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Alzheimer’s disease (AD)

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Alzheimer’s disease (AD), also referred to simply as Alzheimer’s, is a chronic neurodegenerative disease that usually starts slowly and gradually worsens over time. It is the cause of 60–70% of cases of dementia. The most common early symptom is difficulty in remembering recent events. As the disease advances, symptoms can include problems with language, disorientation (including easily getting lost), mood swings, loss of motivation, not managing self-care, and behavioural issues. As a person’s condition declines, they often withdraw from family and society.  Gradually, bodily functions are lost, ultimately leading to death. Although the speed of progression can vary, the typical life expectancy following diagnosis is three to nine years.

The cause of Alzheimer’s disease is poorly understood. AD affects many different types of neurons in many parts of the brain. This poses a convoluted problem for repairing and/or rejuvenating of the brain. Research does shows that new neurons can be formed but transplanting cells into the brain or signalling-associated proteins  is not an easy task.

Pre-dementia

 

The first symptoms are often mistakenly attributed to ageing or stress. Detailed neuropsychological testing can reveal mild cognitive difficulties up to eight years before a person fulfils the clinical criteria for diagnosis of AD. These early symptoms can affect the most complex activities of daily living. The most noticeable deficit is short term memory loss, which shows up as difficulty in remembering recently learned facts and inability to acquire new information.

Subtle problems with the executive functions of attentiveness, planning, flexibility, and abstract thinking, or impairments in semantic memory (memory of meanings, and concept relationships) can also be symptomatic of the early stages of AD. Apathy and depression can be seen at this stage, with apathy remaining as the most persistent symptom throughout the course of the disease. The preclinical stage of the disease has also been termed mild cognitive impairment (MCI). This is often found to be a transitional stage between normal ageing and dementia. MCI can present with a variety of symptoms, and when memory loss is the predominant symptom, it is termed “amnestic MCI” and is frequently seen as a prodromal stage of Alzheimer’s disease.

 

 

Early

 

In people with AD, the increasing impairment of learning and memory eventually leads to a definitive diagnosis. In a small percentage, difficulties with language, executive functions, perception (agnosia), or execution of movements (apraxia) are more prominent than memory problems. AD does not affect all memory capacities equally. Older memories of the person’s life (episodic memory), facts learned (semantic memory), and implicit memory (the memory of the body on how to do things, such as using a fork to eat or how to drink from a glass) are affected to a lesser degree than new facts or memories.

Language problems are mainly characterized by a shrinking vocabulary and decreased word fluency, leading to a general impoverishment of oral and written language.] In this stage, the person with Alzheimer’s is usually capable of communicating basic ideas adequately. While performing fine motor tasks such as writing, drawing, or dressing, certain movement coordination and planning difficulties (apraxia) may be present, but they are commonly unnoticed. As the disease progresses, people with AD can often continue to perform many tasks independently, but may need assistance or supervision with the most cognitively demanding activities.

 

Moderate

 

Progressive deterioration eventually hinders independence, with subjects being unable to perform most common activities of daily living. Speech difficulties become evident due to an inability to recall vocabulary, which leads to frequent incorrect word substitutions (paraphasias). Reading and writing skills are also progressively lost. Complex motor sequences become less coordinated as time passes and AD progresses, so the risk of falling increases. During this phase, memory problems worsen, and the person may fail to recognize close relatives. Long-term memory, which was previously intact, becomes impaired.

Behavioural and neuropsychiatric changes become more prevalent. Common manifestations are wandering, irritability and labile affect, leading to crying, outbursts of unpremeditated aggression, or resistance to care giving. Sundowning can also appear. Approximately 30% of people with AD develop illusionary misidentifications and other delusional symptoms. Subjects also lose insight of their disease process and limitations (anosognosia). Urinary incontinence can develop. These symptoms create stress for relatives and care givers, which can be reduced by moving the person from home care to other long-term care facilities.

