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Term paper on alzhiemers

Current day supplements and medications are failing miserably. Due to the advancements of modern health care people will now live longer, hence leading to an increase in the number of people with AD. According to Healy, there has been 5.

It currently afflicts about 4 million Americans and is the fourth leading cause of death in the United States. AD is characterized by decreasing cognitive function, memory impairment, and neuronal loss. There are complications with detecting and diagnosing AD in I performed basic laboratory procedures and often worked independently to develop our experiments.

Investing three years in They do not want to think or do something about it. Nobody can blame them. They have just been handed a life sentence of doubt. When do they Be it due to life style changes or due to inheritance… the number of cases in this domain of medicine are on constant rise. Over the years, adults have continually led busy lives. In the advent of technology, some find themselves with increased business opportunities and by extension, more responsibilities.

Between juggling work and rest, it has become increasingly difficult to set aside time for regular fitness activities, leading Alzheimer disease is a intelligence disease in which our understanding cells break down to connect all otherfeel difficulty speaking and cause confusion when a task performed by the patient because for the reason that a greater quantity of protein which is rubbery and twisted protein The right choice of menu components allows you to activate memory, increase the ability to concentrate, has a positive effect on brain activity.

Patients with a-MCI present with memory deficits greater than would be expected based on age and education; however functional abilities remain relatively preserved and independence intact [ 8 ]. Regardless of this variation, annual conversion rate of those with MCI is far greater than the baseline incidence rate [ 4 ].

By identifying AD in its early stages, recommendations for the most current or efficacious interventions can be made, with the goal of slowing disease progression. Also, implementing caregiver interventions, such as referral to support groups, psychoeducation, and counseling or psychotherapy [ 9 ], can also assist patients and their families. Over the past 20 years, researchers have made great strides in the areas of AD, with respect to etiology, prevention, diagnosis, and treatment.

However, while the exact etiology still remains a mystery, definitive diagnosis can only be made postmortem, and current treatments can only slow disease progression temporarily. Late-onset AD, the most common form of the disease, occurs in individuals over the age of While researchers have not found any causal determinants for this particular type, they have identified several associated risk factors, including age, female gender, low educational and occupational attainment, prior head injury, sleep disorders e.

Depending on the combination of APOE alleles that an individual possesses, he or she may have a three to eight times higher risk. The much rarer, early-onset from of AD, occurring in fewer than five percent of individuals with the disease, typically affects individuals between the ages of approximately thirty and sixty. This form of the disease is caused by one of three identified genetic mutations that are passed down in an autosomal dominant fashion among families: the amyloid precursor protein APP , presenilin-1, and presenilin-2 genes [ 4 , 10 ].

AD is characterized by progressive degenerative neuronal changes, with associated global deterioration of cognitive and personality functioning. This pathological sequence preferentially begins in the medial temporal lobe structures responsible for memory the entorhinal cortex and hippocampus and then progresses to the frontal, temporal, and parietal areas, with relative sparing of the motor and sensory cortical regions and subcortical regions [ 11 ].

NFTs are composed of an abnormal form of the intraneuronal protein tau, which normally plays a role in structural support and cellular communication. The accumulation of NFTs occurs in a hierarchical pattern, beginning primarily in the medial temporal lobe especially, the entorhinal cortex , gradually progressing into the limbic system hippocampus and amygdala , and eventually spreading throughout the neocortex [ 4 , 11 , 15 ].

There is evidence that the presence of both amyloid plaques and NFTs is required for AD to develop [ 8 ]. Researchers continue to search for tools that can offer the same degree of diagnostic certainty during life that postmortem brain tissue examinations offer. There are currently five biomarkers which show the most promise as indicators of AD pathology organized into two categories: biomarkers of beta-amyloid accumulation and biomarkers of neuronal degeneration or injury [ 16 ].

The accumulation of beta-amyloid can be detected through the use of radioactive tracers in conjunction with positron emission tomography PET imaging [ 17 ], as well as through the analysis of beta-amyloid levels in the cerebrospinal fluid CSF [ 18 ]. Analysis of CSF levels of tau has also been found to indicate neuronal degeneration associated with NFT accumulation [ 8 , 18 ].

