Abstract :

Alzheimer’s disease (AD) is one of the age-related infections which can develop to Dementia and nowadays both pervasiveness and rate of dementia rise considerably with propelling age Aβ plaques are commonly found in Alzheimer’s patients. neurofibrillary tangles are irregular growth of protein in the brain. Paul Block and George Mannesco believe that Aβ plaques exist, after they discovered circular buildup. AD is eventually caused by neuronal malfunction and death. Aβ cellulose bodies are considered to be less poisonous than Aβ oligomers. A union of blood pressure in adulthood will increase their risk of dementia and Alzheimer’s disease. In the research they found out that old people with 75+ years and the following period are having more risk of dementia and AD. BMI has a bifacial association with dementia and AD has several studies. Due to the uncertain pathophysiological mechanism of Alzheimer’s disease, it is crucial for selecting a precise target population, need for a large sample size, and high cost of the prevention research, it has been a main issue to conduct primary prevention trials. Commonly, healthy seniors are a primary target demographic. Non-pharmacological treatments are helping the patient by enhancing a protective lifestyle like doing physical exercise and a healthy diet. Biomarkers have a priority role to design which group will get in preventative trials, a higher risk of progression of dementia will cut down the studies, however it will decrease the general public’s ability to find the entire community. Primary prevention will evade illness and accomplice pathologies before they arise. Additionally, secondary prevention contains screening to detect disease in its early stages. Tertiary prevention is treating an illness to avoid complex injuries and disability. In a research study, the use of drugs, vitamins, or lifestyle treatments can prevent Alzheimer’s disease, according to the natural definition term the outcome can be a lot of different paths. The possibility of clinical research of AD prevention is full of obstacles.

---

Keywords :

Alzheimer’s disease, Environmental risk factors Prevention, Risk-Reduction, Vascular risk factors.

---

References :

