The goal of the Johns Hopkins Alzheimer's Disease Research Center (ADRC) is to accelerate the discovery of new treatments that are directed at the basic mechanisms of disease, and to hasten the time when effective treatments for AD and related disorders become a reality. We have a strong commitment to basic research regarding the underlying mechanisms of Alzheimer's Disease and related disorders, and how this may translate into effective treatment. We perform clinical research seeking to identify medications to delay or treat the symptoms of dementia. We also provided many educational programs for family members and professionals.

The Esther Oh Lab is interested in developing biological markers for pre-clinical stages of Alzheimer's disease (AD). Our current research involves using transgenic models of AD to develop peripheral injections of monoclonal antibodies against amyloid-beta as a tool to detect a level of amyloid-beta that would be correlative to the amyloid-beta level in the brain.

The Philip Wong Lab seeks to understand the molecular mechanisms and identification of new therapeutic targets of neurodegenerative diseases, particularly Alzheimer's disease (AD) and amyotrophic lateral sclerosis (ALS). Taking advantage of discoveries of genes linked to these diseases (mutant APP and PS in familial AD and mutant SOD1, dynactin p150glued ALS4and ALS2 in familial ALS), our laboratory is taking a molecular/cellular approach, including transgenic, gene targeting and RNAi strategies in mice, to develop models that facilitate our understanding of pathogenesis of disease and the identification and validation of novel targets for mechanism-based therapeutics. Significantly, these mouse models are instrumental for study of disease mechanisms, as well as for design and testing of therapeutic strategies for AD and ALS.

In the Lee Martin Laboratory, we are testing the hypothesis that selective vulnerability--the phenomenon in which only certain groups of neurons degenerate in adult onset neurological disorders like amyotrophic lateral sclerosis and Alzheimer's disease--is dictated by brain regional connectivity, mitochondrial function and oxidative stress. We believe it is mediated by excitotoxic cell death resulting from abnormalities in excitatory glutamatergic signal transduction pathways, including glutamate transporters and glutamate receptors as well as their downstream intracellular signaling molecules. We are also investigating the contribution of neuronal/glial apoptosis and necrosis as cell death pathways in animal (including transgenic mice) models of acute and progressive neurodegeneration. We use a variety of anatomical and molecular neurobiological approaches, including neuronal tract-tracing techniques, immunocytochemistry, immunoblotting, antipeptide antibody production, transmission electron microscopy and DNA analysis to determine the precise regional and cellular vulnerabilities and the synaptic and molecular mechanisms that result in selective neuronal degeneration.

The Hey-Kyoung Lee Lab is interested in exploring the cellular and molecular changes that happen at synapses to allow memory storage. We use various techniques, including electrophysiological recording, biochemical and molecular analysis, and imaging, to understand the cellular and molecular changes that happen during synaptic plasticity. Currently, we are examining the molecular and cellular mechanisms of global homeostatic synaptic plasticity using sensory cortices as model systems. In particular, we found that loss of vision elicits global changes in excitatory synaptic transmission in the primary visual cortex. Vision loss also triggers specific synaptic changes in other primary sensory cortices, which we postulate underlies sensory compensation in the blind. One of our main research goals is to understand the mechanisms underlying such cross-modal synaptic plasticity. We are also interested in elucidating the events that occur in diseased brains. In collaboration with other researchers, we are analyzing various mouse models of Alzheimer's disease, especially focusing on the possible alterations in synaptic plasticity mechanisms.

Research in the Bakker Memory Laboratory is focused on understanding the mechanisms and brain networks underlying human cognition with a specific focus on the mechanisms underlying learning and memory and the changes in memory that occur with aging and disease. We use a variety of techniques including neuropsychological assessments, experimental behavioral assessments and particularly advanced neuroimaging methods to study these questions in young and older adults and patients with mild cognitive impairment, Alzheimer’s disease, Parkinson’s disease and epilepsy. Through our collaborations with investigators in both basic science and clinical departments, including the departments of Psychiatry and Behavioral Sciences, Psychological and Brain Sciences, Neurology and Public Health, our research also focuses on brain systems involved in spatial navigation and decision-making as well as cognitive impairment in neuropsychiatric conditions such as schizophrenia, eating disorders, obsessive-compulsive disorders, depression and anxiety.

The Kathryn Carson Lab investigates ways to improve medical research, particularly in the areas of brain and thyroid cancer, Alzheimer’s disease, atherosclerosis, hypertension, HIV and lupus. Our team seeks to help researchers optimize their studies through better study design, protocol and grant writing, data cleaning and analysis, and publication writing. We work with investigators from a wide range of departments through the Johns Hopkins Institute for Clinical and Translational Research.

Psychiatric Neuroimaging (PNI) is active in neuropsychiatric research using imaging methods such as MRI, fMRI, PET and DTI to understand the mechanisms and brain networks underlying human cognition. PNI faculty have published hundreds of papers on a variety of brain disorders which include but are not limited to Alzheimer's disease, Parkinson's disease, bipolar disorder, and eating disorders. Faculty in the division have been awarded numerous peer-reviewed grants by the National Institutes of Health, foundations and other funding organizations.

Founded in the late 1980s, our Lab explores the fundamental mechanisms of neural responses to traumatic and degenerative signals and works to identify targets for treating injury/degeneration with small molecules, peptides and cells. We currently focus on traumatic and degenerative axonopathies as they occur in traumatic brain injury (diffuse axonal injury), neurodegenerative diseases i.e. Alzheimer's disease and other white matter conditions, e.g. hypoxic ischemic encephalopathy, demyelination. We are especially interested in the role of the MAPK cascade of injury, NAD metabolism and SARM1 signaling and their convergence on Wallerian degeneration.

Dr. Hua's research has centered on the development of novel MRI technologies for in vivo functional and physiological imaging in the brain, and the application of such methods for studies in healthy and diseased brains. These include the development of human and animal MRI methods to measure functional brain activities, cerebral perfusion and oxygen metabolism at high (3 Tesla) and ultra-high (7 Tesla and above) magnetic fields. He is particularly interested in novel MRI approaches to image small blood and lymphatic vessels in the brain. Collaborating with clinical investigators, these techniques have been applied 1) to detect functional, vascular and metabolic abnormalities in the brain in neurodegenerative diseases such as Huntingdon's disease (HD), Parkinson's disease (PD), Alzheimer's disease (AD) and mental disorders such as schizophrenia; and 2) to map brain functions and cerebrovascular reactivity for presurgical planning in patients with vascular malformations, brain tumors and epilepsy.