Fluorodeoxyglucose- FDG- PET imaging can be employed to detect hypometabolism in the temporoparietal region, which has been shown to effectively differentiate AD from normal controls [ 19 ]. Finally, structural magnetic resonance imaging MRI can be used to detect the characteristic pattern of pronounced atrophy in the medial temporal lobes that often occurs in mild to moderate AD [ 20 ].

While biomarker research holds promise for early detection and diagnosis of AD, standardized guidelines are still being developed for determining cut-points for diagnosis [ 8 ]. Thus, the use of biomarker data is currently indicated primarily for research purposes. Newly approved amyloid imaging techniques via PET scan are beginning to be used in order to supplement the results of other diagnostic evaluations.

It is imperative for clinicians to familiarize themselves with these revised criteria, listed within the Neurocognitive Disorders section, as the criteria contained in the prior DSM-IV-TR are not reflective of the current state of the AD literature [ 21 ]. The initial presentation of AD typically involves anterograde amnesia resulting from progressive declines in episodic memory. Specific memory tests may reveal deficits in the encoding and consolidating of new information into long term memory as evidenced by rapid forgetting after a time delay and lack of improvement even when recognition cues are provided.

On episodic memory tasks, AD patients commonly commit more errors of intrusion and perseveration, have difficulty employing semantic encoding tactics, and demonstrate less of a primacy effect when compared to normal elderly individuals [ 3 , 5 , 23 ]. As memory impairment begets functional decline, some of the first overt signs of AD often noted by family members include repeating oneself in conversations, misplacing items , becoming lost while driving familiar routes , burning meals while cooking, and difficulty managing finances [ 4 , 24 ].

With regard to remote memory, a pattern emerges in the early stages of the disease in which older memories are relatively spared, while those from the more recent past are lost [ 5 , 23 ]. Deficits in semantic memory and language may become evident early in the course of AD, as well.

Impairment may be detected on tests of verbal fluency, with the tendency to perform relatively worse on tasks requiring generation of words from a given category versus generation of words that begin with a particular letter of the alphabet. Patients are unable to employ clustering strategies to boost their performances and are also unaided by category retrieval cues [ 3 , 23 ]. Given that AD leads to a loss of semantic knowledge, the failure to demonstrate semantic knowledge for a particular item or concept has been shown to be consistent across test methods [ 3 ].

Poor performance is also typically seen on confrontation naming tests and semantic categorization i. Language discourse becomes increasingly filled with circumlocutions and overlearned phrases, accompanied by diminished meaning and spontaneity [ 23 ]. Decline in executive functioning can be seen on tests of complex problem solving, working memory, mental flexibility, and sequencing; deficits in these areas may be detected relatively early on tests such as the Tower of London puzzle, Porteus Maze task, Trail-Making Test, and Wisconsin Card Sorting Task and are implicated in the decline of instrumental activities of daily living IADLs.

Tests of immediate attention span and focus, such as digit span and mental control, may remain intact until later in the disease progression [ 3 , 5 , 23 ]. Visuospatial functioning tends not to be a prominent early feature of AD, but instead it regresses over the course of the disease [ 5 ].

In particular, visuoconstructional deficits may be apparent on the Clock Drawing task and on complex copying tasks using drawing or blocks [ 23 , 24 ]. Additionally, visuoperceptual and visual orientation abilities may become disturbed over time [ 5 ]. While extrapyramidal motor signs are more prominent in the latter stages of AD, patients may show deficits in ideomotor skilled movement to verbal command or imitation and ideational performing a planned series of motor tasks to achieve a goal praxis, even in the early stages of the disease [ 24 ].

This has implications for their ability to independently perform daily living tasks [ 23 ]. Determining the primary cause of cognitive decline can be challenging, given the common comorbidity of cerebrovascular disease, Lewy body disease, and AD [ 6 , 8 ]. Additionally, temporal conditions, such as delirium, depression, anxiety, metabolic disorders, vitamin deficiencies, normal pressure hydrocephalus NPH , and adverse reactions to medication, may resemble AD particularly in individuals who are young, newly symptomatic or whose symptoms are mild [ 24 ].