1. T. Fulop et al., “Can an infection hypothesis explain the beta amyloid hypothesis of Alzheimer’s disease?,” Frontiers in aging neuroscience, vol. 10, p. 224, 2018.
2. C. Zucchella et al., “The multidisciplinary approach to Alzheimer’s disease and dementia. A narrative review of non-pharmacological treatment,” Frontiers in neurology, vol. 9, p. 1058, 2018.
3. M. McMaster et al., “Lifestyle Risk Factors and Cognitive Outcomes from the Multidomain Dementia Risk Reduction Randomized Controlled Trial, Body Brain Life for Cognitive Decline (BBL‐CD),” Journal of the American Geriatrics Society, vol. 68, no. 11, pp. 2629-2637, 2020.
4. L. Vermunt et al., “Duration of preclinical, prodromal, and dementia stages of Alzheimer’s disease in relation to age, sex, and APOE genotype,” Alzheimer’s & Dementia, vol. 15, no. 7, pp. 888-898, 2019.
5. R. D. Hallam, “Bolstered Neuronal Antioxidant Response May Confer Resistance to Development of Dementia in Individuals with Alzheimer’s Neuropathology by Ameliorating Amyloid-β-Induced Oxidative Stress,” Journal of Neuroscience, vol. 41, no. 29, pp. 6187-6189, 2021.
6. S. H. Choi and R. E. Tanzi, “Is Alzheimer’s disease a neurogenesis disorder?,” Cell Stem Cell, vol. 25, no. 1, pp. 7-8, 2019.
7. A. Myers and P. McGonigle, “Overview of transgenic mouse models for Alzheimer’s disease,” Current protocols in neuroscience, vol. 89, no. 1, p. e81, 2019.
8. F. Jessen et al., “Design and first baseline data of the DZNE multicenter observational study on predementia Alzheimer’s disease (DELCODE),” Alzheimer’s research & therapy, vol. 10, no. 1, pp. 1-10, 2018.
9. P. Dev, “Introduction to Different Kinds of Cognitive Disorders,” in Bio-Inspired Algorithms and Devices for Treatment of Cognitive Diseases Using Future Technologies: IGI Global, 2022, pp. 39-55.
10. R. J. Caselli, D. S. Knopman, and G. Bu, “An agnostic reevaluation of the amyloid cascade hypothesis of Alzheimer’s disease pathogenesis: The role of APP homeostasis,” Alzheimer’s & Dementia, vol. 16, no. 11, pp. 1582-1590, 2020.
11. R. Loera‐Valencia et al., “Current and emerging avenues for Alzheimer’s disease drug targets,” Journal of Internal Medicine, vol. 286, no. 4, pp. 398-437, 2019.
12. T. Ozben and S. Ozben, “Neuro-inflammation and anti-inflammatory treatment options for Alzheimer’s disease,” Clinical biochemistry, vol. 72, pp. 87-89, 2019.
13. S.-i. Choi, B. Lee, J. H. Woo, J. B. Jeong, I. Jun, and E. K. Kim, “APP processing and metabolism in corneal fibroblasts and epithelium as a potential biomarker for Alzheimer’s disease,” Experimental Eye Research, vol. 182, pp. 167-174, 2019.
14. H. Li, C.-C. Liu, H. Zheng, and T. Y. Huang, “Amyloid, tau, pathogen infection and antimicrobial protection in Alzheimer’s disease–conformist, nonconformist, and realistic prospects for AD pathogenesis,” Translational neurodegeneration, vol. 7, no. 1, pp. 1-16, 2018.
15. J. Z. A. Tan and P. A. Gleeson, “The role of membrane trafficking in the processing of amyloid precursor protein and production of amyloid peptides in Alzheimer’s disease,” Biochimica et Biophysica Acta (BBA)-Biomembranes, vol. 1861, no. 4, pp. 697-712, 2019.
16. E. Chipi, N. Salvadori, L. Farotti, and L. Parnetti, “Biomarker-based signature of Alzheimer’s disease in pre-MCI individuals,” Brain Sciences, vol. 9, no. 9, p. 213, 2019.
17. C. P. Boix, I. Lopez-Font, I. Cuchillo-Ibañez, and J. Sáez-Valero, “Amyloid precursor protein glycosylation is altered in the brain of patients with Alzheimer’s disease,” Alzheimer’s Research & Therapy, vol. 12, no. 1, pp. 1-15, 2020.
18. E. L. Abner et al., “Diffuse amyloid-β plaques, neurofibrillary tangles, and the impact of ApoE in elderly persons’ brains lacking neuritic amyloid plaques,” Journal of Alzheimer’s Disease, vol. 64, no. 4, pp. 1307-1324, 2018.
19. A. Tsatsanis et al., “Amyloidogenic processing of Alzheimer’s disease β-amyloid precursor protein induces cellular iron retention,” Molecular Psychiatry, vol. 25, no. 9, pp. 1958-1966, 2020.
20. H. Hampel et al., “The β-secretase BACE1 in Alzheimer’s disease,” Biological psychiatry, vol. 89, no. 8, pp. 745-756, 2021.
21. S. M. Nassibi, “The Protective Effect of Astaxanthin on Scopolamine-Induced Alzheimer Model in Mice,” 2021.
