Yaakov Stern

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Yaakov Stern is an American cognitive neuroscientist, professor of neuropsychology at Columbia University.

Contents

Early life

Stern has an undergraduate degree in psychology from Touro College, and a doctorate in psychology from the Graduate Center of the City University of New York. He joined the faculty at Columbia University after completing his doctorate. He now is a Florence Irving professor of neuropsychology and chief of the Cognitive Neuroscience Division of the Neurology department. [1]

Cognitive reserve

Stern's major contribution is the concept of cognitive reserve, which helps to explain differential susceptibility to age- or disease-related brain changes. In 2002 he published his first systematic treatment of the concept. [2] Stern's work in cognitive reserve is the most cited in the list of 300 papers in Alzheimer's Disease research compiled by the Journal of Alzheimer's Disease [3] and has been quoted in news articles. [4] [5] [6]

In 1992, he demonstrated that when patients with Alzheimer's disease are matched for clinical severity, those with higher education had more extensive neurodegeneration, indicating that they could cope more successfully with the underlying pathology. [7] He was one of the first to use prospective incidence studies to demonstrate that individuals with higher educational or occupational attainment, [8] or who engage in more late life leisure activities [9] have a reduced risk of developing Alzheimer's. He was the first to observe that patients with higher reserve had a more rapid rate of decline. [10] Much of his later work has focused on the potential neural basis of cognitive reserve using imaging studies. [11]

Stern has authored or co-authored and published over 600 articles in academic journals. His H index according to Google scholar is over 150. He edited a book on cognitive reserve. [12]

Other research

Stern's earliest work focused on identifying cognitive changes in nondemented patients with idiopathic Parkinson's disease, which helped identify the cognitive role of the basal ganglia when it was widely believed to have a role only in motor function. [13] He validated these observations in patients with MPTP-induced Parkinson's. [14]

In the long-standing Predictors study, Stern has been working to clarify the heterogeneity of the course of Alzheimer's disease. He identified a set of disease features that are associated with more rapid decline, and created prediction algorithms for disease course. [15]

Stern directs the Reference Ability Neural Network (RANN) study, which is examining the neural basis for key cognitive domains in aging. [16]

Related Research Articles

<span class="mw-page-title-main">Dementia</span> Long-term brain disorders causing impaired memory, thinking and behavior

Dementia is the general name for a decline in cognitive abilities that impacts a person's ability to perform everyday activities. This typically involves problems with memory, thinking, and behavior. Aside from memory impairment and a disruption in thought patterns, the most common symptoms include emotional problems, difficulties with language, and decreased motivation. The symptoms may be described as occurring in a continuum over several stages. Dementia ultimately has a significant effect on the individual, caregivers, and on social relationships in general. A diagnosis of dementia requires the observation of a change from a person's usual mental functioning and a greater cognitive decline than what is caused by normal aging.

<span class="mw-page-title-main">Parkinsonism</span> Medical condition

Parkinsonism is a clinical syndrome characterized by tremor, bradykinesia, rigidity, and postural instability. These are the four motor symptoms found in Parkinson's disease (PD) – after which it is named – dementia with Lewy bodies (DLB), Parkinson's disease dementia (PDD), and many other conditions. This set of symptoms occurs in a wide range of conditions and may have many causes, including neurodegenerative conditions, drugs, toxins, metabolic diseases, and neurological conditions other than PD.

Vascular dementia (VaD) is dementia caused by problems in the blood supply to the brain, resulting from a cerebrovascular disease. Restricted blood supply (ischemia) leads to cell and tissue death in the affected region, known as an infarct. The three types of vascular dementia are subcortical vascular dementia, multi-infarct dementia, and stroke related dementia. Subcortical vascular dementia is brought about by damage to the small blood vessels in the brain. Multi-infarct dementia is brought about by a series of mini-strokes where many regions have been affected. The third type is stroke related where more serious damage may result. Such damage leads to varying levels of cognitive decline. When caused by mini-strokes, the decline in cognition is gradual. When due to a stroke, the cognitive decline can be traced back to the event.