Neuropsychological testing can contribute to differentiating a true dementia process from a pseudo-dementia, as well as distinguishing between different forms of dementia. However, there are times when patients meet the diagnostic criteria for AD, and have a comorbid condition that may be contributing to cognitive impairment, thus causing a mixed dementia. The NIA-AA criteria differentiate between probable and possible AD and designate patients with mixed dementias to the latter category [ 16 ].

Table 1 offers a schematic for diagnostic guidance when evaluating a patient for dementia. Generally, when a clinician suspects changes in mental status, a screening test is performed to assess global cognitive abilities. This global assessment tool measures orientation to time and place, word recall, language abilities, attention and calculation, and visuospatial skills. The MMSE yields a perfect score of 30, with cut-off points between 24 and 26 suggesting dementia [ 25 ].

Age and education adjustments should be utilized for MMSE scoring, as performance may be affected by demographic factors, particularly education [ 25 ]. Temporal orientation and factual understanding of current events may be problematic even in early AD, which may be revealed by the MMSE.

However, the MoCA includes more difficult tasks, making it more sensitive in differentiating normal cognition from mild cognitive impairment. An appropriate set of medical tests i. The neuropsychologist should utilize a battery of assessment measures that are sensitive to the cognitive deficits seen in AD and capable of distinguishing between age-related cognitive decline, MCI, AD, and other forms of dementia.

Additional evidence of episodic memory impairment may be gathered from word list memory tasks, which can help identify deficits in encoding, storage, and retrieval. Combined visuoconstructional and visual memory tasks may be used which require the patient to copy shapes and then to recall those shapes after a delay, both from memory and with recognition cues.

A diverse range of skills may be assessed by administering a Clock Drawing task, including planning, visual attention, spatial orientation, and graphomotor control [ 28 ]. Finally, since many patients with dementia have never undergone previous neuropsychological assessment, an estimate of premorbid IQ may be obtained by administering a word list reading task, such as the Wechsler Test of Adult Reading WTAR. Ability to perform basic activities of daily living BADLs must also be examined e.

A global rating of dementia severity is calculated, along with the CDR sum of boxes score CDR-SB , which allows for a detailed, continuous measure of the subtle differences between levels of impairment and has been found to be able to discriminate MCI from early AD [ 30 ]. In the management of AD, a multimodal approach is warranted. Table 2 provides an outline of eight intervention areas to address. These interventions include pharmaceutical, nutraceutical, medical foods, neurophysiological, physical health, cognitive, behavioral, and future planning.

At this time, there are no established therapeutic interventions that have been found which can stop the progression or reverse the neural deterioration caused by AD. However, there are four FDA approved pharmaceuticals currently prescribed which temporarily halt or slow cognitive, functional, and behavioral decline. Three of the medications are cholinesterase inhibitors, namely, Donepezil, Rivastigmine, and Galantamine, which work to increase the levels of acetylcholine, a neurotransmitter in the brain that is involved in learning and memory.

The cholinesterase inhibitors are indicated for the treatment of individuals in the mild to moderate stages of AD [ 31 , 32 ]. Memantine works by increasing the levels of glutamate, another neurotransmitter implicated in learning and memory.

This drug is indicated for the treatment of moderate to severe AD. There is also evidence that Memantine may provide added benefits for individuals with AD who are already taking Donepezil [ 33 ]. Overall, the benefits of AD drugs are limited, as they are effective for approximately one year and in only about half of individuals to whom they are prescribed [ 31 ].

Currently, there are no other evidence-supported treatments for AD, however ongoing research aims to find disease-modifying treatments. Recent breakthroughs include results from a phase II clinical trial of IVIG, an immunotherapy agent, which was found to stabilize cognition and functioning, in a small sample of AD patients, for three years [ 35 ].

Additionally, Alpha GPC, phosphatidylserine, Huperzine A, and choline show promise as nutraceutical agents for enhancing cognitive performance and slowing cognitive decline. Alpha GPC, also known as L-Alpha Glycerylphosphorylcholine, a naturally occurring form of choline, acts as a parasympathomimetic acetylcholine precursor and has shown promise in improving cognitive symptoms related to AD, vascular dementia, and multi-infarct dementia.

Phosphatidylserine is a widely abundant anionic phospholipid in the human body and has been shown to improve age-related cognitive changes. Huperzine A a natural cholinesterase inhibitor has been linked to improved memory performance in elderly people with benign forgetfulness, as well as patients with AD and vascular dementia. Cholinesterase inhibitors have been shown to have neuroprotective properties in patients with mild [ 37 ] as well as moderate-to-advanced AD [ 38 ].

