.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">43. Narengaowa, Kong, W., Lan, F., Awan, U. F., <em>et al<\/em>. (2021). The oral-gut-brain AXIS: the influence of microbes in Alzheimer\u2019s disease.&nbsp;<em>Frontiers in cellular neuroscience<\/em>,&nbsp;<em>15<\/em>, 633735.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">44. Song, S., Li, T., Lin, W., <em>et al<\/em>. (2025). Application of artificial intelligence in Alzheimer\u2019s disease: A bibliometric analysis.&nbsp;<em>Frontiers in Neuroscience<\/em>,&nbsp;<em>19<\/em>, 1511350.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">45. Lu, L., Yu, X., Cai, Y., <em>et al<\/em>. (2021). Application of CRISPR\/Cas9 in Alzheimer\u2019s disease.&nbsp;<em>Frontiers in neuroscience<\/em>,&nbsp;<em>15<\/em>, 803894.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">46. Liu, X. Y., Yang, L. P., &amp; Zhao, L. (2020). Stem cell therapy for Alzheimer&#8217;s disease.&nbsp;<em>World journal of stem cells<\/em>,&nbsp;<em>12<\/em>(8), 787.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">47. Deb, A., Thornton, J. D., Sambamoorthi, U., <em>et al<\/em>. (2017). Direct and indirect cost of managing Alzheimer\u2019s disease and related dementias in the United States.&nbsp;<em>Expert review of pharmacoeconomics &amp; outcomes research<\/em>,&nbsp;<em>17<\/em>(2), 189-202.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">48. Elif, K., Ta\u015fkapilio\u011flu, \u00d6., &amp; Bakar, M. (2017). Caregiver burden in different stages of Alzheimer\u2019s disease.&nbsp;<em>Archives of Neuropsychiatry<\/em>,&nbsp;<em>54<\/em>(1), 82.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">49. Karlawish, J. (2011). Addressing the ethical, policy, and social challenges of preclinical Alzheimer disease.&nbsp;<em>Neurology<\/em>,&nbsp;<em>77<\/em>(15), 1487-1493.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">50. Rio, R. (2018). A community-based music therapy support group for people with Alzheimer&#8217;s disease and their caregivers: A sustainable partnership model.&nbsp;<em>Frontiers in medicine<\/em>,&nbsp;<em>5<\/em>, 293.<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Alzheimer\u2019s is a neurodegenerative disorder marked by amyloid plaques and tau tangles that lead to progressive memory loss and brain inflammation. With rising global prevalence, it poses immense medical and social challenges. 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