DOCSLIB.ORG

Memory Loss What Can You Do About

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Memory Loss What Can You Do About Joyce Cheng RN Community Health Nurse November 16, 2016 Dementia- an umbrella term used to describe a set of symptoms, including impairment in memory, reasoning, judgment, language and other thinking skills Normal age-related memory loss doesn’t prevent you from living a full and productive life. These changes in memory are generally manageable and do not disrupt your ability to work, live independently or maintain a social life Alzheimer’s disease Vascular dementia (multi-infarct dementia) Frontotemporal dementia Lewy body dementia • Alzheimer's is the most common form of dementia, accounts for 60 to 80 percent of dementia cases. • Alzheimer's is not a normal part of aging, although the greatest known risk factor is increasing age, and the majority of people with Alzheimer's are 65 and older • Alzheimer's worsens over time. Alzheimer's is the sixth leading cause of death in the United States. • Alzheimer's has no current cure, but treatments for symptoms are available and research continues. Asking the same questions repeatedly Forgetting common words when speaking Mixing words up Taking longer to complete familiar tasks Misplacing items in inappropriate places Getting lost while walking or driving around a familiar neighborhood Undergoing sudden changes in mood or behavior for no apparent reason Becoming less able to follow directions Vascular cognitive impairment- Sleep deficiency- Medications Nutritional Deficiency Stress, Anxiety, and Depression Caused by reduced blood flow to the brain or blockage. Reduced blood flow lead to depriving of oxygen and essential nutrients. Hypertension High Cholesterol Stroke- forgetfulness may be an early warning sign of stroke Sleep Apnea- wake up with a headache, daytime fatigue, snoring. Insomnia Deep sleep (REM rapid eye movement) plays an important role in memory Sleep Stages Non-REM Sleep- Stage 1- 5-10 minutes Stage 2- light sleep, lower heart rate & body temp Stage 3 &4- body repair, regrow tissue, build bone/ muscle, strengthen immune system Stage 5 REM Sleep- Increase Heart Rate & breathing, intense dreams, brain active, learning, thinking organizing into storing memories, balance mood, Several types of drugs can affect memory(FDA) Sleeping pills Antihistamines Anti-anxiety medications Antidepressants Certain Pain killers Cholesterol-lowering medication- statins Diabetes medication-metformin Lack of Vitamin B12- can lead to confusion and dementia Food contains Vitamin B12- dairy products, meat, and fish or Vitamin B12 fortified cereals Significant stress or anxiety can lead to problems with attention and memory Especially true if combined with poor sleep Untreated chronic stress can lead to depression which could affect brain function. (Journal of Pharmacy & Bioallied Sciences) Infection- Syphilis Head injury- concussion Brain Tumors and its treatments Alcoholism, substance Abuse- A study found that men who drank heavily showed signs of mental decline one to six years earlier than light drinkers Talk to your Primary doctor, to get a timely diagnosis and appropriate care Adopt ways to cope memory loss Treatment for memory loss depends on the cause. In many cases, it may be reversible with treatment. In others, memory may improve over time. Treatments may also be specific to conditions related to memory loss. For example, drugs are available to treat memory problems related to Alzheimer’s disease Symptoms: Confusion Trouble paying attention and concentrating Reduced ability to organize thoughts or actions Decline in ability to analyze a situation, develop an effective plan and communicate that plan to others Difficulty deciding what to do next Problems with memory Restlessness and agitation Unsteady gait Sudden or frequent urge to urinate or inability to control passing urine Depression Alzheimer's is a type of dementia that causes problems with memory, thinking and behavior. Symptoms usually develop slowly and get worse over time, becoming severe enough to interfere with daily tasks. Alzheimer's is the most common form of dementia, a general term for memory loss and other intellectual abilities serious enough to interfere with daily life. Alzheimer's disease accounts for 60 to 80 percent of dementia cases. Alzheimer's is not a normal part of aging, although the greatest known risk factor is increasing age, and the majority of people with Alzheimer's are 65 and older. But Alzheimer's is not just a disease of old age. Up to 5 percent of people with the disease have early onset Alzheimer's (also known as younger-onset), which often appears when someone is in their 40s or 50s. Alzheimer's worsens over time. Alzheimer's is a progressive disease, where dementia symptoms gradually worsen over a number of years. In its early stages, memory loss is mild, but with late-stage Alzheimer's, individuals lose the ability to carry on a conversation and respond to their environment. Alzheimer's is the sixth leading cause of death in the United States. Those with Alzheimer's live an average