Andrew E. Budson | |
---|---|
Nationality | American |
Occupation(s) | Neurologist, academic and researcher |
Awards | Elected member, Memory Disorders Research Society Member, American Neurological Association Norman Geschwind Prize in Behavioral Neurology Research Award in Geriatric Neurology Member, The Academy, Harvard Medical School |
Academic background | |
Education | B.A., Chemistry & Philosophy M.D. |
Alma mater | Haverford College, Haverford Pennsylvania Harvard Medical School, Boston, Massachusetts |
Academic work | |
Institutions | Boston University School of Medicine Harvard Medical School |
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. [1]
As a cognitive behavioral neurologist,Budson has published over 150 papers and book chapters on clinical and cognitive neuroscience aspects of Alzheimer's disease (AD),Chronic Traumatic Encephalopathy (CTE),others dementias,and normal aging. [2] He has co-authored or edited eight books,including Memory Loss,Alzheimer's Disease,and Dementia:A Practical Guide for Clinicians and Seven Steps to Managing Your Memory.
Budson is a member of the American Academy of Neurology, [3] Memory Disorders Research Society, [4] and the American Neurological Association. [5] He is on the Board of Directors,and the Medical and Scientific Advisory Committee of Alzheimer's Association of Massachusetts and New Hampshire. [1]
Budson received his Bachelor's degree with majors in Chemistry and Philosophy from Haverford College in 1988. He enrolled at Harvard Medical School,and earned his M.D. in 1993. [6] He completed his internship in Internal Medicine at Brigham and Women's Hospital,Boston,followed by his residency in Neurology at the Harvard Longwood Program,also serving as chief resident. Later,he completed a clinical fellowship in cognitive and behavioral neurology and dementia under Kirk Daffner at Brigham and Women's Hospital in 1999,and a research fellowship in experimental psychology and cognitive neuroscience under Daniel Schacter at Harvard University,Cambridge in 2000. [7]
Budson started his academic career as an Instructor in Neurology at Harvard Medical School in 1998,and was promoted to Assistant Professor of Neurology in 2001,and to Lecturer in Neurology in 2005. He held his next appointment at Boston University School of Medicine as an Associate Professor of Neurology from 2005 until 2009,and subsequently became Professor of Neurology,as well as Faculty Member in the Division of Graduate Medical Sciences there. In 2014,he held another appointment at Harvard Medical School as a Member of the Academy,and later on,in 2017,as a Chair of Science of Learning Interest Group in The Academy. [8]
Along with academic appointments,at VA Boston Healthcare System,Budson served as Deputy Chief of Staff from 2010 to 2012,and has been serving as Chief of Cognitive and Behavioral Neurology Section,and Program Director for VA Boston/Boston Medical Center UCNS-Certified Cognitive Behavioral Neurology Fellowship since 2011,and as Associate Chief of Staff for Education since 2012. He also serves as Associate Director and Leader of Outreach,Recruitment,&Engagement Core at Boston University Alzheimer's Disease Research Center,and as Consultant Neurologist at Brigham and Women's Hospital. [9]
Budson's research primarily focuses on understanding memory and memory distortions in patients with Alzheimer's disease and other neurological disorders,while using the techniques of experimental psychology and cognitive neuroscience. [10] For his research in the field,he was awarded the Norman Geschwind Prize in Behavioral Neurology in 2008 and the Research Award in Geriatric Neurology in 2009,both from the American Academy of Neurology. He has received federal funding since 1998 including F32,K23,R01,and VA Merit grants,all related to aging and AD. [11]
Budson has focused his research on understanding false memory in patients with Alzheimer's disease (AD) dementia,with particular attention on investigating the underlying mechanisms that cause an increased incidence of false memory in these patients,and determining if there are methods to help reduce the amount of false memory that occurs in these patients. [12]
Budson discussed structural network differences in individuals with mild cognitive impairment (MCI) with high versus low executive abilities,and found that patients with AD have an increased reliance on gist-based memory,which leads to their increased incidence of false memory relative to healthy older controls. In this work,he discovered that patients with AD have impairments in item-specific recollection mechanisms. [13] This prevents them from using their recall of "true" memories to combat information they never encountered (false memories). [14]
He introduced and evaluated strategies that patients with AD can use to reduce false memories. He highlighted that healthy older adults are able to use two strategies to reduce their false memory,the "distinctiveness heuristic" and the "recall-to-reject" strategy. [15] His research indicated that patients with AD are aware of these strategies,but can only use them to a limited capacity due to their general episodic memory impairment. [16] In another study,he described the underlying neural correlates associated with the recollection and familiarity in both healthy populations and patients with AD and other dementias using electroencephalography (EEG) event-related potentials (ERPs) as well as structural and functional MRI. [17] He demonstrated that false memory is generally associated with diminished N400 and Late Frontal Effects,and ERPs associated with the memorial mechanisms of familiarity and recollection are enhanced when perceptually rich stimuli are used,such as pictures. [18]
Budson,along with co-workers,worked extensively to understand better chronic traumatic encephalopathy (CTE),a cause of dementia that has been discovered to be more prevalent than previously thought. He discovered new findings related to CTE including the diversity of its clinical presentation,the spectrum of its neuropathology,possible mechanisms related to blast injury,and its relation to motor neuron disease. [19]