 

Advanced

 

During the final stages, the patient is completely dependent upon caregivers. Language is reduced to simple phrases or even single words, eventually leading to complete loss of speech. Despite the loss of verbal language abilities, people can often understand and return emotional signals. Although aggressiveness can still be present, extreme apathy and exhaustion are much more common symptoms. People with Alzheimer’s disease will ultimately not be able to perform even the simplest tasks independently; muscle mass and mobility deteriorates to the point where they are bedridden and unable to feed themselves. The cause of death is usually an external factor, such as infection of pressure ulcers or pneumonia, not the disease itself.

TREATMENT

At World Stem Cell Clinic and The Royal British Medical Center we practice Precision medicine (PM) which is a treatment model that proposes the customization of the treatment to each unique patients based on their medical history, stage of disease, exam results, time available for treatment and a patient orientation meeting with our Doctors before determining the best treatment for each unique patient.

 

 

References

  1. ^ Jump up to:ab c d e f g h i j k l m Burns A, Iliffe S (February 2009). “Alzheimer’s disease”. BMJ. 338: b158. doi:1136/bmj.b158. PMID 19196745. S2CID 8570146.
  2. ^ Jump up to:ab c d e f g h “Dementia Fact sheet”. World Health Organization. 12 December 2017.
  3. ^ Jump up to:ab Mendez MF (November 2012). “Early-onset Alzheimer’s disease: nonamnestic subtypes and type 2 AD”. Archives of Medical Research. 43 (8): 677–85. doi:1016/j.arcmed.2012.11.009. PMC 3532551. PMID 23178565.
  4. ^ Jump up to:ab c d e Ballard C, Gauthier S, Corbett A, Brayne C, Aarsland D, Jones E (March 2011). “Alzheimer’s disease”. Lancet. 377 (9770): 1019–31. doi:1016/S0140-6736(10)61349-9. PMID 21371747. S2CID 20893019.
  5. ^ Jump up to:ab “Dementia diagnosis and assessment” (PDF). National Institute for Health and Care Excellence (NICE). Archived from the original(PDF) on 5 December 2014. Retrieved 30 November 2014.
  6. ^Commission de la transparence (June 2012). “Drugs for Alzheimer’s disease: best avoided. No therapeutic advantage” [Drugs for Alzheimer’s disease: best avoided. No therapeutic advantage]. Prescrire International. 21 (128): 150. PMID 22822592.
  7. ^ Jump up to:ab Querfurth HW, LaFerla FM (January 2010). “Alzheimer’s disease”. The New England Journal of Medicine. 362 (4): 329–44. doi:1056/NEJMra0909142. PMID 20107219. S2CID 205115756.
  8. ^ Jump up to:ab GBD 2015 Disease Injury Incidence Prevalence Collaborators (October 2016). “Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015”. Lancet. 388 (10053): 1545–1602. doi:1016/S0140-6736(16)31678-6. PMC 5055577. PMID 27733282.
  9. ^ Jump up to:ab GBD 2015 Mortality Causes of Death Collaborators (October 2016). “Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980-2015: a systematic analysis for the Global Burden of Disease Study 2015”. Lancet. 388(10053): 1459–1544. doi:1016/S0140-6736(16)31012-1. PMC 5388903. PMID 27733281.
  10. ^“About Alzheimer’s Disease: Symptoms”. National Institute on Aging. Archived from the original on 15 January 2012. Retrieved 28 December2011.
  11. ^Todd S, Barr S, Roberts M, Passmore AP (November 2013). “Survival in dementia and predictors of mortality: a review”. International Journal of Geriatric Psychiatry. 28 (11): 1109–24. doi:1002/gps.3946. PMID 23526458. S2CID 25445595.