of eight years after their symptoms become noticeable to others, but survival can range from four to 20 years, depending on age and other health conditions. Alzheimer's has no current cure, but treatments for symptoms are available and research continues. Although current Alzheimer's treatments cannot stop Alzheimer's from progressing, they can temporarily slow the worsening of dementia symptoms and improve quality of life for those with Alzheimer's and their caregivers. Today, there is a worldwide effort under way to find better ways to treat the disease, delay its onset, and prevent it from developing. Overview of disease progression The symptoms of Alzheimer's disease worsen over time, although the rate at which the disease progresses varies. On average, a person with Alzheimer's lives four to eight years after diagnosis, but can live as long as 20 years, depending on other factors. Changes in the brain related to Alzheimer's begin years before any signs of the disease. This time period, which can last for years, is referred to as preclinical Alzheimer's disease. Three different categories: May overlap Mild Alzheimer's disease (early-stage) In the early stages of Alzheimer's, a person may function independently. He or she may still drive, work and be part of social activities. Despite this, the person may feel as if he or she is having memory lapses, such as forgetting familiar words or the location of everyday objects. Friends, family or neighbors begin to notice difficulties. During a detailed medical interview, doctors may be able to detect problems in memory or concentration. Common difficulties include: Problems coming up with the right word or name Trouble remembering names when introduced to new people Having greater difficulty performing tasks in social or work settings Forgetting material that one has just read Losing or misplacing a valuable object Increasing trouble with planning or organizing Moderate Alzheimer's disease (middle-stage) is typically the longest stage and can last for many years. As the disease progresses, the person with Alzheimer's will require a greater level of care. You may notice the person with Alzheimer's confusing words, getting frustrated or angry, or acting in unexpected ways, such as refusing to bathe. Damage to nerve cells in the brain can make it difficult to express thoughts and perform routine tasks. At this point, symptoms will be noticeable to others and may include: Forgetfulness of events or about one's own personal history Feeling moody or withdrawn, especially in socially or mentally challenging situations Being unable to recall their own address or telephone number or the high school or college from which they graduated Confusion about where they are or what day it is The need for help choosing proper clothing for the season or the occasion Trouble controlling bladder and bowels in some individuals Changes in sleep patterns, such as sleeping during the day and becoming restless at night An increased risk of wandering and becoming lost Personality and behavioral changes, including suspiciousness and delusions or compulsive, repetitive behavior like hand-wringing or tissue shredding Severe Alzheimer's disease (late-stage) In the final stage of this disease, individuals lose the ability to respond to their environment, to carry on a conversation and, eventually, to control movement. They may still say words or phrases, but communicating pain becomes difficult. As memory and cognitive skills continue to worsen, personality changes may take place and individuals need extensive help with daily activities. Require full-time, around-the-clock assistance with daily personal care Lose awareness of recent experiences as well as of their surroundings Require high levels of assistance with daily activities and personal care Experience changes in physical abilities, including the ability to walk, sit and, eventually, swallow Have increasing difficulty communicating Become vulnerable to infections, especially pneumonia This type of dementia resembles Alzheimer's disease in that it also involves a progressive degeneration of brain cells that is irreversible. With this form of dementia, a person may have symptoms such as sudden onset of memory loss, behavior changes, or difficulties with speech and movement. Changes in behavior may include becoming either withdrawn or disinhibited (e.g., losing the ability to restrain one's behavior and actions). The person may lose interest in
Load more

Recommended publications
  • Psychogenic and Organic Amnesia. a Multidimensional Assessment of Clinical, Neuroradiological, Neuropsychological and Psychopathological Features
