History Of Alzheimer Research Articles

136 Ambulatory Follow-up After Emergency Department Discharge and Association With Outcomes Among Older Adults With Alzheimer’s Disease and Related Dementia

136 Ambulatory Follow-up After Emergency Department Discharge and Association With Outcomes Among Older Adults With Alzheimer’s Disease and Related Dementia

0856 Correcting Sleep/Wake Cycle and Reducing Combativeness in an 84-year-old Patient

Abstract Introduction Sleep disruption is a common occurrence in hospitalized geriatric patients. Such patients frequently arrive at the emergency department for behavioral changes due to delirium, which can often be mistaken for, or compounded by, underlying dementia. Behavioral symptoms may vary, including disinhibition, aggression, distress during care, mood disturbance, and paranoia, affecting approximately 90% of patients. Effectively treating these patients is challenging; antipsychotic use is a commonly implemented treatment in hospitalized settings, but is complicated by adverse side effects and an increased risk of CVA. In this case report, we discuss the use of an antipsychotic, olanzapine, to treat an 84 year old hospitalized patient presenting with sleep disruption and changes in mental status. Report of Cases: An 84 year old gentleman with a history of Alzheimer’s dementia with worsening behavioral changes was admitted for urinary tract infection, humeral fracture secondary to mechanical fall, and increasing aggression toward his caretaker. At home the patient was sleeping during the day and more was active and combative at night. While hospitalized, he had become aggressive with hospital staff due to his distress and was minimally oriented at baseline. We trialed the patient on olanzapine 5mg at night to facilitate sleep and reduce his aggression, in addition to environmental changes to reorient day and night. After a few days of this treatment, this patient was much more pleasant and oriented, able to hold conversation, and no longer aggressive. His initial disposition was to be transferred to a memory care facility, given increasing safety concerns expressed by the caretaker. However, following these changes, he was able to return home in the comfort of his family and caretaker. Conclusion Antipsychotic use in the elderly for sleep disruption and behavioral disturbances is heavily debated, though there may be some benefit to their use. The CATIE-AD trial and a Cochrane Review suggest Olanzapine may reduce aggression, particularly in Alzheimer’s disease, and has the added benefit of sedation which aids in establishing sleep cycles. However, many patients discontinue antipsychotic treatment due to side effects and routine use is discouraged. When in use, regular monitoring should take place to evaluate for side effects associated with pharmacotherapy and continued therapeutic benefit should be reassessed. Support (If Any)

The offspring of mothers harboring APP/PS1 mutations presents early changes in memory and brain metabolism.

Previous studies suggested that individuals with a maternal history of Alzheimer's Disease (AD) are at higher risk of developing AD than individuals with a paternal history of AD. One could suggest that intra-uterine interactions might be responsible for elevating this risk. In this context, AD rodent models are highly suited for improving our understanding of this matter since animals reach adulthood in a few months. Here, we aimed at investigating changes in memory-related processes and brain metabolism on the offspring born to transgenic mothers harboring human APP/PS1 mutations. We hypothesized that offspring born to AD-transgenic mothers will present early memory and brain glucose metabolism changes. Rats born to F344-AD (Tg-AD) mothers and wild-type fathers (WT), the maternal AD group, and rats born to WT mothers and Tg-AD fathers, the paternal AD group, were evaluated in two different time-points: ∼5.5, and ∼9.5 months. To assess spatial working memory, spontaneous alternation behavior was evaluated in the Y-maze test. Furthermore, micro-PET [18 F]FDG was used to assess brain glucose metabolism (SUVr normalization, pons as reference region). Y-maze test demonstrated that rats born to transgenic mothers presented memory disturbances, indexed by spontaneous alternation, at ∼5.5 months (p = 0.0028, Figure 1A) and ∼9.5 months (p = 0.0062, Figure 1B), while rats born to WT mothers and Tg-AD fathers exhibited a decline in spontaneous alternation only at ∼9.5 months (p = 0.0181, Figure 1B). No changes were found in brain glucose metabolism at ∼5.5 months for both groups. However, rats born to AD-Tg mothers present brain glucose hypermetabolism at ∼9,5 months. Our findings demonstrate that rats born to AD-Tg mothers harboring APP/PS1 mutations present cognitive decline and brain glucose metabolism abnormalities earlier than those born to WT mothers. Further studies are needed to understand the biological basis behind this phenomenon.