Normal pressure hydrocephalus (NPH), also called malresorptive hydrocephalus, is a form of communicating hydrocephalus in which excess cerebrospinal fluid (CSF) builds up in the ventricles, leading to normal or slightly elevated cerebrospinal fluid pressure. The fluid build-up causes the ventricles to enlarge and the pressure inside the head to increase, compressing surrounding brain tissue and leading to neurological complications. Although the cause of idiopathicNPH remains unclear, it has been associated with various co-morbidities including hypertension, diabetes mellitus, Alzheimer's disease, and hyperlipidemia. Causes of secondary NPH include trauma, hemorrhage, or infection. The disease presents in a classic triad of symptoms, which are memory impairment, urinary frequency, and balance problems/gait deviations. The disease was first described by Salomón Hakim and Raymond Adams in 1965.

Semantic dementia (SD), also known as semantic variant primary progressive aphasia (svPPA), is a progressive neurodegenerative disorder characterized by loss of semantic memory in both the verbal and non-verbal domains. However, the most common presenting symptoms are in the verbal domain. Semantic dementia is a disorder of semantic memory that causes patients to lose the ability to match words or images to their meanings. However, it is fairly rare for patients with semantic dementia to develop category specific impairments, though there have been documented cases of it occurring. Typically, a more generalized semantic impairment results from dimmed semantic representations in the brain.

Progressive nonfluent aphasia (PNFA) is one of three clinical syndromes associated with frontotemporal lobar degeneration. PNFA has an insidious onset of language deficits over time as opposed to other stroke-based aphasias, which occur acutely following trauma to the brain. The specific degeneration of the frontal and temporal lobes in PNFA creates hallmark language deficits differentiating this disorder from other Alzheimer-type disorders by the initial absence of other cognitive and memory deficits. This disorder commonly has a primary effect on the left hemisphere, causing the symptomatic display of expressive language deficits and sometimes may disrupt receptive abilities in comprehending grammatically complex language.

J. William Langston is the founder and chief scientific officer, movement disorder specialist, and chief executive officer of the Parkinson's Institute and Clinical Center in Sunnyvale, California, the founding member of the Scientific Advisory Board for the Michael J. Fox Foundation and the Co-Editor-in-Chief of the Journal of Parkinson's Disease. He is a graduate of the University of Missouri School of Medicine. Langston was formerly a faculty member at Stanford University and Chairman of Neurology at Santa Clara Valley Medical Center in San Jose, California. Langston has authored or co-authored some 360 peer-reviewed articles in the field of neurology, most of which are on Parkinson's disease and related disorders. Langston gained national and international recognition in 1982 for the discovery of the link between a "synthetic heroin" contaminant (MPTP) and parkinsonism.

<span class="mw-page-title-main">Apolipoprotein E</span> Cholesterol-transporting protein most notably implicated in Alzheimers disease

Apolipoprotein E (Apo-E) is a protein involved in the metabolism of fats in the body of mammals. A subtype is implicated in the Alzheimer's disease and cardiovascular diseases. It is encoded in humans by the gene APOE.

Cognitive reserve is the mind's and brain's resistance to damage of the brain. The mind's resilience is evaluated behaviorally, whereas the neuropathological damage is evaluated histologically, although damage may be estimated using blood-based markers and imaging methods. There are two models that can be used when exploring the concept of "reserve": brain reserve and cognitive reserve. These terms, albeit often used interchangeably in the literature, provide a useful way of discussing the models. Using a computer analogy, brain reserve can be seen as hardware and cognitive reserve as software. All these factors are currently believed to contribute to global reserve. Cognitive reserve is commonly used to refer to both brain and cognitive reserves in the literature.