    Behavioural Neurology 18 (2007) 53–64 53 IOS Press Psychogenic and organic amnesia. A multidimensional assessment of clinical, neuroradiological, neuropsychological and psychopathological features Laura Serraa,∗, Lucia Faddaa,b, Ivana Buccionea, Carlo Caltagironea,b and Giovanni A. Carlesimoa,b aFondazione IRCCS Santa Lucia, Roma, Italy bClinica Neurologica, Universita` Tor Vergata, Roma, Italy Abstract. Psychogenic amnesia is a complex disorder characterised by a wide variety of symptoms. Consequently, in a number of cases it is difficult distinguish it from organic memory impairment. The present study reports a new case of global psychogenic amnesia compared with two patients with amnesia underlain by organic brain damage. Our aim was to identify features useful for distinguishing between psychogenic and organic forms of memory impairment. The findings show the usefulness of a multidimensional evaluation of clinical, neuroradiological, neuropsychological and psychopathological aspects, to provide convergent findings useful for differentiating the two forms of memory disorder. Keywords: Amnesia, psychogenic origin, organic origin 1. Introduction ness of the self – and a period of wandering. According to Kopelman [33], there are three main predisposing Psychogenic or dissociative amnesia (DSM-IV- factors for global psychogenic amnesia: i) a history of TR) [1] is a clinical syndrome characterised by a mem- transient, organic amnesia due to epilepsy [52], head ory disorder of nonorganic origin. Following Kopel- injury [4] or alcoholic blackouts [20]; ii) a history of man [31,33], psychogenic amnesia can either be sit- psychiatric disorders such as depressed mood, and iii) uation specific or global. Situation specific amnesia a severe precipitating stress, such as marital or emo- refers to memory loss for a particular incident or part tional discord [23], bereavement [49], financial prob- of an incident and can arise in a variety of circum- lems [23] or war [21,48].
    [Show full text]
  • What Is It Like to Be Confabulating?
    What is it like to be Confabulating? Sahba Besharati, Aikaterini Fotopoulou and Michael D. Kopelman Kings College London, Institute of Psychiatry, London UK Different kinds of confabulations may arise in neurological and psychiatric disorders. This chapter first offers conceptual distinctions between spontaneous and momentary (“provoked”) confabulations, as well as between these types of confabulation and other kinds of false memories. The chapter then reviews current explanatory theories, emphasizing that both neurocognitive and motivational factors account for the content of confabulations. We place particular emphasis on a general model of confabulation that considers cognitive dysfunctions in memory and executive functioning in parallel with social and emotional factors. It is argued that all these dimensions need to be taken into account for a phenomenologically rich description of confabulation. The role of the motivated content of confabulation and the subjective experience of the patient are particularly relevant in effective management and rehabilitation strategies. Finally, we discuss a case example in order to illustrate how seemingly meaningless false memories are actually meaningful if placed in the context of the patient’s own perspective and autobiographical memory. Key words: Confabulation; False memory; Motivation; Self; Rehabilitation. 1 Memory is often subject to errors of omission and commission such that recollection includes instances of forgetting, or distorting past experience. The study of pathological forms of exaggerated memory distortion has provided useful insights into the mechanisms of normal reconstructive remembering (Johnson, 1991; Kopelman, 1999; Schacter, Norman & Kotstall, 1998). An extreme form of pathological memory distortion is confabulation. Different variants of confabulation are found to arise in neurological and psychiatric disorders.
    [Show full text]
  • How the Brain and Memory Works 10
    Caring For A Loved One With Dementia 10 How the Brain and Memory Works Introduction The way our brain stores memories is a complex process across many areas of the brain. Luckily, memories are not all stored in one place. They are spread out across different brain regions, or lobes, and allow us to keep and recall memories even if one area of the brain is damaged. Although the brain’s process for storing memories is sometimes compared to a filing cabinet, the processes are extremely complex and still not fully understood. 2 Creating memories 3. Store information The human brain is made up of neurons. Neurons are nerve cells that talk to each other through a synapse- a connection This is the process of retaining the information in short term, or between cells that sends information. Neurons receive and more permanently in long term memory. An area of the brain carry information to the parts of the brain to process or store called the Hippocampus plays an important role in storing long information. The brain has approximately 100 billion nerve term memories. cells, give or take 15 billion. 4. Recall To create memories, the brain must accomplish the following processes: Memories that are frequently recalled become stronger than those accessed less frequently. The neurons linked to this 1. Encode information information create a neural pathway- a road to that memory. Think of it as walking along a path. The more frequently you This process allows something of interest to be stored in the walk on the same path, the more defined the trail becomes.
