Case Study 7 Chapter 18 Disorders Of Thought, Emotion, And M

Case Study7 Chapter 18 Disorders Of Thought Emotion And Memorynor

Analyze a clinical case involving an elderly patient, Ella, who exhibits signs of memory decline, personality changes, and impulsive behaviors. Address the key questions regarding dementia, particularly Alzheimer disease, including its diagnostic criteria, brain pathology, and affected brain regions. Discuss the macroscopic and microscopic features characteristic of Alzheimer disease and explain the neurological mechanisms underlying specific behavioral symptoms, such as forgetfulness of recent events, which indicate damage to particular brain structures.

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Alzheimer disease (AD) is a progressive neurodegenerative disorder characterized primarily by a decline in cognitive functions, particularly memory, reasoning, and alterations in personality. It is classified as a dementia, a broad term describing a set of symptoms caused by various brain diseases that result in the decline of intellectual and social abilities severe enough to interfere with daily functioning. The diagnosis of Alzheimer disease is based on a "diagnosis of exclusion," meaning that clinicians rule out other potential causes of dementia, such as vascular disorders, infections, metabolic imbalances, and other neurodegenerative conditions, before confirming AD. This classification underscores the complexity of AD diagnosis, which relies strongly on clinical assessments supported by neuroimaging and, in some cases, postmortem histopathological examination.

The macroscopic features of the brain in Alzheimer disease mainly include cerebral atrophy, particularly noticeable in the cerebral cortex, hippocampus, and entorhinal cortex—areas crucial for memory formation. The atrophy results from widespread neuronal loss, loss of synapses, and spongiform degeneration. The ventricles are often enlarged, a consequence of cortical tissue loss, and the sulci are widened. Microscopically, AD is characterized by the presence of amyloid plaques composed of beta-amyloid peptides and neurofibrillary tangles made of hyperphosphorylated tau protein. These pathological hallmarks are distributed preferentially in regions associated with memory and cognition, with plaques frequently observed in the cortical regions and tangles particularly abundant in the hippocampus, entorhinal cortex, and other limbic structures. The accumulation of these abnormal proteins disrupts neural networks and leads to neuronal death, which underpins the progressive cognitive decline evident in patients.

In Ella’s case, her forgetfulness of recent events and her difficulty in recognizing her belongings, such as her slippers, suggest impairment in memory consolidation, an underlying function of the hippocampus. The hippocampus is part of the medial temporal lobe and plays a vital role in forming new memories. Damage to this region results in an inability to transfer new information from short-term to long-term memory—a hallmark of early Alzheimer disease. Additionally, her behavioral changes and withdrawal may reflect degeneration in other brain regions such as the prefrontal cortex, which is involved in personality, decision-making, and social behaviors.

The specific behavioral symptom described—Ella forgetting the slippers shortly after receiving them—indicates a compromise in the hippocampus's function. Pathophysiologically, the accumulation of neurofibrillary tangles and amyloid plaques in the hippocampal neurons disrupts intracellular and extracellular functioning, leading to neuronal death. This results in the impairment of synaptic transmission, especially in the circuits responsible for encoding and storing new memories. As these neurons degenerate, the neural network sustaining memory consolidation deteriorates, causing the failure to retain recent events or information. The progression of tau pathology disrupts axonal transport and induces cytoskeletal destabilization, further promoting neuronal loss. Consequently, Ella’s inability to remember the slippers reflects underlying hippocampal damage typical in the early stages of Alzheimer disease.

In summary, Alzheimer disease is a complex disorder with characteristic macroscopic and microscopic changes in the brain. Its diagnosis relies on excluding other causes and identifying key pathological features. The hippocampus’s vulnerability to neurodegeneration explains many of the clinical features seen in Ella’s case, emphasizing the critical role of this brain region in memory formation and the devastating effects of Alzheimer pathology when it is compromised.

References

• Braak, H., & Braak, E. (1991). Neuropathological stageing of Alzheimer-related changes. Acta Neuropathologica, 82(4), 239–259.
• Hyman, B. T., et al. (2012). National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease. Alzheimer's & Dementia, 8(1), 1-13.
• Morris, J. C. (2005). Pathologic correlates of nondemented aging, mild cognitive impairment, and early-stage Alzheimer disease. Journal of Neural Transmission. Supplementum, (69), 163–170.
• Ritchie, C. W., et al. (2017). Diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging and the Alzheimer's Association workgroup. Alzheimer's & Dementia, 13(3), 235-262.
• Serrano-Pozo, A., et al. (2011). Neuropathological alterations in Alzheimer disease. Cold Spring Harbor Perspectives in Medicine, 1(1), a006189.
• Selkoe, D. J., & Hardy, J. (2016). The amyloid hypothesis of Alzheimer’s disease at 25 years. EMBO Molecular Medicine, 8(6), 595-608.
• Jack, C. R., et al. (2013). Alzheimer’s disease neuroimaging initiative (ADNI): MRI methods. Alzheimer's & Dementia, 9(4), e42–e55.
• Price, J. L., et al. (2012). Neuropathology of Alzheimer’s disease: a critical review. Alzheimer's & Dementia, 8(4), 261–272.
• Gordon, M. F., et al. (2002). The neuropathology of Alzheimer’s disease: a review. Journal of Clinical Pathology, 55(4), 255–262.
• Cummings, J. L. (2004). Alzheimer’s disease: Advances in diagnosis and treatment. Journal of Geriatric Psychiatry and Neurology, 17(3), 159–160.