In 2022,Budson,with his colleagues Kenneth Richman and Elizabeth Kensinger,published a new theory of consciousness in the journal Cognitive and Behavioral Neurology. In their paper they suggested that consciousness developed as part of episodic memory and the other explicit memory systems to facilitate the flexible recombination of information needed by the episodic memory system to plan for the future. Building on Daniel Kahneman's and Amos Tversky's research into System 1 unconscious processing and System 2 conscious processing,Budson and colleagues argued that humans do not directly consciously perceive,decide,and act,but rather they perform these activities unconsciously and subsequently consciously remember the perception,decision,and action. Budson and colleagues suggested that this consciousness-as-memory theory can explain postdictive effects as well as why conscious decisions and actions (such as dieting and mindfulness) are difficult. As what they suggest are logical consequences of their theory,they made several other claims including (1) that all areas of the cerebral cortex contribute to consciousness but none is critical,(2) consciousness can arise from any "region" of the cerebral cortex (size of region not defined),(3) all mammals and other vertebrates experience some form of consciousness,(4) there are many disorders of consciousness including strokes,delirium,dementia,migraines,epilepsy,dissociative disorders,schizophrenia,and autism. [20]
Although the article built on the work of others,such as Endel Tulving and,more recently,Joseph LeDoux and Hakwan Lau, [21] the paper by Budson,Richman,and Kensinger was recognized as original,being covered by news outlets and the February 2023 print magazine edition of the French magazine,Science &Vie. [22] It also generated published commentaries in Cognitive and Behavioral Neurology by Hinze Hogendoorn, [23] Amnon Dafni-Merom and Shahar Arzy, [24] and Howard Kirshner. [25]
Dementia is a syndrome associated with many neurodegenerative diseases,characterized by a general decline in cognitive abilities that impacts a person's ability to perform everyday activities. This typically involves problems with memory,thinking,behavior,and motor control. Aside from memory impairment and a disruption in thought patterns,the most common symptoms of dementia 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,their caregivers,and their 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 might be caused by the normal aging process.
Binswanger's disease,also known as subcortical leukoencephalopathy and subcortical arteriosclerotic encephalopathy,is a form of small-vessel vascular dementia caused by damage to the white brain matter. White matter atrophy can be caused by many circumstances including chronic hypertension as well as old age. This disease is characterized by loss of memory and intellectual function and by changes in mood. These changes encompass what are known as executive functions of the brain. It usually presents between 54 and 66 years of age,and the first symptoms are usually mental deterioration or stroke.
Anosognosia is a condition in which a person with a disability is cognitively unaware of having it due to an underlying physical condition. Anosognosia results from physiological damage to brain structures,typically to the parietal lobe or a diffuse lesion on the fronto-temporal-parietal area in the right hemisphere,and is thus a neuropsychiatric disorder. A deficit of self-awareness,the term was first coined by the neurologist Joseph Babinski in 1914,in order to describe the unawareness of hemiplegia.
Frontotemporal dementia (FTD),also called frontotemporal degeneration disease or frontotemporal neurocognitive disorder, encompasses several types of dementia involving the progressive degeneration of the brain's frontal and temporal lobes. FTD is the second most prevalent type of early onset dementia after Alzheimer's disease. Men and women appear to be equally affected. FTD generally presents as a behavioral or language disorder with gradual onset. Signs and symptoms tend to appear in late adulthood,typically between the ages of 45 and 65,although it can affect people younger or older than this. Currently,no cure or approved symptomatic treatment for FTD exists,although some off-label drugs and behavioral methods are prescribed.
Donepezil,sold under the brand name Aricept among others,is a medication used to treat dementia of the Alzheimer's type. It appears to result in a small benefit in mental function and ability to function. Use,however,has not been shown to change the progression of the disease. Treatment should be stopped if no benefit is seen. It is taken by mouth or via a transdermal patch.
Cognitive disorders (CDs),also known as neurocognitive disorders (NCDs),are a category of mental health disorders that primarily affect cognitive abilities including learning,memory,perception,and problem-solving. Neurocognitive disorders include delirium,mild neurocognitive disorders,and major neurocognitive disorder. They are defined by deficits in cognitive ability that are acquired,typically represent decline,and may have an underlying brain pathology. The DSM-5 defines six key domains of cognitive function:executive function,learning and memory,perceptual-motor function,language,complex attention,and social cognition.
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.
Neurofibrillary tangles (NFTs) are intracellular aggregates of hyperphosphorylated tau protein that are most commonly known as a primary biomarker of Alzheimer's disease. Their presence is also found in numerous other diseases known as tauopathies. Little is known about their exact relationship to the different pathologies.
Primary progressive aphasia (PPA) is a type of neurological syndrome in which language capabilities slowly and progressively become impaired. As with other types of aphasia,the symptoms that accompany PPA depend on what parts of the left hemisphere are significantly damaged. However,unlike most other aphasias,PPA results from continuous deterioration in brain tissue,which leads to early symptoms being far less detrimental than later symptoms.