22. J. M. Long, B. Maloney, J. T. Rogers, and D. K. Lahiri, “Novel upregulation of amyloid-β precursor protein (APP) by microRNA-346 via targeting of APP mRNA 5′-untranslated region: Implications in Alzheimer’s disease,” Molecular psychiatry, vol. 24, no. 3, pp. 345-363, 2019.
23. V. V. Giridharan, F. Masud, F. Petronilho, F. Dal-Pizzol, and T. Barichello, “Infection-induced systemic inflammation is a potential driver of Alzheimer’s disease progression,” Frontiers in aging neuroscience, vol. 11, p. 122, 2019.
24. A. De la Rosa et al., “Physical exercise in the prevention and treatment of Alzheimer’s disease,” Journal of sport and health science, vol. 9, no. 5, pp. 394-404, 2020.
25. M. Van Zeller, D. Dias, A. M. Sebastião, and C. A. Valente, “NLRP3 inflammasome: a starring role in amyloid-β-and tau-driven pathological events in Alzheimer’s disease,” Journal of Alzheimer’s Disease, vol. 83, no. 3, pp. 939-961, 2021.
26. L. Zhang et al., “Advance of sporadic Alzheimer’s disease animal models,” Medicinal research reviews, vol. 40, no. 1, pp. 431-458, 2020.
27. R. Zhou, G. Yang, and Y. Shi, “Macromolecular complex in recognition and proteolysis of amyloid precursor protein in Alzheimer’s disease,” Current Opinion in Structural Biology, vol. 61, pp. 1-8, 2020.
28. F. H. Bouwman et al., “Clinical application of CSF biomarkers for Alzheimer’s disease: From rationale to ratios,” Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring, vol. 14, no. 1, p. e12314, 2022.
29. A. Nakajima and Y. Ohizumi, “Potential benefits of nobiletin, a citrus flavonoid, against Alzheimer’s disease and Parkinson’s disease,” International journal of molecular sciences, vol. 20, no. 14, p. 3380, 2019.
30. S. F. Lichtenthaler, S. K. Tschirner, and H. Steiner, “Secretases in Alzheimer’s disease: Novel insights into proteolysis of APP and TREM2,” Current Opinion in Neurobiology, vol. 72, pp. 101-110, 2022.
31. J. Cao, J. Hou, J. Ping, and D. Cai, “Advances in developing novel therapeutic strategies for Alzheimer’s disease,” Molecular neurodegeneration, vol. 13, no. 1, pp. 1-20, 2018.
32. S. O. Bachurin, S. I. Gavrilova, A. Samsonova, G. E. Barreto, and G. Aliev, “Mild cognitive impairment due to Alzheimer disease: Contemporary approaches to diagnostics and pharmacological intervention,” Pharmacological research, vol. 129, pp. 216-226, 2018.
33. B.-L. Sun et al., “Clinical research on Alzheimer’s disease: progress and perspectives,” Neuroscience bulletin, vol. 34, no. 6, pp. 1111-1118, 2018.
34. F. S. Dafsari and F. Jessen, “Depression—an underrecognized target for prevention of dementia in Alzheimer’s disease,” Translational Psychiatry, vol. 10, no. 1, pp. 1-13, 2020.
35. A. G. Ording et al., “Cancer and risk of Alzheimer’s disease: Small association in a nationwide cohort study,” Alzheimer’s & Dementia, vol. 16, no. 7, pp. 953-964, 2020.
36. M. Lilamand et al., “Relationship between brain amyloid deposition and instrumental activities of daily living in older adults: a longitudinal study from the Multidomain Alzheimer Prevention Trial,” Journal of the American Geriatrics Society, vol. 66, no. 10, pp. 1940-1947, 2018.
37. G. Torrandell‐Haro, G. L. Branigan, F. Vitali, N. Geifman, J. M. Zissimopoulos, and R. D. Brinton, “Statin therapy and risk of Alzheimer’s and age‐related neurodegenerative diseases,” Alzheimer’s & Dementia: Translational Research & Clinical Interventions, vol. 6, no. 1, p. e12108, 2020.
38. D. Barthold, G. Joyce, R. Diaz Brinton, W. Wharton, P. G. Kehoe, and J. Zissimopoulos, “Association of combination statin and antihypertensive therapy with reduced Alzheimer’s disease and related dementia risk,” PloS one, vol. 15, no. 3, p. e0229541, 2020.
39. E. Olmastroni et al., “Statin use and risk of dementia or Alzheimer’s disease: a systematic review and meta-analysis of observational studies,” European Journal of Preventive Cardiology, vol. 29, no. 5, pp. 804-814, 2022.
40. A. Rosenberg, F. Mangialasche, T. Ngandu, A. Solomon, and M. Kivipelto, “Multidomain interventions to prevent cognitive impairment, Alzheimer’s disease, and dementia: From FINGER to World-Wide FINGERS,” The Journal of Prevention of Alzheimer’s Disease, vol. 7, no. 1, pp. 29-36, 2020.