Motor neuron disease beginning with frontotemporal dementia: clinical features and progression

Objective: To study disease characteristics, progression and outcome in a group of motor neuron disease (MND) patients beginning with frontotemporal dementia (FTD) by comparing them with patients with the typical motor-onset. Methods: 849 patients recruited from tertiary centers were studied according to FTD-onset and motor-onset. We studied clinical data, functional decline and survival. Results: Twenty six patients (3.1%) had FTD-onset of whom seven (26.9%) had coincident motor dysfunction. In those with isolated FTD-onset, motor symptoms developed after a median of 12 months (IQR: 4–18). FTD-onset patients were older at presentation; the bulbar-region was more frequently first affected than in the motor-onset group; there was a predominant upper motor neuron (UMN) phenotype; fasciculations were less common than in motor onset disease but facial and upper limb apraxia was more frequent; as well as ALS and FTD familial history. No differences were observed for gender, frequency of C9orf72 hexanucleotide repeat expansion, family history of Alzheimer’s and Parkinson’s diseases, median delay from motor symptoms to diagnosis, median ALSFRS-R rate of change, handedness, emotional lability, depression, weight loss, resting tremor, bradykinesia, sensory changes or neuropathy. Clinical and demographic features were similar between FTD-onset patients developing bulbar MND and bulbar-onset ALS patients. Once bulbar symptoms manifested functional progression and survival were similar to those of bulbar-onset ALS patients. Conclusions: MND patients with FTD-onset have a distinctive phenotype characterized by predominant UMN presentation and rapid progression to bulbar involvement. The main factor impacting functional decline and survival is the onset of bulbar dysfunction.

Two separate, large cohorts reveal potential modifiers of age-associated variation in visual reaction time performance

To identify potential factors influencing age-related cognitive decline and disease, we created MindCrowd. MindCrowd is a cross-sectional web-based assessment of simple visual (sv) reaction time (RT) and paired-associate learning (PAL). svRT and PAL results were combined with 22 survey questions. Analysis of svRT revealed education and stroke as potential modifiers of changes in processing speed and memory from younger to older ages (ntotal = 75,666, nwomen = 47,700, nmen = 27,966; ages 18–85 years old, mean (M)Age = 46.54, standard deviation (SD)Age = 18.40). To complement this work, we evaluated complex visual recognition reaction time (cvrRT) in the UK Biobank (ntotal = 158,249 nwomen = 89,333 nmen = 68,916; ages 40–70 years old, MAge = 55.81, SDAge = 7.72). Similarities between the UK Biobank and MindCrowd were assessed using a subset of MindCrowd (UKBb MindCrowd) selected to mirror the UK Biobank demographics (ntotal = 39,795, nwomen = 29,640, nmen = 10,155; ages 40–70 years old, MAge = 56.59, SDAge = 8.16). An identical linear model (LM) was used to assess both cohorts. Analyses revealed similarities between MindCrowd and the UK Biobank across most results. Divergent findings from the UK Biobank included (1) a first-degree family history of Alzheimer’s disease (FHAD) was associated with longer cvrRT. (2) Men with the least education were associated with longer cvrRTs comparable to women across all educational attainment levels. Divergent findings from UKBb MindCrowd included more education being associated with shorter svRTs and a history of smoking with longer svRTs from younger to older ages.

Manifestation of cognitive impairments after a prior coronavirus infection COVID-19 in a patient with ApoE ε4 genotype

Nowadays, the novel coronavirus infection (COVID-19) pandemic is one of the most important global health problems. There is increasing evidence that COVID-19 affects central and peripheral nervous system as well. The paper presents a clinical case of a 47 old patient with the ApoE ε4 haplotype and family history of Alzheimer’s disease who developed cognitive impairment after acute COVID-19. Before the infection the patient has no cognitive complaints and preserved everyday activity. After novel coronavirus infection, which was observed in mild form, the patient had started to complain on constant excessive forgetfulness. Neuropsychological assessment confirmed the presence of pre-mild cognitive impairment of predominantly single domain amnestic type. However, brain MRI showed only subtle periventricular white matter changes usually attributed to small vessel disease. Memory complaints were observed for 3 months of follow up despite intensive cognitive training, optimization of lifestyle and therapy with choline alphoscerate. Probable links between coronavirus infectious and cognitive impairment manifestation are discussed. There is data that ApoE ε4 haplotype is associated with increase of microglia mediated neuro-inflammation and it can be significant for accelerating of progression of neurodegenerative diseases after COVID-19. Further follow up of the patient is necessary for determination of nosological diagnosis explaining manifested predominantly amnestic type pre-mild cognitive impairment.

