Of the approximately 6.8 million Americans who have been diagnosed with dementia, over 5 million have been diagnosed with Alzheimer's Disease (AD). Due to the rise in the aging population, these figures are expected to double by 2050. The following paper provides an up-to-date review of clinical issues and relevant research. Research related to the methods of the earliest possible detection of AD is ongoing. Health care professionals should play a critical role in differentially diagnosing AD patients, as well as supporting their families. Novel interventions, including medications, natural supplements, and behavioral techniques, are constantly appearing in the literature. It is necessary for the health practitioner to remain current, regarding AD, as such information will facilitate better care for patients and their families. 1. Introduction Approximately 6.8 million individuals in the United States are affected by dementia [1], and approximately 5.3 million have been diagnosed with Alzheimer’s Disease (AD) [2]. As the elderly population continues to grow, these numbers are only expected to increase. AD has emerged as a serious public health concern, placing an immense burden on the individual, family, community, and health care resources. AD most frequently presents with episodic memory impairment as the earliest and most prominent feature, with additional deficits in language, semantic memory, executive functioning, visuospatial abilities, and functional impairment that emerge over the disease course [3]. A common misconception is that AD is a “normal” or expected occurrence of aging, and it is part of the typical trajectory of age-related cognitive decline. Rather, healthy aging has been found to be associated with relatively stable performance on measures of cognitive functioning when measured longitudinally. However, cross-sectional studies have indicated that some domains of cognitive functioning do in fact decline with age [4]. As individuals live to advanced ages (e.g., over the age of 80), it can become more challenging to differentiate between the subtle cognitive declines that accompany aging and those that signify early dementia [5]. The trajectory of AD is characterized along a continuum, ranging from healthy aging to preclinical AD, mild cognitive impairment (MCI), and dementia. Pathological changes that underlie AD begin to accumulate for years, or even decades, before emotional, physical, or cognitive symptoms emerge, eventually reaching a threshold at which the onset of a gradual and progressive decline in cognition occurs [5].
References
[1]
NINDS, “Dementia: hope through research,” 2012, http://www.ninds.nih.gov/disorders/dementias/detail_dementia.html.
S. Weintraub, A. H. Wicklund, and D. P. Salmon, “The neuropsychological profile of Alzheimer disease,” Cold Spring Harbor Perspectives in Medicine, vol. 2, no. 4, Article ID a006171, 2012.
[4]
J. M. Burns and J. C. Morris, Mild Cognitive Impairment and Early Alzheimer's Disease: Detections and Diagnosis, John Wiley & Sons, 2008.
[5]
M. W. Bondi, D. P. Salmon, and A. W. Kaszniak, “The neuropsychology of dementia,” in Neuropsychological Assessment of Neuropsychiatric and Neuromedical Disorders, I. Grant and K. Adams, Eds., pp. 159–198, Oxford University Press, New York, NY, USA, 2009.
[6]
C. R. Jack Jr., M. S. Albert, D. S. Knopman et al., “Introduction to the recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease,” Alzheimer's and Dementia, vol. 7, no. 3, pp. 257–262, 2011.
[7]
R. C. Petersen, “Conceptual overview,” in Mild Cognitive Impairment: Aging to Alzheimer's Disease, R. C. Petersen, Ed., pp. 1–14, Oxford University Press, New York, NY, USA, 2003.
[8]
M. S. Albert, S. T. DeKosky, D. Dickson et al., “The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease,” Alzheimer's and Dementia, vol. 7, no. 3, pp. 270–279, 2011.
[9]
Association As, “Alzheimer's disease facts and figures,” 2012, http://www.alz.org/downloads/facts_figures_2012.pdf.
[10]
NIA, 2011-2012 Alzheimer's Disease Progress Report: Intensifying the Research Effort, 2012.
[11]
H. Braak and E. Braak, “Neuropathological stageing of Alzheimer-related changes,” Acta Neuropathologica, vol. 82, no. 4, pp. 239–259, 1991.
[12]
D. J. Selkoe, “The molecular pathology of Alzheimer's disease,” Neuron, vol. 6, no. 4, pp. 487–498, 1991.
[13]
J. Hardy and D. J. Selkoe, “The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics,” Science, vol. 297, no. 5580, pp. 353–356, 2002.