The prevention of dementia involves reducing the number of risk factors for the development of dementia, and is a global health priority needing a global response. Initiatives include the establishment of the International Research Network on Dementia Prevention (IRNDP) which aims to link researchers in this field globally, and the establishment of the Global Dementia Observatory a web-based data knowledge and exchange platform, which will collate and disseminate key dementia data from members states. Although there is no cure for dementia, it is well established that modifiable risk factors influence both the likelihood of developing dementia and the age at which it is developed. Dementia can be prevented by reducing the risk factors for vascular disease such as diabetes, high blood pressure, obesity, smoking, physical inactivity and depression. A study concluded that more than a third of dementia cases are theoretically preventable. Among older adults both an unfavorable lifestyle and high genetic risk are independently associated with higher dementia risk. A favorable lifestyle is associated with a lower dementia risk, regardless of genetic risk. In 2020, a study identified 12 modifiable lifestyle factors, and the early treatment of acquired hearing loss was estimated as the most significant of these factors, potentially preventing up to 9% of dementia cases.

<span class="mw-page-title-main">Alzheimer's disease</span> Progressive neurodegenerative disease

Alzheimer's disease (AD) is a neurodegenerative disease that usually starts slowly and progressively worsens, and is the cause of 60–70% of cases of dementia. The most common early symptom is difficulty in remembering recent events. As the disease advances, symptoms can include problems with language, disorientation, mood swings, loss of motivation, self-neglect, and behavioral issues. As a person's condition declines, they often withdraw from family and society. Gradually, bodily functions are lost, ultimately leading to death. Although the speed of progression can vary, the average life expectancy following diagnosis is three to twelve years.

Subcortical dementias includes those diseases which predominantly affects the basal ganglia along with features of cognitive decline.

<span class="mw-page-title-main">Montreal Cognitive Assessment</span> Screening assessment for detecting cognitive impairment

The Montreal Cognitive Assessment (MoCA) is a widely used screening assessment for detecting cognitive impairment. It was created in 1996 by Ziad Nasreddine in Montreal, Quebec. It was validated in the setting of mild cognitive impairment (MCI), and has subsequently been adopted in numerous other clinical settings. This test consists of 30 points and takes 10 minutes for the individual to complete. The original English version is performed in seven steps, which may change in some countries dependent on education and culture. The basics of this test include short-term memory, executive function, attention, focus, and more.

<span class="mw-page-title-main">Rivastigmine</span> Chemical compound

Rivastigmine is a cholinesterase inhibitor used for the treatment of mild to moderate Alzheimer's disease. The drug can be administered orally or via a transdermal patch; the latter form reduces the prevalence of side effects, which typically include nausea and vomiting.

Parkinson's disease dementia (PDD) is dementia that is associated with Parkinson's disease (PD). Together with dementia with Lewy bodies (DLB), it is one of the Lewy body dementias characterized by abnormal deposits of Lewy bodies in the brain.

Corticobasal syndrome (CBS) is a rare, progressive atypical Parkinsonism syndrome and is a tauopathy related to frontotemporal dementia. CBS is typically caused by the deposit of tau proteins forming in different areas of the brain.

<span class="mw-page-title-main">Gladys Maestre</span> Venezuela-born Neuroscientist

Gladys Elena Maestre is a neuroscientist from Venezuela who is a professor at the University of Texas Rio Grande Valley School of Medicine. She is known for her work on Alzheimer's disease and other forms of dementia.

Nicole Schupf is an American epidemiologist and neuroscientist who is Professor of Epidemiology in Neurology, Psychiatry, the Gertrude H. Sergievsky Center, and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Faculty of Medicine. She studies aging and Alzheimer's disease in individuals with Down syndrome.

<span class="mw-page-title-main">Andrew E. Budson</span> American neurologist

Andrew E. Budson is an American neurologist, academic and researcher. He is a Professor of Neurology at Boston University School of Medicine, Lecturer in Neurology at Harvard Medical School, Chief of Cognitive and Behavioral Neurology and Associate Chief of Staff for Education at the Veterans Affairs (VA) Boston Healthcare System, where he also serves as a Director of the Center for Translational Cognitive Neuroscience. He is Associate Director and Outreach, Recruitment, and Engagement Core Leader at the Boston University Alzheimer's Disease Research Center.