The complexity of Alzheimer's disease: an evolving puzzle.

The history of Alzheimer's disease (AD) started in 1907, but we needed to wait until the end of the century to identify the components of pathological hallmarks and genetic subtypes and to formulate the first pathogenic hypothesis. Thanks to biomarkers and new technologies, the concept of AD then rapidly changed from a static view of an amnestic dementia of the presenium to a biological entity that could be clinically manifested as normal cognition or dementia of different types. What is clearly emerging from studies is that AD is heterogeneous in each aspect, such as amyloid composition, tau distribution, relation between amyloid and tau, clinical symptoms, and genetic background, and thus it is probably impossible to explain AD with a single pathological process. The scientific approach to AD suffers from chronological mismatches between clinical, pathological, and technological data, causing difficulty in conceiving diagnostic gold standards and in creating models for drug discovery and screening. A recent mathematical computer-based approach offers the opportunity to study AD in real life and to provide a new point of view and the final missing pieces of the AD puzzle.

History of Alzheimer’s disease (AD) from the perspective of leading research theories

Alzheimer’s disease is the leading cause of cognitive deterioration. Alois Alzheimer described it for the first time in 1907. In the last five decades, there were emerging numerous hypotheses about the pathomechanism of this condition. The first one, the cholinergic hypothesis resulted in important antidementia medications. Amyloid cascade theory set the direction for many years in Alzheimer research. Currently, it also contributed to the licencing of a novel pharmaceutical Aducanumab. Additionally, the latest hypotheses shed light on the new aspects of the pathology of dementia. This study emphasizes the historical landmarks of Alzheimer’s research and reveals their interactions as well.

S3402 Toxic Megacolon Disguised as Fecal Impaction

INTRODUCTION: Clostridium difficile colitis is a disease rising in incidence over the years with increasing mortality, especially with complications such as toxic megacolon which can affect 0.4-3% of cases. This case report shows the need to keep a high index of suspicion, especially with atypical presentations to help reduce the mortality rate. CASE DESCRIPTION/METHODS: A 77 year old male with a history of Alzheimer’s Disease had a prolonged hospital course after admission for a fracture requiring surgery after a ground level fall. One and a half month into the hospital course, the patient was diagnosed with suppurative parotitis with associated leukocytosis up to 33,000. He was begun on empiric antibiotics which were eventually de-escalated to daptomycin & zosyn with subsequent resolution in leukocytosis one week into the planned two week antibiotic course. On the last day of antibiotics, patient was noted to having uptrending leukocytosis up to 24,000 despite staying afebrile, vitally stable, and with no symptoms reported including abdominal pain or diarrhea. His antibiotics were escalated with continued worsening of leukocytosis up to 42K. At that time, patient began complaining of abdominal pain with subsequent CT scan noting significant colonic stool with possible fecal impaction. Given the leukocytosis and imaging, he was evaluated by surgery due to concern of possible perforation. Surgery had low concern for perforation and recommended aggressive bowel regimen after which patient began stooling frequently. Shortly thereafter, he became hypotensive requiring vasopressor support. He subsequently tested positive for clostridium difficile and was begun on treatment for fulminant C. difficile with toxic megacolon. However, the patient died a few days later. DISCUSSION: C. difficile colitis and its complications, including toxic megacolon, are important to recognize early to ensure prompt treatment of this potentially fatal disease. There are the known expected signs and symptoms including abdominal pain, diarrhea, fevers, lactic acidosis, elevated creatinine, significant leukocytosis. However, it is important to not be confounded by unusual presentations such as in this case. Other rare case reports include Burke et al. who describe a patient with toxic megacolon from C. difficile without diarrhea. Malkan et al. also describe a case series of uncommon presentations though most are noted to have known risk factors including prolonged hospital or antibiotic courses.