    [Show full text]
  • Primary and Secondary Prevention Interventions for Cognitive Decline
    2016 Primary and secondary prevention interventions for cognitive decline and dementia Overview of reviews Published by The Norwegian Institute of Public Health Section for evidence summaries in the Knowledge Centre Title Primary and secondary prevention interventions for cognitive decline and dementia Norwegian title Primær‐ og sekundærforebyggende tiltak for kognitiv svikt og demens Responsible Camilla Stoltenberg, direktør Authors Gerd M Flodgren, project leader, researcher, the Knowledge Centre Rigmor C Berg, Head of Unit, for Social Welfare Research at the Knowledge Centre ISBN 978‐82‐8082‐745‐6 Projectnumber 798 Type of publication Overview of reviews No of pages 69 (110 inklusiv vedlegg) Client Nasjonalforeningen for folkehelsen MeSH terms Alzheimer’s disease, dementia, cognition, cognitive impairment, cognitive disorders, memory complaints, primary prevention, secondary prevention Citation Flodgren GM, Berg RC. Primary and secondary prevention interventions for cognitive decline and dementia. [Primær‐ og sekundærforebyggende tiltak for kognitiv svikt og demens] Rapport −2016. Oslo: Folkehelseinstituttet, 2016. 2 Table of contents Table of contents TABLE OF CONTENTS 3 KEY MESSAGES 5 EXECUTIVE SUMMARY 6 Background 6 Objectives 6 Methods 6 Results 6 Discussion 8 Conclusions 8 HOVEDFUNN (NORSK) 9 SAMMENDRAG (NORSK) 10 Bakgrunn 10 Problemstillinger 10 Metoder 10 Resultat 10 Diskusjon 12 Konklusjon 12 PREFACE 13 OBJECTIVES 15 BACKGROUND 16 Description of the condition 16 How the interventions may work 18 Why is it important to do this
    [Show full text]
  • Effect of Phosphatidylserine Administration on Symptoms of Attention-Deficit/Hyperactivity Disorder in Children S
    AGRO SET_OTT_06.qxp 27-10-2006 10:14 Pagina 16 Effect of phosphatidylserine administration on symptoms of attention-deficit/hyperactivity disorder in children S. HIRAYAMA1*,Y. MASUDA2,R. RABELER3 *Corresponding author 1. Department of Early Childhood Education and Care, Kurashiki City College, 160 Hieda, Kurashikishi, Okayama, Japan 2. Kojima first High School, Okayama, Japan 3. Cargill Food Ingredients GmbH, Freising, Germany PURPOSE the emotional response in the frontal lobe, due to a problem of disinhibition (1). Disinhibition consists of disinhibition of To clarify whether the administration of phosphatidylserine attention (inattention) and that of behaviour (hyperactivity ("PS") can improve the attention-deficit ("AD") and and impulsiveness). hyperactivity disorder ("HD") symptoms in children. with AD/HD patients are classified into inattention-predominant Infant nutrition AD/HD. type, hyperactivity and impulsiveness -dominant type and mixed type. Each symptom causes problems in learning and relation between family members. Though the cause of STUDY DESIGN AND SUBJECTS disorders has yet to be identified (2), central stimulants (a type of psycho stimulant) are used in the treatment. These A pilot study in 15 AD/HD children 6 to 12 years old (including drugs can alleviate the AD/HD symptoms to some extent (3, 6 suspected to have AD/HD) who had rarely received 4). However, there is no consensus on the long term use of medication before. These 15 children took 200 mg/day of PS these drugs and adverse events (adverse reactions) may in a capsule every day for 2 months. The following items were occur during or years after the treatment (5). Accordingly, investigated at the start of study ("pre-study") and upon supplementary and substitute medication is frequently completion of study ("post-study): 1) AD/HD symptoms advised.