41. T. T. Nguyen, T. T. D. Nguyen, T. K. O. Nguyen, and T. K. Vo, “Advances in developing therapeutic strategies for Alzheimer’s disease,” Biomedicine & Pharmacotherapy, vol. 139, p. 111623, 2021.
42. J. F. Hodes et al., “Alzheimer’s “prevention” vs.“risk reduction”: transcending semantics for clinical practice,” Frontiers in neurology, vol. 9, p. 1179, 2019.
43. R. S. Isaacson et al., “The clinical practice of risk reduction for Alzheimer’s disease: a precision medicine approach,” Alzheimer’s & Dementia, vol. 14, no. 12, pp. 1663-1673, 2018.
44. L. Parnetti, E. Chipi, N. Salvadori, K. D’Andrea, and P. Eusebi, “Prevalence and risk of progression of preclinical Alzheimer’s disease stages: a systematic review and meta-analysis,” Alzheimer’s research & therapy, vol. 11, no. 1, pp. 1-13, 2019.
45. C. Green et al., “Assessing cost-effectiveness of early intervention in Alzheimer’s disease: An open-source modeling framework,” Alzheimer’s & Dementia, vol. 15, no. 10, pp. 1309-1321, 2019.
46. A. K. Sahoo, J. Dandapat, U. C. Dash, and S. Kanhar, “Features and outcomes of drugs for combination therapy as multi-targets strategy to combat Alzheimer’s disease,” Journal of Ethnopharmacology, vol. 215, pp. 42-73, 2018.
47. F. H. Bazzari, D. M. Abdallah, and H. S. El-Abhar, “Pharmacological interventions to attenuate Alzheimer’s disease progression: the story so far,” Current Alzheimer Research, vol. 16, no. 3, pp. 261-277, 2019.
48. J. Blackman, M. Swirski, J. Clynes, S. Harding, Y. Leng, and E. Coulthard, “Pharmacological and non‐pharmacological interventions to enhance sleep in mild cognitive impairment and mild Alzheimer’s disease: A systematic review,” Journal of sleep research, vol. 30, no. 4, p. e13229, 2021.
49. H. Zhang and Y. Zheng, “β amyloid hypothesis in Alzheimer’s disease: pathogenesis, prevention, and management,” Zhongguo yi xue ke xue Yuan xue bao. Acta Academiae Medicinae Sinicae, vol. 41, no. 5, pp. 702-708, 2019.
50. V. N. Bukke et al., “The dual role of glutamatergic neurotransmission in Alzheimer’s disease: From pathophysiology to pharmacotherapy,” International journal of molecular sciences, vol. 21, no. 20, p. 7452, 2020.
51. B. C. Beckelman et al., “Genetic reduction of eEF2 kinase alleviates pathophysiology in Alzheimer’s disease model mice,” The Journal of clinical investigation, vol. 129, no. 2, pp. 820-833, 2019.
52. W. Jagust, “Imaging the evolution and pathophysiology of Alzheimer disease,” Nature Reviews Neuroscience, vol. 19, no. 11, pp. 687-700, 2018.
53. M. M. Ali, R. G. Ghouri, A. H. Ans, A. Akbar, and A. Toheed, “Recommendations for anti-inflammatory treatments in Alzheimer’s disease: a comprehensive review of the literature,” Cureus, vol. 11, no. 5, 2019.
54. S. Cordone, S. Scarpelli, V. Alfonsi, L. De Gennaro, and M. Gorgoni, “Sleep-based interventions in Alzheimer’s disease: promising approaches from prevention to treatment along the disease trajectory,” Pharmaceuticals, vol. 14, no. 4, p. 383, 2021.
55. G. L. Bowman et al., “A blood-based nutritional risk index explains cognitive enhancement and decline in the multidomain Alzheimer prevention trial,” Alzheimer’s & Dementia: Translational Research & Clinical Interventions, vol. 5, pp. 953-963, 2019.
56. T. Desmidt et al., “Benzodiazepine use and brain amyloid load in nondemented older individuals: a florbetapir PET study in the Multidomain Alzheimer Preventive Trial cohort,” Neurobiology of Aging, vol. 84, pp. 61-69, 2019.
57. N. Costa et al., “The cost-effectiveness of three prevention strategies in Alzheimer’s disease: results from the Multidomain Alzheimer Preventive Trial (MAPT),” The Journal of Prevention of Alzheimer’s Disease, vol. 8, no. 4, pp. 425-435, 2021.
58. A. Atri, “Current and future treatments in Alzheimer’s disease,” 2019, vol. 39: Thieme Medical Publishers, 02 ed., pp. 227-240.
59. H. McGurran, J. Glenn, E. Madero, and N. Bott, “Risk Reduction and Prevention of Alzheimer’s Disease: Biological Mechanisms of Diet,” Current Alzheimer Research, vol. 17, no. 5, pp. 407-427, 2020.
60. M. D. Sweeney et al., “Vascular dysfunction—the disregarded partner of Alzheimer’s disease,” Alzheimer’s & Dementia, vol. 15, no. 1, pp. 158-167, 2019.