S1788 A Rare Case of an Adult Ingesting a Disk Battery With Impaction in the Lower Gastrointestinal Tract

INTRODUCTION: Disk battery ingestion is commonly seen in the pediatric population and rarely in adults. There are no guidelines on how to manage these in the lower GI tract. We present a rare case of a disk battery impacted in the lower GI tract in an adult patient. CASE DESCRIPTION/METHODS: A 96 year-old-male with a history of Alzheimer's disease presented for concerns that he had ingested a battery. Physical examination was remarkable for altered mental status. Abdominal x-ray revealed a coin like lesion in the RLQ (Figure 1). CT scan of abdomen and pelvis confirmed a radiopaque object at the ileo-cecal junction (Figure 2), believed to be a disk battery. Colorectal surgery was consulted for colonoscopic removal with possible surgical conversion but the health care proxy refused and instead opted for conservative management/non-invasive measures. Multiple trials of bowel regimens including polyethylene glycol were initiated to induce dislodgement without success as serial abdominal x-rays revealed that the battery remained impacted in the same location (Figure 3). At this point, the health-care proxy opted for discharge to a nursing home with supportive measures. DISCUSSION: Current guidelines recommend removal if the battery is lodged in the esophagus, if the battery is in the stomach and is less than 2 cm in size, conservative management is advised as it will likely pass through the GI tract. Progression should be followed with serial abdominal x-rays every 3 days and if impaction is suspected, the battery should be removed. Currently no guidelines on impacted objects in the lower GI tract exist, but we hypothesize that if the object is less than 2 cm, it will likely be evacuated. The major risk of foreign body ingestion is perforation. This occurs from penetration of the mucosa or via pressure injury from impaction. Lithium-Ion batteries have a high risk of electrical thermal injury leading to liquefaction necrosis and Nickel-Cadmium batteries can cause caustic injuries. Regardless, they both carry an increased risk of perforation, especially with impaction. In our case, the patient was given multiple bowel regimens to induce dislodgement. Although serial imaging did not show progression of the battery, to our knowledge, there are no other cases in which bowel regimens have been used for managing lower GI tract foreign objects and this creates a need for further investigation.Figure 1.: Abdominal X-Ray showing radiopaque object in RLQ (Red Arrow).Figure 2.: CT Abdomen and Pelvis showing radiopaque object at the Ileocecal Valve (Red Arrow).Figure 3.: Abdominal X-Ray showing unchanged location of radiopaque object in RLQ (Red Arrow).

Hypothermia induced by quetiapine

An 89-year-old woman was brought to the emergency department, responding only to pain (GCS 6), with a rectal temperature of 28.5°C, hypotension (68/40), bradycardia (35/min) and bradypnoea. The remainder of...

No apparent effect of naproxen onCSFmarkers of innate immune activation

We studied 78 participants having a parental or multiple‐sibling history of Alzheimer’s disease (AD) in a two‐year randomized placebo‐controlled trial of naproxen 220 mg b.i.d. for mitigation of early AD pathogenesis. Naproxen was detected in cerebrospinal fluid at concentrations ~100 times lower than in plasma, but produced negligible change in immune markers. The repeated lack of benefit in AD prevention trials using naproxen and related drugs may reflect limited CNS permeability, lack of expected drug effects, or both. These findings suggest reconsideration of implications from results of AD prevention trials using anti‐inflammatory drugs.

Correlation Between Accumulation of Alzheimer's Disease Markers in Brain and Retina of Individuals with Late Stage of the Disease

This study was aimed to determine if there is a correlation between accumulation of various Alzheimer's disease (AD) markers in the brain and retina of individuals in the late stages of the disease. Characterizing the distribution and accumulation of these markers in the retina and brain may be important for early diagnosis of neurodegenerative diseases such as AD.We examined total tau and phosphorylated tau protein accumulations in different areas of the brain and in retinal tissues from aged individuals with AD in order to compare the intensity and sensitivity of these biomarkers.Tissues from the hippocampus and temporal lobe of four different cadavers were analyzed. Two cadavers had diagnosed Alzheimer's disease, and two cadavers served as a non‐AD control. We utilized cryosectioning to prepare tissue sections for immunostaining. Tissues obtained from individuals without a history of Alzheimer's disease or other types of dementia were used as negative controls. Detection of tau was performed using a primary antibody against human tau proteins and amyloid‐b, followed by a universal secondary antibody.Although the staining for AD markers was greater than controls for both brain tissues, the density was higher in the hippocampus than in the temporal lobe. The density of the total tau (TT) was greater than that of phosphorylated tau (PT181) in both the hippocampus and temporal lobe. We also found this to be the case in the brain tissues of a control, indicating that total tau may be a more sensitive biomarker than phosphorylated tau.These data demonstrate that total tau may be a stronger biomarker than phosphorylated tau in quantifying protein accumulations in the brains of Alzheimer's disease cadavers. This raises the intriguing possibility that there may be more sensitive biomarkers that can better predict the course of neurodegenerative diseases such as AD. Thus, future studies will concentrate on the accumulation of tau in the brain and retina of individuals during the earlier stages of Alzheimer's disease, as well as the sensitivity and accuracy of different biomarkers.Support or Funding InformationTouro University Nevada intramural grant.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Diet as a Risk Factor for Cognitive Decline in African Americans and Caucasians with a Parental History of Alzheimer\u2019s Disease: A Cross-Sectional Pilot Study Dietary Patterns