Recently, there is the development of medical foods that are thought to have some promise in improving mental status: Axona, CerefolinNAC, and Souvenaid [ 39 ]. Each works via a different mechanism of action, and all are prescriptive supplements.

However, Souvenaid is not currently available for use in the USA. The application of translational models, such as through animal and cell research, has helped identify certain processes and elements that may deter the neuropathogenetic progression of AD [ 40 ].

Research has begun to explore nonpharmaceutical interventions through translational models that may reduce toxins and prevent cell loss including apoptosis. In other words, once applications of interventions on animals or cells are deemed successful, they can be translated or applied to human participants. Laser light therapy is one such intervention, and animal studies using infrared light treatment have documented positive results in mice with traumatic brain injury [ 41 ]. Stimulation of human mitochondrial processes and cell proliferation due to laser irradiation have also been demonstrated [ 42 ].

Ultimately, the most successful model of treatment for AD will likely include early detection and control of physical factors diabetes, hypertension, hyperlipidemia , followed by application of multifaceted, disease-modifying interventions to prevent the early and continued loss of neurons and to reduce the toxins that result in further cell deterioration [ 34 ].

Changes in personality and behavioral disturbances affect most patients with AD and can range from disinterest and apathy to agitation, affective disinhibition, and restlessness. Specific behaviors can be difficult to manage, such as aimless wandering, emotional outbursts, stubbornness, paranoia, hallucinations, and depression. Behavioral interventions can complement medication management and include creating a structured, safe, low stress environment, promoting regular sleep and eating habits, minimizing unexpected changes, and employing redirection and distraction [ 44 ].

Since ADLs such as self-care, personal hygiene, and dressing tend to worsen with the progression of the disease, patients with advanced AD require a greater level of caretaker commitment. Caregivers should be alerted to the challenges they will face as the disease progresses and be provided with appropriate coping skills, training, and interventions, through support groups and individual therapy.

When at-home care is no longer an option, families will face the decision of placing their loved one in an assisted-living facility. Caregivers should not make this choice in isolation; mental health practitioners can help provide information and allow for the processing of the emotional weight of the decision and any mixed emotions of guilt, hurt, anger, and loss. Considering that IADLs also decrease in AD, issues such as management of medical decisions, financial affairs, and cessation of driving will also emerge.

When the patient is no longer able to perform basic math calculations, securing a financial advisor to oversee assets is often recommended. When insight becomes limited and memory is significantly compromised, medical decision-making and medication management may also need to be shifted to the hands of a caregiver.

Pursuit of guardianship and capacity evaluations are not uncommon, especially when estate and legal issues need to be addressed. AD is believed to emerge as the result of a complicated interplay of genetic, environmental, and lifestyle factors. Due to this complex process, it is difficult to pinpoint a definitive prevention strategy; however, there is mounting evidence that modifying certain lifestyle factors may lower the risk of developing AD [ 45 ].

There is data to suggest that aerobic exercise may improve cognition [ 5 ] and serve a protective role in healthy older adults by inducing neuroplasticity in areas of the brain associated with episodic memory [ 46 ]. Additionally, physical activity has been found to improve scores on cognitive and functional measures in individuals with MCI and dementia [ 47 ].

As cardiovascular risk factors, such as diabetes, hypercholesterolemia, and hypertension, have been found to be associated with AD, it is hypothesized that preventing or managing these conditions may decrease the likelihood of developing AD [ 45 ]. Research has shown that healthy eating, specifically adhering to a Mediterranean diet, correlated with both a lower risk of cardiovascular disease and AD [ 48 ].

While there is ongoing research investigating the effects of various vitamins and dietary supplements in preventing AD, as of yet, clinical trials have not been able to prove their effectiveness [ 45 ].

In addition to maintaining physical health, engagement in cognitively stimulating as well as social activities seems important for promoting healthy brain functioning. Investigators have found that older adults who frequently participate in mentally demanding activities i. Formal interventions involving cognitive training and time spent engaging in physical, cognitive, and social activities have been associated with a lower risk of developing dementia in healthy older adults, especially for individuals who participated in two or three of these endeavors [ 50 ].

