at the Nathan S. Kline Institute for Psychiatric Research
Geriatric Psychiatry Research Program
Our Past Studies
APECS / Merck
These were clinical trials funded by Merck Pharmaceuticals. The purpose of these studies was to evaluate the safety and efficacy of MK8931 in the possible treatment of Alzheimer’s disease. MK8931 reduces the level of Abeta deposits in the brain, which is a small piece of protein that may be involved in causing Alzheimer’s Disease (AD). Accumulation of this particular protein, is also thought to be related to the progression of AD and begins well before the onset of AD dementia and probably even before any cognitive decline associated with AD. Therefore, these trials also assessed the effect of MK-8931 on disease progression (disease worsening).
One study enrolled subjects with a diagnosis of prodromal Alzheimer’s disease, positive PET-Amyloid scan, and between ages 50 and 85 at screening. The second Merck study focused on those diagnosed with mild to moderate AD, positive PET-Amyloid scan, and between ages 55 and 85.
This was a clinical trial that was funded by Accera Pharmaceuticals. The purpose of this study was to evaluate the safety and efficacy of AC-1204 in the treatment of Alzheimer’s disease. A similar product to AC-1204 called Axona, had already been tested by Accera in patients with memory problems, including Alzheimer's disease. People with Alzheimer’s disease can have difficulty using glucose in the brain, which serves as the primary source of energy. Another energy source that your brain can use in place of glucose is ketone bodies. This study determined whether increasing ketone body levels with AC-1204, will improve test scores that measure memory and other mental skills in study participants with Alzheimer’s disease. This study enrolled subjects with a diagnosis of mild to moderate Alzheimer’s disease and 66-90 years of age (inclusive) at screening.
This was a clinical trial that was funded by TauRx Pharmaceuticals. The primary objective of this study was to evaluate the efficacy, safety, and tolerability of Leuco-methylthioninium bis(hydromethanesulfonate) [LMTM] in treating mild Alzheimer’s disease. LMTM, the investigational product, is believed to have the potential to confer benefits over existing treatments for AD due to its ability to affect the process of tau aggregation, which is responsible for the underlying neurofibrillary pathology of Alzheimer’s disease. The secondary objective was to evaluate the effect of LMTM on functional activities of daily living as well as on other aspects of Alzheimer’s disease, including cognition and mood. This study enrolled subjects with a diagnosis of Alzheimer’s disease and are ≤90 years of age at screening.
The Alzheimer's Disease Neuroimaging Initiative (ADNI-2) was a non-treatment study that was funded by the National Institute of Health (NIH). The overall goal of this project was to determine the relationships among clinical, imaging, genetic, and biochemical biomarker characteristics of the entire spectrum of Alzheimer’s disease (AD), as the pathology evolves from normal aging through very mild symptoms, to mild cognitive impairment (MCI), to dementia. Enrolled subjects were between 55-90 (inclusive) years of age. This study enrolled subjects who currently had a diagnosis of Alzheimer’s disease (AD) and subjects who did not have a diagnosis of AD, but had significant memory concerns.
This was a clinical trial funded by Avanir Pharmaceuticals. This study evaluated the efficacy, safety and tolerability of AVP-923 (dextromethorphan/quinidine) for the treatment of symptoms of agitation in patients with Alzheimer’s disease. Alzheimer’s is a brain disease that destroys brain cells and causes problems with memory, thinking and behavior. Agitated behaviors such as irritability and restlessness, physical and verbal aggression, and pacing and wandering are major problems, can be difficult to manage, and can impact one's quality of life. This study included subjects who met a diagnosis for Alzheimer’s dementia and demonstrated symptoms of agitation.
ABETA was a non-treatment study which investigated the link between late-life major depression and Alzheimer’s disease. Individuals who become depressed after age 60 and those with a history of depressive symptoms are known to be at risk for memory decline and Alzheimer’s, even after treatment of their depression. However, not every one of these individuals will go on to develop progressive memory decline. In individuals who are not depressed, higher blood levels of a protein known as amyloid beta 42 (Aβ42) have been found to be helpful in identifying those at risk for Alzheimer's. The purpose of this study was to evaluate if a higher blood level of this protein is found in older individuals with current or past depression and if they can help in identifying those individuals at risk for progressive memory loss. Another goal was to determine if similar changes in this protein are found in the cerebrospinal fluid (CSF).
The purpose of this study was to determine if high blood levels of a certain substance called amyloid beta (1-42) was associated with persistent depression. The study was designed to understand the biological factors that may contribute to treatment-resistant and recurrent depression in the elderly.
The purpose of this research was to determine whether a daily unit dose of lorazepam would lead to a temporary impairment in performance in elderly patients, who were currently on long-term lorazepam treatment for Generalized Anxiety Disorder (GAD).
Dr. Pomara has been involved in clinical practice,
non-treatment studies, and clinical trials for over
Some of our most recent studies include...
The primary objective of this study was to evaluate the safety and efficacy of T-817MA as an adjunct therapy to donepezil (Aricept). In Alzheimer’s disease (AD) the formation of beta amyloid, which is thought to be related to the progression of Alzheimer’s disease, eventually results in neuronal cell malfunction and death. T-817MA is a compound that has a protective effect on neural cells and could potentially prevent the toxic effect of beta amyloid on neuronal cells. Therefore, this trial assessed the effect of T-817MA on disease progression (disease worsening).