BackgroundAfrican Americans (AA) are more likely to develop Alzheimer’s disease (AD) than Caucasians (CC). Dietary modification may have the potential to reduce the risk of developing AD.ObjectiveThe objective of this study is to investigate the relationship between Southern and Prudent diet patterns and cognitive performance in individuals at risk for developing AD.DesignCross-sectional observational study.ParticipantsSixty-six cognitively normal AA and CC individuals aged 46–77 years with a parental history of AD were enrolled.MeasurementsParticipants completed a Food Frequency questionnaire, cognitive function testing, which consisted of 8 neuropsychological tests, and cardiovascular risk factor assessments, including evaluation of microvascular and macrovascular function and ambulatory blood pressure monitoring.ResultsResults revealed a relationship between the Southern diet and worse cognitive performance among AAs. AAs who consumed pies, mashed potatoes, tea, and sugar drinks showed worse cognitive performance (p<0.05) compared with CCs. In addition, gravy (p=0.06) and cooking oil/fat (p=0.06) showed negative trends with cognitive performance in AAs. In both CC and AA adults, greater adherence to a Prudent dietary pattern was associated with better cognitive outcomes. Cardiovascular results show that participants are overall healthy. AAs and CCs did not differ on any vascular measure including BP, arterial stiffness and endothelial function.ConclusionResearch shows that dietary factors can associate with cognitive outcomes. This preliminary crosssectional study suggests that foods characteristic of the Southern and Prudent diets may have differential effects on cognitive function in middle-aged individuals at high risk for AD. Results suggest that diet could be a non-pharmaceutical tool to reduce cognitive decline in racially diverse populations. It is possible that the increased prevalence of AD in AA could be partially reduced via diet modification.

Terahertz Imaging and Electromagnetic Model of Axon Demyelination in Alzheimer's Disease

We investigate the utility of terahertz (THz) spectroscopy in identifying Alzheimer's disease in human brain tissue. Using reflection-mode time-domain THz spectroscopy, two-dimensional images of formalin-fixed and paraffin-embedded tissue samples of the hippocampus area were recorded in the 60 GHz-2 THz band. The THz images were compared with microscopic images of the same samples after hematoxylin and eosin staining. We demonstrate that the THz reflection spectra, particularly from white matter, reveal detectable differences between postmortem brain tissues exhibiting Alzheimer's disease and normal controls. The THz reflectivity of white matter areas was on average 4.2% higher than that of gray matter regions in tissue samples with known Alzheimer's history, whereas for normal control samples the contrast was only 2%. Additional studies further enhance this hypothesis, and the demyelination of white matter in Alzheimer's tissues suggests a possible cause for the differences in the THz reflection spectra. We also compare the THz response of the tissues with conventional Luxol-fast blue staining to demonstrate the correlation between the two methods for predicting demyelination. In addition, we present a simplified electromagnetic model of white matter axons exhibiting various degrees of demyelination to further support this hypothesis through full-wave electromagnetic simulations. This study offers, for the first time, proof of concept for the feasibility of detecting Alzheimer's disease using THz spectroscopy on ex vivo samples.

Professor Alois Alzheimer (1864–1915): Lest we forget

December 19th 2015 marks the centennial anniversary of the death of the great Bavarian psychiatrist and neuropathologist, Alois Alzheimer (1864–1915), a man immortalised by the still incurable dementing process described by him in 1906 and firmly established in his name. Notwithstanding the great wealth of research into the history of Alzheimer’s disease and legacy, the life of this exemplary clinician remains less than widely appreciated today, and it is the purpose of this brief reminiscence to retell the story of the pioneering neuropsychiatrist in this centenary year of his passing.

