Center for the Aging Brain

The Montefiore Einstein Center for the Aging Brain is internationally recognized for paradigm-shifting research studies that continue to reveal the importance across the lifespan of building and sustaining cognitive resilience through brain and body metabolic regulation; low-level inflammation; novel environmental influences; motor control; cellular and neural network plasticity, and homeostasis and rejuvenation; novel forms of gene and genome regulation; mechanisms of multigenerational inheritance; and exceptionally early developmental influences, including processes mediating the fundamental patterning of a three-dimensional brain and cardinal body axes.

Employing the latest cutting-edge, nano- to whole-brain and body, molecular to structural and functional imaging technologies, our Center for the Aging Brain capitalizes on our institutional commitment to training and nurturing an interdisciplinary team of renowned physician-scientists who integrate rapidly emerging insights regarding brain and body aging, healthspan, sleep-wake biology and circadian rhythms, as well as principles underpinning intellectual resilience and longevity, into a program of comprehensive and evolving interdisciplinary care and dynamic therapeutic optimization.

We are ranked in the top 1% of all hospitals in the nation for neurology and neurosurgery, according to U.S. News & World Report, and our scientific depth and discoveries, breadth of educational programs, and leading clinical care innovations have resulted in recognition as an international referral site for managing complex cases in older adults.

The richness of our culture of scientific innovations, cross-disciplinary scholarship and novel clinical care models has allowed us to continue to advance effective therapeutic interventions where others have failed.

Neurological Services

The Montefiore Einstein Center for the Aging Brain distinguishes itself by fielding a broad-based team of world-renowned experts in the disciplines that impact our understanding of normal aging, healthspan, mechanisms of longevity and the pathophysiology of degenerative dementias. Our academic neurologists have subspecialty expertise in aging and dementia, cognitive neuroscience, neuromuscular medicine, motor control, movement disorders, sleep-wake disorders, headache medicine, neuroimmunology, neurogenetics, metabolic disorders, neuro-ophthalmology, epilepsy and neurovascular disorders. 

Our neurologic subspecialists draw upon the expertise of neuroradiology, neurorehabilitation medicine, cardiology, psychiatry and behavioral sciences, geriatrics, bioengineering, systems biology/AI, stem cell biology, epigenetics and regenerative medicine.

Dementia is the loss of cognitive functioning—the ability to think, remember or reason—to such an extent that it interferes with a person's daily life and activities. These functions include memory, language skills, visual perception, problem-solving, self-management and the ability to focus and pay attention. Some people with dementia cannot control their emotions, and their personalities may change. Several diseases and conditions can cause dementia or dementia-like symptoms, but dementia itself is not a specific disease. 

Dementia ranges in severity from the mildest stage, when it is just beginning to affect a person's functioning, to the most severe stage, when the person must depend completely on others for basic activities of daily living. 

A diagnosis of dementia can be frightening for those affected by the syndrome, their family members and caretakers. Learning more about this medical condition can help, keeping in mind that depending on the cause, some symptoms may be reversible. This overview discusses the various types of dementia, how the disorders are diagnosed and treated, and research supported by the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute on Aging (NIA), both part of the National Institutes of Health (NIH).

The different forms of age-related dementia, as well as many age-related neurodegenerative diseases, are thought to be caused by changes in various proteins. These diseases are called proteinopathies because they involve the abnormal buildup of specific proteins in the brain. Mutations in genes that provide instructions for making these proteins have been found to cause dementia in families. 

In the vast majority of affected individuals, dementia is not inherited, and the cause is unknown. 