    [Show full text]
  • The Importance of Sleep in Fear Conditioning and Posttraumatic Stress Disorder
    Biological Psychiatry: Commentary CNNI The Importance of Sleep in Fear Conditioning and Posttraumatic Stress Disorder Robert Stickgold and Dara S. Manoach Abnormal sleep is a prominent feature of Axis I neuropsychia- fear and distress are extinguished. Based on a compelling tric disorders and is often included in their DSM-5 diagnostic body of work from human and rodent studies, fear extinction criteria. While often viewed as secondary, because these reflects not the erasure of the fear memory but the develop- disorders may themselves diminish sleep quality, there is ment of a new safety or “extinction memory” that inhibits the growing evidence that sleep disorders can aggravate, trigger, fear memory and its associated emotional response. and even cause a range of neuropsychiatric conditions. In this issue, Straus et al. (3 ) report that total sleep Moreover, as has been shown in major depression and deprivation can impair the retention of such extinction mem- attention-deficit/hyperactivity disorder, treating sleep can ories. In their study, healthy human participants in three improve symptoms, suggesting that disrupted sleep contri- groups successfully learned to associate a blue circle (condi- butes to the clinical syndrome and is an appropriate target for tioned stimulus) with the occurrence of an electric shock treatment. In addition to its effects on symptoms, sleep (unconditioned stimulus) during a fear acquisition session. disturbance, which is known to impair emotional regulation The following day, during extinction learning, the blue circle and cognition in otherwise healthy individuals, may contribute was repeatedly presented without the shock. The day after to or cause disabling cognitive deficits. For sleep to be a target that, extinction recall was tested by again repeatedly present- for treatment of symptoms and cognitive deficits in neurop- ing the blue circle without the shock.
    [Show full text]
  • Memory Dysfunction in Neurological Practice Andrew E Budson, Bruce H Price
    Downloaded from pn.bmj.com on 5 February 2007 42 Practical Neurology HOW TO UNDERSTAND IT Pract Neurol 2007; 7: 42–47 Memory dysfunction in neurological practice Andrew E Budson, Bruce H Price A E Budson Geriatric Research Educational Clinical Center, Edith Nourse Rogers Memorial Veterans Hospital, Bedford, MA; Boston University Alzheimer’s Disease Center, Boston University, Boston, MA; Division of Cognitive and Behavioral Neurology, Department of Neurology, Brigham and Women’s Hospital, Boston, MA; Harvard Medical School, Boston, MA, USA B H Price Department of Neurology, McLean Hospital, Belmont, MA and Harvard Medical School, Boston, MA, USA Correspondence to: Dr A E Budson Building 62, Room B30, Edith Nourse Rogers Memorial Veterans Hospital, 200 Springs Road, Bedford, MA 01730, USA; [email protected] Downloaded from pn.bmj.com on 5 February 2007 Budson, Price 43 omplaints of impaired memory are Episodic memory is the explicit and declarative among the most common symptoms reported to neurologists. Moreover, memory system that we all use to recall our C impairment of memory is one of the personal experience most disabling aspects of many neurological disorders, including neurodegenerative dis- eases, strokes, tumours, head trauma, collection of mental abilities that use hypoxia, cardiac surgery, malnutrition, atten- different systems within the brain. A memory tion deficit disorder, depression, anxiety, system is a way that the brain processes medication adverse effects, and just normal information in order to make it available for aging. This memory loss often impairs the use at a later time. Some systems are patient’s daily activities, profoundly affecting associated with conscious awareness (explicit) not just them but also their families.
