Rotation #1: Journal Article Summary
Title: “Memory Loss in Alzheimer’s Disease” by Holgan Jahn, MD
Alzheimer’s is one of the most common causes of dementia and is often on top of a provider’s differential when a patient comes in complaining of memory loss. This article focuses on the relation between memory loss and Alzheimer’s and how this disease affects short term memory, long term memory, and how other outside factors affect the severity of this disease.
Earlier onset of dementia can become evident in patients as early as in their forties; genetics plays a strong role in such cases. However, this is a rare case, occurring in 1% of all patients with AD. More commonly, onset of dementia begins around age 65. According to the article, the most common genetic risk factor for late-onset Alzheimer’s is the apolipoprotein E4 genotype, which increases the risk for AD by 4-10x.
Patients with AD typically have amyloid plaques or neurofibrillary tangles found in their brain autopsies. These lesions first appear in poorly myelinated limbic neurons in areas related to memory and learning such as the hippocampus—thus affecting short-term memory. When assessing patients, the effect of these lesions on the hippocampus directly correlated with performance in memory tasks and a decline of performance in the Boston Naming Test Mini-Mental Status Exam.
Patients with AD may come to the clinician initially complaining of cognitive decline which further develops into cognitive impairment, which progresses to dementia. These deficits in attention and working memory often impair the patient’s ability to plan, problem-solve, and impairs goal-directed behavior.
The impact AD had on memory was tested in a study where patients with subjective memory underwent an episodic memory task where they had to match face to professions (including processes such as encoding, recall, and recognition) as well as a working memory task all while the patient was observed using a functional MRI. The result was that there was a reduction in the right hippocampal activation during episodic recall, further proving the connection between memory loss and the way AD affects the brain.
Moreover, sleep disturbances have also been associated with AD, which also affects a patient’s cognitive state. These sleep disturbances include daytime napping and insomnia, and they affect 25-40% of patients with mild-moderate AD. Sleep changes in patients who are already experiencing mild cognitive impairment, can experience worsened memory deficits due to interference to sleep-dependent memory consolidation.
Using this information, it would be useful as future clinicians to notice these “red flags” that may indicate possible early development of AD in our patients. We can then hope to implement therapeutic interventions which can prolong the cognitive impairment process.