Various neurodegenerative disorders and factors contribute to the development of dementia through a progressive and irreversible loss of neurons and brain functioning. Types of dementia include:

• Alzheimer’s disease, the most common dementia diagnosis among older adults. It is caused by changes in the brain, including abnormal buildups of proteins known as amyloid plaques and tau tangles.
• Frontotemporal dementia, a rare form of dementia that tends to occur in people younger than 60. It is associated with abnormal amounts or forms of the proteins tau and TDP-43.
• Lewy body dementia, a form of dementia caused by abnormal deposits of the protein alpha-synuclein, called Lewy bodies.
• Vascular dementia, a form of dementia caused by conditions that damage blood vessels in the brain or interrupt the flow of blood and oxygen to the brain.
• Mixed dementia, a combination of two or more types of dementia. For example, through autopsy studies involving older adults who had dementia, researchers have identified that many people had a combination of brain changes associated with different forms of dementia.

Doctors have identified many other conditions that can cause dementia or dementia-like symptoms. The diseases have different symptoms that involve body and brain functions, and affect mental health and cognition.

Alzheimer’s disease is a brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out the simplest tasks. In most people with the disease, symptoms first appear when they are in their mid-60s. Early-onset Alzheimer’s occurs between a person’s 30s and mid-60s and is very rare. Alzheimer’s disease is the most common cause of dementia among older adults.

The disease is named after Dr. Alois Alzheimer. In 1906, Dr. Alzheimer noticed changes in the brain tissue of a woman who had died of an unusual mental illness. Her symptoms included memory loss, language problems and unpredictable behavior. After she died, he examined her brain and found many abnormal clumps (now called amyloid plaques) and tangled bundles of fibers (now called neurofibrillary, or tau, tangles).

These plaques and tangles in the brain are still considered some of the main features of Alzheimer’s disease. Another feature is the loss of connections between nerve cells (neurons) in the brain. Neurons transmit messages between different parts of the brain, and from the brain to muscles and organs in the body. Many other complex brain changes are thought to play a role in Alzheimer’s, too.

This damage initially takes place in parts of the brain involved in memory, including the entorhinal cortex and hippocampus. It later affects areas in the cerebral cortex, such as those responsible for language, reasoning and social behavior. Eventually, many other areas of the brain are damaged.

In some dementias, changes in the tau protein, which plays an important role in the structure and formation of brain cells, cause it to form clumps inside nerve cells in the brain, which is believed to make the cells stop functioning properly and die. Disorders that are associated with the abnormal buildup of tau are called tauopathies.

In Alzheimer’s disease, the tau protein aggregates (accumulates into abnormal clumps) and becomes twisted and tangled, forming fibers—neurofibrillary or tau tangles—inside neurons. Abnormal clumps (plaques) of the beta-amyloid protein (a protein believed to play a role in the communication between brain cells) are prominent in spaces between brain cells. Both plaques and tangles are thought to contribute to reduced function and nerve-cell death in AD and are hallmarks of the disease.

There are two types of Alzheimer's—early-onset and late-onset. Both types have a genetic component. Most people with Alzheimer's have late-onset disease, in which symptoms become apparent in their mid-60s. 

Researchers have not found a specific gene that directly causes the late-onset form of the disease. However, one genetic risk factor—having one form, or allele, of the apolipoprotein E (APOE) gene on chromosome 19—does increase a person's risk. APOE ɛ4 is called a risk-factor gene because it increases a person's risk of developing the disease. However, inheriting an APOE ɛ4 allele does not mean that a person will definitely develop Alzheimer's. Some people with an APOE ɛ4 allele never get the disease, and others who develop Alzheimer's do not have any APOE ɛ4 alleles.

Signs of late-onset Alzheimer’s:

• Signs first appear in a person’s mid-60s
• Most common type of Alzheimer’s disease
• May involve a gene called APOE ɛ4

Early-onset Alzheimer's disease occurs between a person's 30s to mid-60s and represents fewer than 10 percent of all people with Alzheimer's. Some cases are caused by an inherited change in one of three genes. For other cases, research shows that other genetic components are involved. Researchers are working to identify additional genetic risk variants for early-onset Alzheimer’s disease.

Signs of early-onset Alzheimer’s:

• Signs first appear between a person’s 30s and mid-60s
• Very rare
• Usually caused by gene changes passed down from parent to child