    [Show full text]
  • The Three Amnesias
    The Three Amnesias Russell M. Bauer, Ph.D. Department of Clinical and Health Psychology College of Public Health and Health Professions Evelyn F. and William L. McKnight Brain Institute University of Florida PO Box 100165 HSC Gainesville, FL 32610-0165 USA Bauer, R.M. (in press). The Three Amnesias. In J. Morgan and J.E. Ricker (Eds.), Textbook of Clinical Neuropsychology. Philadelphia: Taylor & Francis/Psychology Press. The Three Amnesias - 2 During the past five decades, our understanding of memory and its disorders has increased dramatically. In 1950, very little was known about the localization of brain lesions causing amnesia. Despite a few clues in earlier literature, it came as a complete surprise in the early 1950’s that bilateral medial temporal resection caused amnesia. The importance of the thalamus in memory was hardly suspected until the 1970’s and the basal forebrain was an area virtually unknown to clinicians before the 1980’s. An animal model of the amnesic syndrome was not developed until the 1970’s. The famous case of Henry M. (H.M.), published by Scoville and Milner (1957), marked the beginning of what has been called the “golden age of memory”. Since that time, experimental analyses of amnesic patients, coupled with meticulous clinical description, pathological analysis, and, more recently, structural and functional imaging, has led to a clearer understanding of the nature and characteristics of the human amnesic syndrome. The amnesic syndrome does not affect all kinds of memory, and, conversely, memory disordered patients without full-blown amnesia (e.g., patients with frontal lesions) may have impairment in those cognitive processes that normally support remembering.
    [Show full text]
  • Disordered Recognition Memory: Recollective Confabulation
    cortex xxx (2013) 1e12 Available online at www.sciencedirect.com Journal homepage: www.elsevier.com/locate/cortex Special issue: Research report Disordered recognition memory: Recollective confabulation Chris J.A. Moulin* Laboratoire d’Etude de l’Apprentissage et du De´veloppement, CNRS UMR 5022, Universite´ de Bourgogne, Dijon, France article info abstract Article history: Recollective confabulation (RC) is encountered as a conviction that a present moment is a Received 31 January 2012 repetition of one experienced previously, combined with the retrieval of confabulated Reviewed 12 April 2012 specifics to support that assertion. It is often described as persistent de´ja` vu by family Revised 24 September 2012 members and caregivers. On formal testing, patients with RC tend to produce a very high Accepted 24 January 2013 level of false positive errors. In this paper, a new case series of 11 people with dementia or Published online xxx mild cognitive impairment (MCI) and with de´ja` vu-like experiences is presented. In two experiments the nature of the recognition memory deficit is explored. The results from Keywords: these two experiments suggest e contrary to our hypothesis in earlier published case re- Dementia ports e that recollection mechanisms are relatively spared in this group, and that patients De´ja` vu experience familiarity for non-presented items. The RC patients tended to be overconfident Reduplicative paramnesia in their assessment of recognition memory, and produce inaccurate assessments of their Familiarity performance. These findings are discussed with reference to delusions more generally, and Metacognition point to a combined memory and metacognitive deficit, possibly arising from damage to temporal and right frontal regions.
    [Show full text]
  • Nutrition and Brain Aging: Role of Fatty Acids with an Epidemiological Perspective
    THESIS AWARD Nutrition and brain aging: role of fatty acids with an epidemiological perspective Cecilia SAMIERI Abstract: In the absence of identified etiologic treatment for dementia, the potential Pascale BARBERGER-GATEAU preventive role of nutrition may offer an interesting perspective. The objective of the thesis of C. Samieri was to study the association between nutrition and brain aging in Inserm, U897, 1,796 subjects, aged 65 y or older, from the Bordeaux sample of the Three-City study, Equipe Epidemiologie de la nutrition with a particular emphasis on fatty acids. Considering the multidimensional nature of et des comportements alimentaires, nutritional data, several complementary strategies were used. At the global diet level, Universite Bordeaux Segalen, dietary patterns actually observed in the population were identified by exploratory Case 11, methods. Older subjects with a ‘‘healthy’’ pattern, who consumed more than 3.5 weekly 146 rue Leo-Saignat, servings of fish in men and more than 6 daily servings of fruits and vegetables in women, F-33076 Bordeaux cedex, showed a better cognitive and psychological health. Adherence to the Mediterranean France diet, measured according to a score-based confirmatory method, was associated with <[email protected]. slower global cognitive decline after 5 y of follow-up. At the nutrient biomarker level, fr> higher plasma eicosapentaenoic acid (EPA), a long-chain omega-3 fatty acid, was associated with a decreased dementia risk, and the omega-6-to-omega-3 fatty acids ratio to an increased risk, particularly in depressed subjects. EPA was also related to slower working memory decline in depressed subjects or in carriers of the e4 allele of the ApoE gene.