  12. ^“So, What Can You Do?”. National Institute on Aging. 29 July 2016. Archived from the original on 3 April 2017.
  13. ^ Jump up to:ab c d e Hsu D, Marshall GA (2017). “Primary and Secondary Prevention Trials in Alzheimer Disease: Looking Back, Moving Forward”. Current Alzheimer Research. 14 (4): 426–40. doi:2174/1567205013666160930112125. PMC 5329133. PMID 27697063.
  14. ^ Jump up to:ab c d Thompson CA, Spilsbury K, Hall J, Birks Y, Barnes C, Adamson J (July 2007). “Systematic review of information and support interventions for caregivers of people with dementia”. BMC Geriatrics. 7: 18. doi:1186/1471-2318-7-18. PMC 1951962. PMID 17662119.
  15. ^Forbes D, Forbes SC, Blake CM, Thiessen EJ, Forbes S (April 2015). “Exercise programs for people with dementia”. The Cochrane Database of Systematic Reviews (Submitted manuscript). 132 (4): CD006489. doi:1002/14651858.CD006489.pub4. PMID 25874613.
  16. ^National Institute for Health and Clinical Excellence. “Low-dose antipsychotics in people with dementia”. National Institute for Health and Care Excellence (NICE). Archived from the original on 5 December 2014. Retrieved 29 November 2014.
  17. ^“Information for Healthcare Professionals: Conventional Antipsychotics”. US Food and Drug Administration. 16 June 2008. Archived from the original on 29 November 2014. Retrieved 29 November 2014.
  18. ^ Jump up to:ab c Berchtold NC, Cotman CW (1998). “Evolution in the conceptualization of dementia and Alzheimer’s disease: Greco-Roman period to the 1960s”. Neurobiology of Aging. 19 (3): 173–89. doi:1016/S0197-4580(98)00052-9. PMID 9661992. S2CID 24808582.
  19. ^ Jump up to:ab c d Bonin-Guillaume S, Zekry D, Giacobini E, Gold G, Michel JP (January 2005). “[The economical impact of dementia]”. Presse Médicale(in French). 34 (1): 35–41. doi:1016/s0755-4982(05)83882-5. PMID 15685097.
  20. ^ Jump up to:ab c d e Meek PD, McKeithan K, Schumock GT (1998). “Economic considerations in Alzheimer’s disease”. Pharmacotherapy. 18 (2 Pt 2): 68–73, discussion 79–82. doi:1002/j.1875-9114.1998.tb03880.x(inactive 11 November 2020). PMID 9543467.
  21. ^“Evaluating Prescription Drugs Used to Treat: Alzheimer’s Disease Comparing Effectiveness, Safety, and Price” (PDF). Consumer Reports Drug Effectiveness Review Project. Consumer Reports. May 2012. Archived from the original (PDF) on 5 September 2012. Retrieved 1 May 2013.
  22. ^ Jump up to:ab c d e Waldemar G, Dubois B, Emre M, Georges J, McKeith IG, Rossor M, Scheltens P, Tariska P, Winblad B (January 2007). “Recommendations for the diagnosis and management of Alzheimer’s disease and other disorders associated with dementia: EFNS guideline”. European Journal of Neurology. 14 (1): e1–26. doi:1111/j.1468-1331.2006.01605.x. PMID 17222085. S2CID 2725064.
  23. ^ Jump up to:ab c Bäckman L, Jones S, Berger AK, Laukka EJ, Small BJ (September 2004). “Multiple cognitive deficits during the transition to Alzheimer’s disease”. Journal of Internal Medicine. 256 (3): 195–204. doi:1111/j.1365-2796.2004.01386.x. PMID 15324363. S2CID 37005854.
  24. ^Nygård L (2003). “Instrumental activities of daily living: a stepping-stone towards Alzheimer’s disease diagnosis in subjects with mild cognitive impairment?”. Acta Neurologica Scandinavica. Supplementum. 179(s179): 42–6. doi:1034/j.1600-0404.107.s179.8.x. PMID 12603250. S2CID 25313065.