Fortunately, research geared towards enhancing disease-modifying and preventative interventions is gaining momentum. Neuropsychological evaluation continues to play a critical role in early detection and differential diagnosis of normal aging versus MCI and the various types of dementia. Health care practitioners can offer strategies and support for patients, as well as their families and caregivers, related to the disruptions that AD has upon daily functioning.

As researchers continue to make strides in our understanding of the disease, it is imperative for clinicians to remain abreast of the dementia literature in order to assist patients in obtaining the most effective care. Jonathan Fellus has been a consultant on the speakers bureau of and holds stock in the company Avanir. The authors have no conflict of interests related to this article.

DeFina et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Article of the Year Award: Outstanding research contributions of , as selected by our Chief Editors. Read the winning articles. Journal overview. Special Issues. Academic Editor: Michelle M. Received 05 Jun Accepted 22 Jul Published 04 Sep Abstract Of the approximately 6.

Introduction Approximately 6. Epidemiology and Pathogenesis Over the past 20 years, researchers have made great strides in the areas of AD, with respect to etiology, prevention, diagnosis, and treatment.

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Between juggling work and rest, it has become increasingly difficult to set aside time for regular fitness activities, leading Alzheimer disease is a intelligence disease in which our understanding cells break down to connect all otherfeel difficulty speaking and cause confusion when a task performed by the patient because for the reason that a greater quantity of protein which is rubbery and twisted protein The right choice of menu components allows you to activate memory, increase the ability to concentrate, has a positive effect on brain activity.

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Term paper on alzhiemers Please review our privacy policy. Are empirically derived subtypes of mild cognitive impairment consistent term paper on alzhiemers conventional subtypes? Bondi, D. Parker, Ian B. Atiya, B. At this time, there are no established therapeutic interventions that have been found which can stop the progression or reverse the neural deterioration caused by AD. Novel interventions, including medications, natural supplements, and behavioral techniques, are constantly appearing in the literature.
Mla research papers fill in Dickson et al. Salmon serves as a consultant for Bristol-Myers Squibb. Irwin, James B. Trojanowski, H. A major tragedy was averted after we had to call the police and she was discovered after she backed her car into the side of her home.
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Term paper on alzhiemers One of the great challenges faced by neuropsychologists over the past 50 years is to understand the cognitive and behavioral manifestations of dementia and their relationship to underlying brain pathology. She once got lost and we had to go out searching for her. The right choice argument papers examples menu components allows you to activate memory, increase the ability to concentrate, has a positive effect on brain activity. The s continued these efforts and began to identify the specific cognitive mechanisms affected by various neuropathologic substrates. Impaired recall and the term paper on alzhiemers disturbance in presenile dementia.
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Preclinical AD is the period during which early AD brain changes are present but cognitive symptoms have not yet manifest. The presence of AD brain Authors: Sayeh Bayat, Ganesh M. Babulal, Suzanne E. Schindler, Anne M. Fagan, John C. Morris, Alex Mihailidis and Catherine M. Published on: 14 June Although increasing evidence supports this opinion, the underlying mechanisms are still unknown.

Na, Juhee Chin, Liana G. Content type: Mini review. Published on: 12 June This situation urges t Authors: Nian Xiong, Martin R. Content type: Commentary. However, the underlying mechanisms responsible for this complication remain unclear. A better understanding Pieper, Lara Jehi and Feixiong Cheng. Published on: 9 June Language impairment is an important marker of neurodegenerative disorders. Despite this, there is no universal system of terminology used to describe these impairments and large inter-rater variability can exi Kaufman and Fariya Mostafa.

Published on: 4 June Subjective cognitive decline, perceived worsening of cognitive ability without apparent performance issues on clinical assessment, may be an important precursor to dementia. While previous cross-sectional rese Authors: Raymond P. Viviano and Jessica S. Published on: 31 May As bl Published on: 27 May In animal models, it mediates impaired synaptic dysfunction in the hippocampus, causing memory deficits, and is invol Authors: Niels D.