    [Show full text]
  • Memory Dysfunction
    The new england journal of medicine review article current concepts Memory Dysfunction Andrew E. Budson, M.D., and Bruce H. Price, M.D. From the Geriatric Research Education emory function is vulnerable to a variety of pathologic Clinical Center, Edith Nourse Rogers Me- processes including neurodegenerative diseases, strokes, tumors, head trau- morial Veterans Hospital, Bedford, Mass., m ma, hypoxia, cardiac surgery, malnutrition, attention-deficit disorder, de- the Department of Neurology, Boston Uni- 1,2 versity, Boston, and the Department of pression, anxiety, the side effects of medication, and normal aging. As such, memory Neurology, Division of Cognitive and Be- impairment is commonly seen by physicians in multiple disciplines including neurol- havioral Neurology, Brigham and Wom- en’s Hospital, Boston (A.E.B.); and Har- ogy, psychiatry, medicine, and surgery. Memory loss is often the most disabling feature vard Medical School, Boston, and McLean of many disorders, impairing the normal daily activities of the patients and profoundly Hospital, Belmont, Mass. (B.H.P.). Address affecting their families. reprint requests to Dr. Budson at GRECC, Bldg. 62, Rm. B30, Edith Nourse Rogers Some perceptions about memory, such as the concepts of “short-term” and “long- Memorial Veterans Hospital, 200 Springs term,” have given way to a more refined understanding and improved classification Rd., Bedford, MA 01730, or at abudson@ systems. These changes result from neuropsychological studies of patients with focal partners.org. brain lesions, neuroanatomical studies in humans and animals, experiments in animals, N Engl J Med 2005;352:692-9. positron-emission tomography, functional magnetic resonance imaging, and event- Copyright © 2005 Massachusetts Medical Society.
    [Show full text]
  • Is Sleep Disruption a Cause Or Consequence of Alzheimer's
    International Journal of Molecular Sciences Review Is Sleep Disruption a Cause or Consequence of Alzheimer’s Disease? Reviewing Its Possible Role as a Biomarker Maria-Angeles Lloret 1, Ana Cervera-Ferri 2,* , Mariana Nepomuceno 3, Paloma Monllor 3 , Daniel Esteve 3 and Ana Lloret 3 1 Department of Clinical Neurophysiology, University Clinic Hospital of Valencia, Avda. Blasco Ibanez, 17, 46010 Valencia, Spain; [email protected] 2 Department of Human Anatomy and Embryology, Faculty of Medicine, University of Valencia, Avda. Blasco Ibanez, 15, 46010 Valencia, Spain 3 Department of Physiology, Faculty of Medicine, University of Valencia, Health Research Institute INCLIVA, Avda. Blasco Ibanez, 15, 46010 Valencia, Spain; [email protected] (M.N.); [email protected] (P.M.); [email protected] (D.E.); [email protected] (A.L.) * Correspondence: [email protected]; Tel.: +34-9639-835-07 Received: 27 December 2019; Accepted: 8 February 2020; Published: 10 February 2020 Abstract: In recent years, the idea that sleep is critical for cognitive processing has gained strength. Alzheimer’s disease (AD) is the most common form of dementia worldwide and presents a high prevalence of sleep disturbances. However, it is difficult to establish causal relations, since a vicious circle emerges between different aspects of the disease. Nowadays, we know that sleep is crucial to consolidate memory and to remove the excess of beta-amyloid and hyperphosphorilated tau accumulated in AD patients’ brains. In this review, we discuss how sleep disturbances often precede in years some pathological traits, as well as cognitive decline, in AD. We describe the relevance of sleep to memory consolidation, focusing on changes in sleep patterns in AD in contrast to normal aging.
    [Show full text]