  25. ^ Jump up to:ab Arnáiz E, Almkvist O (2003). “Neuropsychological features of mild cognitive impairment and preclinical Alzheimer’s disease”. Acta Neurologica Scandinavica. Supplementum. 179: 34–41. doi:1034/j.1600-0404.107.s179.7.x. PMID 12603249. S2CID 22494768.
  26. ^Deardorff WJ, Grossberg GT (2019). “Behavioral and psychological symptoms in Alzheimer’s dementia and vascular dementia”. Handbook of Clinical Neurology. 165: 5–32. doi:1016/B978-0-444-64012-3.00002-2. ISBN 9780444640123. PMID 31727229.
  27. ^Murray ED, Buttner N, Price BH (2012). “Depression and Psychosis in Neurological Practice”. In Bradley WG, Daroff RB, Fenichel GM, Jankovic J (eds.). Bradley’s neurology in clinical practice (6th ed.). Philadelphia, PA: Elsevier/Saunders. ISBN 978-1-4377-0434-1.
  28. ^Grundman M, Petersen RC, Ferris SH, et al. (January 2004). “Mild cognitive impairment can be distinguished from Alzheimer disease and normal aging for clinical trials”. Archives of Neurology. 61 (1): 59–66. doi:1001/archneur.61.1.59. PMID 14732621.
  29. ^ Jump up to:ab c d e f g h i j k l m n o p q r s Förstl H, Kurz A (1999). “Clinical features of Alzheimer’s disease”. European Archives of Psychiatry and Clinical Neuroscience. 249 (6): 288–90. doi:1007/s004060050101. PMID 10653284. S2CID 26142779.
  30. ^Carlesimo GA, Oscar-Berman M (June 1992). “Memory deficits in Alzheimer’s patients: a comprehensive review”. Neuropsychology Review. 3 (2): 119–69. doi:1007/BF01108841. PMID 1300219. S2CID 19548915.
  31. ^Jelicic M, Bonebakker AE, Bonke B (1995). “Implicit memory performance of patients with Alzheimer’s disease: a brief review”. International Psychogeriatrics. 7 (3): 385–92. doi:1017/S1041610295002134. PMID 8821346.
  32. ^ Jump up to:ab Taler V, Phillips NA (July 2008). “Language performance in Alzheimer’s disease and mild cognitive impairment: a comparative review”. Journal of Clinical and Experimental Neuropsychology. 30 (5): 501–56. doi:1080/13803390701550128. PMID 18569251. S2CID 37153159.
  33. ^ Jump up to:ab c Frank EM (September 1994). “Effect of Alzheimer’s disease on communication function”. Journal of the South Carolina Medical Association. 90 (9): 417–23. PMID 7967534.
  34. ^Volicer L, Harper DG, Manning BC, Goldstein R, Satlin A (May 2001). “Sundowning and circadian rhythms in Alzheimer’s disease”. The American Journal of Psychiatry. 158 (5): 704–11. doi:1176/appi.ajp.158.5.704. PMID 11329390. S2CID 10492607.
  35. ^Gold DP, Reis MF, Markiewicz D, Andres D (January 1995). “When home caregiving ends: a longitudinal study of outcomes for caregivers of relatives with dementia”. Journal of the American Geriatrics Society. 43(1): 10–6. doi:1111/j.1532-5415.1995.tb06235.x. PMID 7806732. S2CID 29847950.
  36. ^‘ Alzheimer’s disease – Causes‘ (NHS)
  37. ^“What We Know Today About Alzheimer’s Disease”. Alzheimer’s Association. Archived from the original on 7 October 2011. Retrieved 1 October 2011. While scientists know Alzheimer’s disease involves progressive brain cell failure, the reason cells fail isn’t clear.
  38. ^Reitz C, Mayeux R (April 2014). “Alzheimer disease: epidemiology, diagnostic criteria, risk factors and biomarkers”. Biochemical Pharmacology. 88 (4): 640–51. doi:1016/j.bcp.2013.12.024. PMC 3992261. PMID 24398425.
  39. ^Wilson RS, Barral S, Lee JH, Leurgans SE, Foroud TM, Sweet RA, Graff-Radford N, Bird TD, Mayeux R, Bennett DA (2011). “Heritability of different forms of memory in the Late Onset Alzheimer’s Disease Family Study”. Journal of Alzheimer’s Disease. 23 (2): 249–55. doi:3233/JAD-2010-101515. PMC 3130303. PMID 20930268.