[14]
J. Hoffman, The Alzheimer's Project: Momentum in Science, PublicAffairs/Home Box Office, New York, NY, USA, 2009.
[15]
Z. Nagy, D. M. Yilmazer-Hanke, H. Braak, E. Braak, C. Schultz, and J. Hanke, “Assessment of the pathological stages of Alzheimer's disease in thin paraffin sections: a comparative study,” Dementia and Geriatric Cognitive Disorders, vol. 9, no. 3, pp. 140–144, 1998.
[16]
G. M. McKhann, D. S. Knopman, H. Chertkow et al., “The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease,” Alzheimer's and Dementia, vol. 7, no. 3, pp. 263–269, 2011.
[17]
W. E. Klunk, H. Engler, A. Nordberg et al., “Imaging brain amyloid in Alzheimer's disease with pittsburgh compound-B,” Annals of Neurology, vol. 55, no. 3, pp. 306–319, 2004.
[18]
J. Q. Trojanowski, H. Vandeerstichele, M. Korecka et al., “Update on the biomarker core of the Alzheimer's disease neuroimaging initiative subjects,” Alzheimer's and Dementia, vol. 6, no. 3, pp. 230–238, 2010.
[19]
W. Jagust, “Positron emission tomography and magnetic resonance imaging in the diagnosis and prediction of dementia,” Alzheimer's and Dementia, vol. 2, no. 1, pp. 36–42, 2006.
[20]
M. Atiya, B. T. Hyman, M. S. Albert, and R. Killiany, “Structural magnetic resonance imaging in established and prodromal Alzheimer disease: a review,” Alzheimer Disease and Associated Disorders, vol. 17, no. 3, pp. 177–195, 2003.
[21]
APA, Diagnostic and Statistical Manual of Mental Disorders, American Psychiatric Association, Washington, DC, USA, 4th edition, 2000.
[22]
J. D. Warren, P. D. Fletcher, and H. L. Golden, “The paradox of syndromic diversity in Alzheimer disease,” Nature Reviews, vol. 8, no. 8, pp. 451–464, 2012.
[23]
M. D. Lezak, Neuropsychological Assessment, Oxford University Press, New York, NY, USA, 5th edition, 2012.
[24]
B. L. Malamut and L. M. Ryan, “Dementia: behavioral and cognitive aspectseds,” in Clinical Neurology of the Older Adult, J. I. Sirven and B. L. Malamut, Eds., pp. 318–338, Wolters Kluwer Health/Lippincott Williams & Wilkins, Philadelphia, Pa, USA, 2nd edition, 2008.
[25]
M. Mitrushina, “Cognitive screening methods,” in Neuropsychological Assessment of Neuropsychiatric and Neuromedical Disorders, I. Grant and K. Adams, Eds., pp. 101–126, Oxford University Press, New York, NY, USA, 2009.
[26]
Z. S. Nasreddine, N. A. Phillips, V. Bédirian et al., “The Montreal Cognitive Assessment, MoCA: a brief screening tool for mild cognitive impairment,” Journal of the American Geriatrics Society, vol. 53, no. 4, pp. 695–699, 2005.
[27]
S. Weintraub, D. Salmon, N. Mercaldo et al., “The Alzheimer's disease denters' Uniform Data Set (UDS): the neuropsychologic test battery,” Alzheimer Disease and Associated Disorders, vol. 23, no. 2, pp. 91–101, 2009.
[28]
M. Freedman, Clock Drawing: A Neuropsychological Analysis, Oxford University Press, 1994.
[29]
J. C. Morris, “Clinical dementia rating: a reliable and valid diagnostic and staging measure for dementia of the Alzheimer type,” International Psychogeriatrics, vol. 9, supplement 1, pp. 173–176, 1997.
[30]
S. E. O'Bryant, L. H. Lacritz, J. Hall et al., “Validation of the new interpretive guidelines for the clinical dementia rating scale sum of boxes score in the national Alzheimer's coordinating center database,” Archives of Neurology, vol. 67, no. 6, pp. 746–749, 2010.
[31]
Association As, Current Alzheimer's Treatments, 2013.
[32]
N. Herrmann, S. A. Chau, I. Kircanski, and K. L. Lanct？t, “Current and emerging drug treatment options for Alzheimers disease: a systematic review,” Drugs, vol. 71, no. 15, pp. 2031–2065, 2011.
[33]
P. N. Tariot, M. R. Farlow, G. T. Grossberg, S. M. Graham, S. McDonald, and I. Gergel, “Memantine treatment in patients with moderate to severe Alzheimer disease already receiving donepezil: a randomized controlled trial,” Journal of the American Medical Association, vol. 291, no. 3, pp. 317–324, 2004.