David A Bennett is a neurologist, Director of the Rush Alzheimer's Disease Center (RADC), and the Robert C Borwell Professor of Neurology at Rush University Medical Center.Bennett is also Visiting Professor, Instituto de Assistencia Medica ao Servidor Publico Estadual (IAMSPE), São Paulo, Brazil.

References

  1. ↑ "Bio". 14 October 2020.
  2. ↑ Stern, Y. (2002). "What is cognitive reserve? Theory and research application of the reserve concept". Journal of the International Neuropsychological Society. 8 (3): 448–460. doi:10.1017/s1355617702813248. PMID   11939702. S2CID   9902333.
  3. ↑ "Journal of Alzheimer's Disease".
  4. ↑ Heidi Godman (December 21, 2018). "Can I Bank Cognition Now for Old Age?". U.S. News & World Report .
  5. ↑ "Five myths about Alzheimer's disease". June 15, 2018.
  6. ↑ Cecilia Pessoa Gingerich (April 17, 2018). "Physicians with Alzheimer's: What Happens When a Doctor Forgets?".
  7. ↑ Stern, Y.; Alexander, GE; Prohovnik, I.; Mayeux, R. (1992). "Inverse relationship between education and parietotemporal perfusion deficit in Alzheimer's disease". Annals of Neurology. 32 (3): 371–375. doi:10.1002/ana.410320311. PMID   1416806. S2CID   20777087.
  8. ↑ Stern, Y.; Gurland, B.; Tatemichi, TK; Tang, MX; Wilder, D.; Mayeux, R. (1994). "Influence of education and occupation on the incidence of Alzheimer's disease". Journal of the American Medical Association. 271 (13): 1004–1010. doi:10.1001/jama.1994.03510370056032. PMID   8139057.
  9. ↑ Scarmeas, N.; Levy, G.; Tang, MX; Manly, J.; Stern, Y. (2001). "Influence of leisure activity on the incidence of Alzheimer's disease". Neurology. 57 (12): 2236–2242. doi:10.1212/wnl.57.12.2236. PMC   3025284 . PMID   11756603.
  10. ↑ Stern, Y.; Albert, S.; Tang, MX; Tsai, WY (1999). "Rate of memory decline in AD is related to education and occupation: Cognitive reserve?". Neurology. 53 (9): 1942–1957. doi:10.1212/wnl.53.9.1942. PMID   10599762. S2CID   5676450.
  11. ↑ Stern, Y. (2009). "Cognitive reserve". Neuropsychologia. 47 (10): 2015–2028. doi:10.1016/j.neuropsychologia.2009.03.004. PMC   2739591 . PMID   19467352.
  12. ↑ Stern, Yaakov (2006). Cognitive Reserve: Theory and Applications (1st ed.). New York and London: Taylor & Francis. ISBN   9781138006263.
  13. ↑ Stern, Y.; Mayeux, R.; Rosen, J.; Ilson, J. (1983). "Perceptual motor dysfunction in Parkinson's disease: a deficit in sequential and predictive voluntary movement". Journal of Neurology, Neurosurgery, and Psychiatry. 46 (2): 145–151. doi:10.1136/jnnp.46.2.145. PMC   1027297 . PMID   6842218.
  14. ↑ Stern, Y.; Langston, JW (1985). "Intellectual changes in patients with MPTP-induced parkinsonism". Neurology. 35 (10): 1506–1509. doi:10.1212/wnl.35.10.1506. PMID   3875807. S2CID   7914649.
  15. ↑ Stern, Y.; Tang, MX; Albert, MS (1997). "Predicting time to nursing home care and death in individuals with Alzheimer disease". Journal of the American Medical Association. 277 (10): 806–812. doi:10.1001/jama.277.10.806. PMID   9052710.
  16. ↑ Stern, Y.; Habeck, C.; Steffener, J. (2014). "The Reference Ability Neural Network Study: motivation, design, and initial feasibility analyses". NeuroImage. 103: 139–151. doi:10.1016/j.neuroimage.2014.09.029. PMC   4312259 . PMID   25245813.
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