Mirrored-self misidentification is the delusional belief that one's reflection in the mirror is another person –typically a younger or second version of one's self,a stranger,or a relative. This delusion occurs most frequently in patients with dementia and an affected patient maintains the ability to recognize others' reflections in the mirror. It is caused by right hemisphere cranial dysfunction that results from traumatic brain injury,stroke,or general neurological illness. It is an example of a monothematic delusion,a condition in which all abnormal beliefs have one common theme,as opposed to a polythematic delusion,in which a variety of unrelated delusional beliefs exist. This delusion is also classified as one of the delusional misidentification syndromes (DMS). A patient with a DMS condition consistently misidentifies places,objects,persons,or events. DMS patients are not aware of their psychological condition,are resistant to correction and their conditions are associated with brain disease –particularly right hemisphere brain damage and dysfunction.
HIV-associated neurocognitive disorders (HAND) are neurological disorders associated with HIV infection and AIDS. It is a syndrome of progressive deterioration of memory,cognition,behavior,and motor function in HIV-infected individuals during the late stages of the disease,when immunodeficiency is severe. HAND may include neurological disorders of various severity. HIV-associated neurocognitive disorders are associated with a metabolic encephalopathy induced by HIV infection and fueled by immune activation of macrophages and microglia. These cells are actively infected with HIV and secrete neurotoxins of both host and viral origin. The essential features of HIV-associated dementia (HAD) are disabling cognitive impairment accompanied by motor dysfunction,speech problems and behavioral change. Cognitive impairment is characterised by mental slowness,trouble with memory and poor concentration. Motor symptoms include a loss of fine motor control leading to clumsiness,poor balance and tremors. Behavioral changes may include apathy,lethargy and diminished emotional responses and spontaneity. Histopathologically,it is identified by the infiltration of monocytes and macrophages into the central nervous system (CNS),gliosis,pallor of myelin sheaths,abnormalities of dendritic processes and neuronal loss.
Memory disorders are the result of damage to neuroanatomical structures that hinders the storage,retention and recollection of memories. Memory disorders can be progressive,including Alzheimer's disease,or they can be immediate including disorders resulting from head injury.
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.
Mild cognitive impairment (MCI) is a neurocognitive disorder which involves cognitive impairments beyond those expected based on an individual's age and education but which are not significant enough to interfere with instrumental activities of daily living. MCI may occur as a transitional stage between normal aging and dementia,especially Alzheimer's disease. It includes both memory and non-memory impairments. The cause of the disorder remains unclear,as well as both its prevention and treatment,with some 50 percent of people diagnosed with it going on to develop Alzheimer's disease within five years. The diagnosis can also serve as an early indicator for other types of dementia,although MCI may remain stable or even remit.
The NINCDS-ADRDA Alzheimer's Criteria were proposed in 1984 by the National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's Disease and Related Disorders Association and are among the most used in the diagnosis of Alzheimer's disease (AD). These criteria require that the presence of cognitive impairment and a suspected dementia syndrome be confirmed by neuropsychological testing for a clinical diagnosis of possible or probable AD;while they need histopathologic confirmation for the definitive diagnosis. They specify as well eight cognitive domains that may be impaired in AD. These criteria have shown good reliability and validity.
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.
In psychology,confabulation is a memory error consisting of the production of fabricated,distorted,or misinterpreted memories about oneself or the world. It is generally associated with certain types of brain damage or a specific subset of dementias. While still an area of ongoing research,the basal forebrain is implicated in the phenomenon of confabulation. People who confabulate present with incorrect memories ranging from subtle inaccuracies to surreal fabrications,and may include confusion or distortion in the temporal framing of memories. In general,they are very confident about their recollections,even when challenged with contradictory evidence.
The Addenbrooke's Cognitive Examination (ACE) and its subsequent versions are neuropsychological tests used to identify cognitive impairment in conditions such as dementia.
Elizabeth Kensinger is Professor of Psychology and Neuroscience at Boston College. She is known for her research on emotion and memory over the human lifespan. She is co-author of the book Why We Forget and How To Remember Better:The Science Behind Memory,published in 2023 by Oxford University Press,which provides an overview of the psychology and neuroscience of memory. She also is the author of the book Emotional Memory Across the Adult Lifespan, which describes the selectivity of memory,i.e.,how events infused with personal significance and emotion are much more memorable than nonemotional events. This book provides an overview of research on the cognitive and neural mechanisms underlying the formation and retrieval of emotional memories. Kensinger is co-author of a third book How Does Emotion Affect Attention and Memory? Attentional Capture,Tunnel Memory,and the Implications for Posttraumatic Stress Disorder with Katherine Mickley Steinmetz,which highlights the roles of emotion in determining what people pay attention to and later remember.
Czech Brain Ageing Study (CBAS) is a longitudinal,observational study on aging and dementia from two large centers in the Czech Republic combining clinical care and clinical research.