[34]
R. Duara, W. Barker, D. Loewenstein, and L. Bain, “The basis for disease-modifying treatments for Alzheimer's disease: the sixth snnual mild cognitive impairment symposium,” Alzheimer's and Dementia, vol. 5, no. 1, pp. 66–74, 2009.
[35]
N. Relkin, L. Bettger, D. Tsakanikas, and L. Ravdin, “Three year follow-up on the IVIG for Alzheimer's phase II study,” Alzheimer's & Dementia, vol. 8, no. 4, article 589, 2012.
[36]
S. Craft, L. D. Baker, T. J. Montine et al., “Intranasal insulin therapy for Alzheimer disease and amnestic mild cognitive impairment: a pilot clinical trial,” Archives of Neurology, vol. 69, no. 1, pp. 29–38, 2012.
[37]
A. Venneri, W. J. McGeown, and M. F. Shanks, “Empirical evidence of neuroprotection by dual cholinesterase inhibition in Alzheimer's disease,” Neuroreport, vol. 16, no. 2, pp. 107–110, 2005.
[38]
R. Howard, R. McShane, J. Lindesay et al., “Donepezil and memantine for moderate-to-severe Alzheimer's disease,” The New England Journal of Medicine, vol. 366, no. 10, pp. 893–903, 2012.
[39]
P. Thaipisuttikul and J. E. Galvin, “Use of medical foods and nutritional approaches in the treatment of Alzheimer's disease,” Clinical Practice, vol. 9, no. 2, pp. 199–209, 2012.
[40]
L. Hong, “Translational research in neurology: dementia,” Archives of Neurology, vol. 69, no. 8, pp. 969–977, 2012.
[41]
Q. Wu, W. Xuan, T. Ando et al., “Low-level laser therapy for closed-head traumatic brain injury in mice: effect of different wavelengths,” Lasers in Surgery and Medicine, vol. 44, no. 3, pp. 218–226, 2012.
[42]
W.-P. Hu, J.-J. Wang, C.-L. Yu, C.-C. E. Lan, G.-S. Chen, and H.-S. Yu, “Helium-neon laser irradiation stimulates cell proliferation through photostimulatory effects in mitochondria,” Journal of Investigative Dermatology, vol. 127, no. 8, pp. 2048–2057, 2007.
[43]
A. P. Sommer, J. Bieschke, R. P. Friedrich et al., “670 nm laser light and EGCG complementarily reduce amyloid-β aggregates in human neuroblastoma cells: basis for treatment of alzheimer's disease?” Photomedicine and Laser Surgery, vol. 30, no. 1, pp. 54–60, 2012.
[44]
C. H. Sadowsky and J. E. Galvin, “Guidelines for the management of cognitive and behavioral problems in dementia,” Journal of the American Board of Family Medicine, vol. 25, no. 3, pp. 350–366, 2012.
[45]
National Institute on Aging NIoH, Department of Health and Human Services, Preventing Alzheimer's Disease: What Do We Know?2012.
[46]
M. W. Voss, K. I. Erickson, R. S. Prakash, et al., “Neurobiological markers of exercise-related brain plasticity in older adults,” Brain, Behavior, and Immunity, vol. 28, pp. 90–99, 2013.
[47]
P. Heyn, B. C. Abreu, and K. J. Ottenbacher, “The effects of exercise training on elderly persons with cognitive impairment and dementia: a meta-analysis,” Archives of Physical Medicine and Rehabilitation, vol. 85, no. 10, pp. 1694–1704, 2004.
[48]
N. Scarmeas, Y. Stern, M.-X. Tang, R. Mayeux, and J. A. Luchsinger, “Mediterranean diet and risk for Alzheimer's disease,” Annals of Neurology, vol. 59, no. 6, pp. 912–921, 2006.
[49]
R. S. Wilson, D. A. Bennett, J. L. Bienias et al., “Cognitive activity and incident AD in a population-based sample of older persons,” Neurology, vol. 59, no. 12, pp. 1910–1914, 2002.
[50]
A. Karp, S. Paillard-Borg, H.-X. Wang, M. Silverstein, B. Winblad, and L. Fratiglioni, “Mental, physical and social components in leisure activities equally contribute to decrease dementia risk,” Dementia and Geriatric Cognitive Disorders, vol. 21, no. 2, pp. 65–73, 2006.