24. Sensorimotor cortex excitability and connectivity in Alzheimer’s disease: An EEG-TMS co-registration study

Several experimental studies have shown that, nevertheless motor symptoms are late events in the natural history of Alzheimer’s disease (AD), neuropathological progression in the motor cortex parallels that in other brain cortices generally considered more specific targets of the aggression. In the last years we have clearly demonstrated that motor cortex excitability is enhanced in AD since the early stages of the disease and this is probably related to its severity and progression. To further investigate, for the first time without peripheral or attentional confounding effects, the neurophysiological hallmarks of motor cortex functionality in AD we used here transcranial magnetic stimulation (TMS) combined with electroencephalography (EEG). We then demonstrated that in mild AD, despite the lack of clinical manifestations, the sensorimotor system is strongly hyper-excitable and its connectivity is deeply rearranged with the recruitment of additional neural sources, the activation of reverberant circuits and their integration in the distributed excitatory network subtending sensorimotor functions.

History of Alzheimer's Disease.

As modern society ages rapidly, the number of people with dementia is sharply increasing. Direct medical costs and indirect social costs for dementia patients are also increasing exponentially. However, the lack of social awareness about dementia results in difficulties to dementia patients and their families. So, understanding dementia is the first step to remove or reduce the stigma of dementia patients and promote the health of our community. Alzheimer's disease is the most common form of dementia. The term, ‘Alzheimer's disease’ has been used for over 100 years since first used in 1910. With the remarkable growth of science and medical technologies, the techniques for diagnosis and treatment of dementia have also improved. Although the effects of the current symptomatic therapy are still limited, dramatic improvement is expected in the future through the continued research on disease modifying strategies at the earlier stage of disease. It is important to look at the past to understand the present and obtain an insight into the future. In this article, we review the etymology and history of dementia and previous modes of recognizing dementia. We also review the historical developments leading to the terminology of Alzheimer's disease.

Acquired Localized Hypertrichosis Induced by Rivastigmine.

Hypertrichosis is the excessive hair growth in any area of the skin surface. Acquired localized hypertrichosis may be secondary to multiple causes and there is a secondary form due to several drugs, which is usually reversible with discontinuation of the causative agent. Rivastigmine is a reversible and competitive inhibitor of acetylcholinesterase and butyrylcholinesterase used for symptomatic treatment of Alzheimer dementia and Parkinson's disease. It has an adequate safety profile and cutaneous side effects are unusual. Irritant contact dermatitis, allergic dermatitis, baboon syndrome, and cutaneous rash due to rivastigmine have been reported. We report on a Caucasian 80-year-old male with personal history of Alzheimer's disease. The patient started therapy with oral rivastigmine one month prior to clinical presentation of localized hypertrichosis on both forearms. Norgalanthamine has been shown to promote hair growth activity via the proliferation of dermal papilla. Acetylcholinesterase inhibitors can induce hair growth.

Apolipoprotein E genotyping and questionnaire-based assessment of lifestyle risk factors in dyslipidemic patients with a family history of Alzheimer's disease: test development for clinical application.

The cholesterol-raising properties of the apolipoprotein E (APOE) epsilon-4 (ε-4) allele has been validated in the South African population. Mounting evidence supports the added value of APOE genotyping for the evaluation of cardiovascular risk in dyslipidemic patients beyond its established role in the diagnosis of late-onset Alzheimer's disease (AD). The aim of this study was to determine the potential benefits of combining AD family history with questionnaire-based lifestyle assessment to facilitate the clinical interpretation of APOE genotyping results. A total of 580 unrelated South African individuals prospectively enrolled in a chronic disease screening program incorporating a genetic component (2010-2015) was selected for inclusion in this study based on the presence (75) or absence (505) of AD family history. Biochemical assessment of their lipid profiles was performed according to standard laboratory protocols. All study participants were genotyped for the APOE ε-2/ε-3/ε-4 alleles using allele-specific TaqMan real-time polymerase chain reaction technology. In patients without a family history of AD, APOE genotype modified the relationship between alcohol intake and body mass index (p = 0.026), with a significant positive correlation noted between these parameters being limited to ε-4 allele carriers. APOE genotype also modified the association between alcohol intake and total serum cholesterol in patients with a positive family history of AD (p = 0.026). We demonstrated the benefits of a questionnaire-based approach for assessment of lifestyle risk factors to facilitate clinical interpretation of APOE genotyping results for targeted intervention in a genetic subgroup of dyslipidemic patients at increased risk for AD.