  40. ^ Jump up to:ab c Blennow K, de Leon MJ, Zetterberg H (July 2006). “Alzheimer’s disease”. Lancet. 368 (9533): 387–403. doi:1016/S0140-6736(06)69113-7. PMID 16876668. S2CID 47544338.
  41. ^ Jump up to:ab Waring SC, Rosenberg RN (March 2008). “Genome-wide association studies in Alzheimer disease”. Archives of Neurology. 65 (3): 329–34. doi:1001/archneur.65.3.329. PMID 18332245.
  42. ^Selkoe DJ (June 1999). “Translating cell biology into therapeutic advances in Alzheimer’s disease”. Nature. 399 (6738 Suppl): A23–31. doi:1038/19866. PMID 10392577. S2CID 42287088.
  43. ^Borchelt DR, Thinakaran G, Eckman CB, et al. (November 1996). “Familial Alzheimer’s disease-linked presenilin 1 variants elevate Abeta1-42/1-40 ratio in vitro and in vivo”. Neuron. 17 (5): 1005–13. doi:1016/S0896-6273(00)80230-5. PMID 8938131. S2CID 18315650.
  44. ^Kim, JH (December 2018). “Genetics of Alzheimer’s Disease”. Dementia and Neurocognitive Disorders. 17 (4): 131–36. doi:12779/dnd.2018.17.4.131. PMC 6425887. PMID 30906402.
  45. ^Strittmatter WJ, Saunders AM, Schmechel D, Pericak-Vance M, Enghild J, Salvesen GS, Roses AD (March 1993). “Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease”. Proceedings of the National Academy of Sciences of the United States of America. 90 (5): 1977–81. Bibcode:..90.1977S. doi:10.1073/pnas.90.5.1977. PMC 46003. PMID 8446617.
  46. ^ Jump up to:ab Mahley RW, Weisgraber KH, Huang Y (April 2006). “Apolipoprotein E4: a causative factor and therapeutic target in neuropathology, including Alzheimer’s disease”. Proceedings of the National Academy of Sciences of the United States of America. 103 (15): 5644–51. Bibcode:.103.5644M. doi:10.1073/pnas.0600549103. PMC 1414631. PMID 16567625.
  47. ^Hall K, Murrell J, Ogunniyi A, Deeg M, Baiyewu O, Gao S, Gureje O, Dickens J, Evans R, Smith-Gamble V, Unverzagt FW, Shen J, Hendrie H (January 2006). “Cholesterol, APOE genotype, and Alzheimer disease: an epidemiologic study of Nigerian Yoruba”. Neurology. 66 (2): 223–27. doi:1212/01.wnl.0000194507.39504.17. PMC 2860622. PMID 16434658.
  48. ^Gureje O, Ogunniyi A, Baiyewu O, et al. (January 2006). “APOE epsilon4 is not associated with Alzheimer’s disease in elderly Nigerians”. Annals of Neurology. 59 (1): 182–85. doi:1002/ana.20694. PMC 2855121. PMID 16278853.
  49. ^ Jump up to:ab Lambert JC, Ibrahim-Verbaas CA, Harold D, et al. (December 2013). “Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer’s disease”. Nature Genetics. 45 (12): 1452–58. doi:1038/ng.2802. PMC 3896259. PMID 24162737.
  50. ^Jonsson T, Stefansson H, Steinberg S, et al. (January 2013). “Variant of TREM2 associated with the risk of Alzheimer’s disease”. The New England Journal of Medicine (Original article). 368 (2): 107–16. doi:1056/NEJMoa1211103. PMC 3677583. PMID 23150908.
  51. ^Guerreiro R, Wojtas A, Bras J, et al. (January 2013). “TREM2 variants in Alzheimer’s disease”. The New England Journal of Medicine(Original article). 368 (2): 117–27. doi:1056/NEJMoa1211851. PMC 3631573. PMID 23150934.
  52. ^Mukherjee S, Mez J, Trittschuh EH, Saykin AJ, Gibbons LE, Fardo DW, Wessels M, Bauman J, Moore M, Choi SE, Gross AL, Rich J, Louden DK, Sanders RE, Grabowski TJ, Bird TD, et al. (December 2018). “Genetic data and cognitively defined late-onset Alzheimer’s disease subgroups”. Molecular Psychiatry. 25 (11): 2942–2951. doi:1038/s41380-018-0298-8. PMC 6548676. PMID 30514930.
