Alzheimer's Research

Alzheimer’s disease is the most common cause of dementia, affecting an estimated 35 million people worldwide. Despite the wide impact of this disease, little is known as a definitive diagnosis can only occur post-mortem. Annually, millions of funding dollars are allocated for preclinical research to further understand Alzheimer’s disease with animal models being at the forefront of this research.

Risk Factors

  • Age
  • Genetics
  • Hypertension
  • Atherosclerosis
  • Diabetes
  • Tobacco Use
  • Mild to Severe Brain Injury


Commonly Used Species in Alzheimer's Research

Mouse Silhouette




non-human primate

Nonhuman Primates



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This paper provides researchers with the following information
a) a summary of the most commonly researched neurological disease and psychiatric disorders
b) observations regarding in vivo physiologic endpoints of interest
c) the products used to collect these endpoints.

CNS, Neuroscience, Preclinical Neuroscience, Animal models of neuroscience, CNS animal models

DSI Solutions are Trusted by Alzheimer's Researchers to Get Meaningful Answers Out of Their Studies

Because of the high impact Alzheimer's disease (AD) has on the aging population and how little is known about the disease, animal models remain critical in driving research success. Many symptoms of Alzheimer's present in organs systems outside of the CNS, making additional endpoints and holistic approaches valuable to researchers studying Alzheimer's and other neurodegenerative diseases. DSI provides a wide range of validated physiological monitoring solutions to fit researcher needs during many different stages of their studies.

Click on a research area below to learn more about endpoints of interest collected in Alzheimer's studies.


Electroencephalogram (EEG) has been used as a tool for diagnosing Alzheimer’s Disease (AD) in clinical populations for several decades. A criticism of historical techniques points to the lack of specificity and difficulty quantifying the EEG data. New data analysis techniques overcome these problems and offer an exciting area of research for both clinical and pre-clinical scientists. Indicators of AD in EEG include
shift of the power spectrum to lower frequencies,1 decrease in coherence of fast rhythms, and EEG complexity changes

Common Endpoints

Resting-state EEG

Power Spectrum Shifts

Reduced Complexity

Decrease in Synchronization

Neuromodulatory Deficits

Event-related EEG

Google Scholar Indexes 72 Publications Citing DSI, EEG and Alzheimer's


Clinical populations affected by AD show distinct sleep architecture compared to control populations.1 A common method of incorporating sleep assessment involves monitoring both EEG and EMG via either implantable telemetry or a tethered hardwired system. EEG is used to identify the type of sleep that is occurring and EMG is used to identify the presence or absence of rapid eye movement (REM).2,3  Some researchers also use skeletal muscle EMG, activity measurements, and/or video to differentiate betwee wakefulness, sleep architecture, and more.

Common Endpoints

Slow Wave Sleep Reduction

Broken Sleep Periods

REM Reduction


Daytime Sleepiness

Sleep Apnea

Google Scholar Indexes 64 Publications Citing DSI, Sleep and Alzheimer's


In AD populations, there is a blurred distinction between the disease and the patient’s actual cause of death. Shortness of breath, disruptions in the flow of oxygen, pneumonia, and other respiratory disorders are often observed; leading to a lower quality of life. Some research suggests a connection between commonly prescribed sedatives to AD patients and its potential risk of increased respiratory complications. Scientists can study respiratory disruptions in normal or AD animal models to better understand its relationship to neurodegenerative disorders.  

Common Endpoints

Respiratory Rate

Minute and Tidal Volume

 Peak Airflow Rates

Inspiratory and Expiratory Time

Lung Resistance

Dynamic and Static Lung Compliance



Google Scholar Indexes 76 Publications Citing Buxco and Alzheimer's


Current research suggests a bidirectional correlation between elevated blood sugar levels and Alzheimer's disease. Some scientists have gone as far to call Alzheimer’s Disease type-3 diabetes. On the other hand, Platt and colleagues1 have found that an Alzheimer model can lead to diabetes complications (type II). A recent study published in the journal Scientific Reports, report that glycation related damage to specific enzymes may be a critical part in the progression Alzheimer's Disease. These scientists now hope to detect similar changes in blood samples rather than brain.2

Common Endpoints


Blood Glucose Levels




Google Scholar Indexes 81 Publications Citing DSI, Glucose and Alzheimer's

Circadian Rhythm

Circadian rhythm is an important component of mammalian physiology and plays a large role in sleep-wake cycles, core body temperature, hormone balance and eating patterns. Disturbances with circadian rhythm are seen in the early stages of Alzheimer’s Disease. One type of circadian disturbance is known as Sundowning Syndrome, which  is a neurological phenomenon that occurs in about 20% of people with Alzheimer’s1 and is presented as confusion, agitation and anxiety occurring in the late afternoon and continuing through the night.

*Behavioral solutions are available from our Harvard Bioscience sister brands Panlab and Coulbourn Instruments. Reach out to us to learn more about how to incorporate these solutions into your current research set-up.

Google Scholar Indexes 61 Publications Citing DSI, Circadian and Alzheimer's

Highlighted Publications and References

AD and EEG

  1. Czigler B, Csikos D, Hidasi Zm et al. Quantitative EEG in early acute Alzheimer’s disease patients—power spectrum and complexity features. International Journal of Psychophysiology. 2008; 68(1):75-80.
  2. Bowyer S. Coherence a measure of the brain networks: past and present. Neuropsychiatric Electrophysiology. 2016; 2(1)
  3. Tsolaki A. Electroencephalogram and Alzheimer’s Disease: Clinical and Research Approaches. Hindawi, 2014.

AD and Sleep

  1. Tsolaki A. Electroencephalogram and Alzheimer’s Disease: Clinical and Research Approaches. Hindawi, 2014.
  2. Skopin MD, Kabadi SV, Viechweg SS, Mong JA, Faden AI. Chronic Decrease in Wakefulness and Disruption of Sleep-Wake Behavior after Experimental Traumatic Brain Injury. Journal of Neurotrauma. September 2014; 32(5):289-296. doi:10.1089/neu.2014.3664.
  3. Petraglia AL, Plog BA, Dayawansa S, Chen M, Dashnaw ML, Czerniecka K, Walker CT, Viterise T, Hyrien O, Iliff JJ, Deane R, Nedergaard M, Huang JH. The Spectrum of Neurobehavioral Sequelae after Repetitive Mild Traumatic Brain Injury: A Novel Mouse Model of Chronic Traumatic Encephalopathy. Journal of Neurotrauma. July 2014; 31(13):1211-1224. doi:10.1089/neu.2013.3255.

AD and Glucose

  1. Platt B, et al. Neuronal human BACE1 knock-in induces systemic diabetes in mice. Diabetologia. 2016.
  2. Kassaar O, et al. Macrophage Migration Inhibitory Factor is subjected to glucose modification and oxidation in Alzheimer's Disease. Scientific Reports. 2017.

AD and Circadian Rhythm

  1. Alzheimer's Association. Sundowning, Sleep, Alzheimer's & Dementia. Accessed 5 June 2017.