Psychology Alzheimer’s Disease
by
Chad Hales, Allan Levey
  • LAST REVIEWED: 20 April 2017
  • LAST MODIFIED: 26 July 2017
  • DOI: 10.1093/obo/9780199828340-0004

Introduction

Memory is a conserved cognitive task that has persisted for thousands of years. Early utilization may have assisted in returning to the best hunting ground or fruit grove, while more-current utilization, although similar concerning basic needs, also imprints sorrows, joyous occasions, and even a foundation for one’s trade. Unfortunately, aging increases the risk for losing memory in addition to other cognitive functions. The most common affliction that can cause this cognitive decline is Alzheimer’s disease (AD). AD is an indolent neurodegenerative disorder that impairs cognitive, occupational, and social functions. AD affects 10–15 percent of the population over age sixty-five, with some estimates of 40–50 percent affected if over eighty-five years of age. More than five million Americans are currently affected, with future projections suggesting that ten million to fifteen million Americans will be afflicted by 2050. The economic impact is significant, nearing $150 billion annually; however, perhaps even more troubling is the constant psychological bombardment endured both by families and patients. At the turn of the 20th century, Alois Alzheimer, a psychiatrist and neuropathologist, described the seminal case. Auguste Deter (Alzheimer referred to her as a patient as Auguste D) experienced progressive short-term memory impairment and behavioral changes. Following her death, Alzheimer discovered abnormal protein collections, or plaques, in addition to neurofibrillary tangles in her brain, and he concluded that these findings were associated with the cognitive decline. These structures are identified in postmortem cases today, and they are used to confirm clinical diagnosis. Several years following Alzheimer’s revelations, his name became used as a descriptor to identify similar cases of AD. The diagnosis of AD is largely based on clinical impression; however, measuring levels of amyloid and tau in cerebrospinal fluid as well as positron emission tomography (PET) imaging of amyloid can provide additional support for the diagnosis. Postmortem brain neuropathological analysis is still the gold standard for confirming a diagnosis of AD.” Patients typically present with memory complaints, but they may also experience language, visuospatial, judgement, behavior, and mood disturbances. Patients may lack insight into their deficits and are often brought for evaluation by concerned family members. Patients decline gradually over five to ten years and typically succumb to a secondary illness such as pneumonia. More than 75,000 articles, books, and reference materials have been published on AD since Alzheimer’s time. Technological advances in science, coupled with ever-increasing life expectancy and a better understanding of abnormal cognition in the elderly, have likely spurred the more recent urgency. Although the hope is that therapeutics currently in clinical trials will alter the course of AD, more work is needed to assimilate the vast quantity of knowledge. In addition, further research at the cellular level is essential to better understand disease pathogenesis.

General Overviews

Many online resources are available in addition to other published works outlining aspects of AD from historical perspectives (Talbott 1969) and basic research concepts (Querfurth and LaFerla 2010) to clinical presentation, diagnosis, and treatment (Alzheimer’s Disease and Alzheimer’s Association websites). Hebert, et al. 2003 and Reitz, et al. 2011 discuss AD epidemiology, and Miller and Boeve 2011 describes other dementia subtypes in addition to AD.

  • Alzheimer’s Association.

    E-mail Citation »

    This website has information for patients, caregivers, professionals, and researchers. The education page has multiple documents available for download, addressing many of the frequently asked questions about AD symptoms, treatment, and disease course.

  • Alzheimer’s Disease. National Institutes of Health.

    E-mail Citation »

    Provides a general overview, with a section describing symptoms at various stages of AD; located at the PubMed Health consumer website produced by the National Institutes of Health.

  • Hebert, L. E., P. A. Scherr, J. L. Bienias, D. A. Bennett, and D. A. Evans. 2003. Alzheimer disease in the US population: Prevalence estimates using the 2000 census. Archives of Neurology 60.8: 1119–1122.

    DOI: 10.1001/archneur.60.8.1119E-mail Citation »

    Provides epidemiological data and projections for new cases.

  • Miller, B., and B. Boeve. 2011. The behavioral neurology of dementia. New York: Cambridge Univ. Press.

    E-mail Citation »

    This textbook provides an excellent summary of the neurodegenerative dementias, including an entire chapter devoted to AD. This text is helpful when trying to compare and contrast characteristics of various disorders that cause cognitive decline.

  • Querfurth, H. W., and F. M. LaFerla. 2010. Mechanisms of disease: Alzheimer’s disease. New England Journal of Medicine 362.4: 329–344.

    DOI: 10.1056/NEJMra0909142E-mail Citation »

    Review discussing multiple cellular changes that could be involved with AD pathogenesis, on the basis of current research.

  • Reitz, C., C. Brayne, and R. Mayeux. 2011. Epidemiology of Alzheimer disease. Nature Reviews Neurology 7.3: 137–152.

    DOI: 10.1038/nrneurol.2011.2E-mail Citation »

    Up-to-date epidemiological data and projections for AD across the globe.

  • Talbott, J. H. 1969. Alois Alzheimer (1864–1915) neurohistopathologist. Journal of the American Medical Association 208.6: 1017–1018.

    DOI: 10.1001/jama.208.6.1017E-mail Citation »

    A brief editorial providing historical commentary on Alois Alzheimer, as well as selected translations of his original presentation on Auguste D. Citations for those original works are included in the article.

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