  53. ^Francis PT, Palmer AM, Snape M, Wilcock GK (February 1999). “The cholinergic hypothesis of Alzheimer’s disease: a review of progress”. Journal of Neurology, Neurosurgery, and Psychiatry. 66 (2): 137–47. doi:1136/jnnp.66.2.137. PMC 1736202. PMID 10071091.
  54. ^Martorana A, Esposito Z, Koch G (August 2010). “Beyond the cholinergic hypothesis: do current drugs work in Alzheimer’s disease?”. CNS Neuroscience & Therapeutics. 16 (4): 235–45. doi:1111/j.1755-5949.2010.00175.x. PMC 6493875. PMID 20560995.
  55. ^Hardy J, Allsop D (October 1991). “Amyloid deposition as the central event in the aetiology of Alzheimer’s disease”. Trends in Pharmacological Sciences. 12 (10): 383–88. doi:1016/0165-6147(91)90609-V. PMID 1763432.
  56. ^ Jump up to:ab Mudher A, Lovestone S (January 2002). “Alzheimer’s disease-do tauists and baptists finally shake hands?”. Trends in Neurosciences. 25(1): 22–26. doi:1016/S0166-2236(00)02031-2. PMID 11801334. S2CID 37380445.
  57. ^Nistor M, Don M, Parekh M, Sarsoza F, Goodus M, Lopez GE, Kawas C, Leverenz J, Doran E, Lott IT, Hill M, Head E (October 2007). “Alpha- and beta-secretase activity as a function of age and beta-amyloid in Down syndrome and normal brain”. Neurobiology of Aging. 28 (10): 1493–506. doi:1016/j.neurobiolaging.2006.06.023. PMC 3375834. PMID 16904243.
  58. ^Lott IT, Head E (March 2005). “Alzheimer disease and Down syndrome: factors in pathogenesis”. Neurobiology of Aging. 26 (3): 383–89. doi:1016/j.neurobiolaging.2004.08.005. PMID 15639317. S2CID 27716613.
  59. ^Polvikoski T, Sulkava R, Haltia M, Kainulainen K, Vuorio A, Verkkoniemi A, Niinistö L, Halonen P, Kontula K (November 1995). “Apolipoprotein E, dementia, and cortical deposition of beta-amyloid protein”. The New England Journal of Medicine. 333 (19): 1242–47. doi:1056/NEJM199511093331902. PMID 7566000.
  60. ^Transgenic mice:

WHAT MAKES OUR TREATMENT DIFFERENT

  • At World Stem Cell Clinic and The Royal British Medical Center we practice “Patient Precision Medicine (PPM)” which is a treatment model that proposes the customization of the treatment to each unique patient based on their medical history, stage of disease, exam results, time available for treatment and a patient orientation meeting with our Doctors before determining the best treatment for each unique patient.

 

  • Our staff physicians are all board certified, in their field with years of experience. Your team includes both primary and ancillary care professionals devoted to maximizing your benefits from the procedures. We enroll you in an open registry to track your changes independently, for up to 5 years.

 

  • To maintain our “Patient Precision Medicine (PPM)” services for you we may use peripheral blood, bone marrow, adipose or umbilical cord derived cells, plasma, proteins and Extracellular Vesicles based your unique treatment needs with mutual agreement.

 

  • As our patient we also keep you abreast of the newest developments in treatment research. This is an ongoing relationship to maintain and enhance your health.

 

  • Our promise is to provide you with travel and lodging support, access to bilingual staff members throughout the entire process and most importantly the best medical care possible.
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