Prins, John E. Alam and Philip Scheltens. Some SCD individuals however may suffer from very e Published on: 25 May Hippocampus is one of the involved regions and its atrophy is a widely used biomarker for AD diagnosis. We have recently developed Den Published on: 24 May Brown adipose tissue BAT is the main thermogenic driver in mammals and its stimulation, thr Published on: 21 May Authors: Laura E. Donovan, Eric B. Dammer, Duc M. Duong, John J. Hanfelt, Allan I.

Levey, Nicholas T. Seyfried and James J. Content type: Correction. Published on: 18 May Neurofilament light in serum sNfL is a biomarker for axonal damage with elevated levels in many neurological disorders, including neurodegenerative dementias. Since within-group variation of sNfL is large an Authors: E. Willemse, P. Scheltens, C. Teunissen and E. Using antemortem MRI and pathologic Authors: L. Wisse, R. Xie, S.

Das, C. McMillan, J. Trojanowski, M. Grossman, E. Lee, D. Irwin, P. Yushkevich and D. Published on: 14 May Authors: Sarah K. Royse, Davneet S. Minhas, Brian J. Jagust and Susan M. Published on: 10 May Content type: Viewpoint. Authors: Manfred Berres, Andreas U. Published on: 7 May The relationship between cancer and dementia is triggering growing research interest.

Several preclinical studies have provided the biological rationale for the repurposing of specific anticancer agents in Alz Content type: Review. Published on: 5 May Alzheimer disease AD is a progressive neurodegenerative disorder affecting the elderly with a prevalence of 7. Sex-related patterns have been reported in prognosis, biomarker stat Strong evidence supports that neuroinflammatory changes such as Published on: 4 May Identifying novel therapeutic targets is crucial for the successful development of drugs.

However, the cost to experimentally identify therapeutic targets is huge and only approximately genes are targets f Published on: 3 May In view of reported associations between high adiposity, particularly in midlife and late-life dementia risk, we aimed to determine associations between body mass index BMI , and BMI changes across adulthood Authors: Christopher A.

Lane, Josephine Barnes, Jennifer M. Nicholas, John W. Baker, Carole H. Sudre, David M. Cash, Thomas D. Parker, Ian B. Published on: 30 April The diagnosis of AD is often Published on: 29 April Remote monitoring technologies RM Published on: 23 April An amendment to this paper has been published and can be accessed via the original article. Published on: 22 April The cholinergic system and M 1 receptor remain an important target for symptomatic treatment of cognitive dysfunction.

The selective M 1 receptor partial agonist HTL is under development for the symptomatic Hart, Erica S. Rather than using a single memory test, a diagnosis of MCI is established on the basis of scores achieved on multiple objective neuropsychological tests that assess a range of cognitive domains without reference to subjective complaints or clinical judgment. This actuarial method was shown to produce greater diagnostic stability than the conventional method i.

Over the past 20 years great progress was made in identifying in vivo biological markers of AD. Klunk and colleagues see Mathis et al. All of these biomarkers have greatly increased the accuracy with which AD pathology in the brain can be detected before the onset of cognitive symptoms, and improved the ability to differentiate AD from other pathologies that lead to dementia. In the current decade, several large-scale longitudinal studies have examined the relationship between various AD biomarkers and the development of cognitive decline and dementia e.

Based on results from these studies, Jack and colleagues proposed a hypothetical model of dynamic biomarker changes in the development of AD. Their model, consistent with the amyloid cascade hypothesis , proposed that amyloid deposition related to abnormal processing of the amyloid precursor protein i.

This in turn leads to tangle-mediated neuronal injury and neurodegeneration, which then produces cognitive and functional impairment see Jack et al. Many biomarker studies align with this temporal sequence of pathophysiologic changes, particularly in early-onset autosomal dominant mutation carriers e.

The hypothesis also provided the framework for revised diagnostic criteria for AD McKhann et al. Despite its wide influence, there is increasing evidence that calls the amyloid cascade hypothesis into question, especially with regard to its invariant temporal sequence of pathological events Drachman, Axonal injury Ryan et al. In addition, a growing number of studies have shown that cognitive measures can be as sensitive as physical biomarkers in predicting progression to dementia Gomar et al.

Taken together, these findings strongly suggest that the neurodegeneration of AD may not depend upon prior amyloidosis Knopman et al. Jack, Knopman, et al. Our prior work Edmonds, Delano-Wood, Galasko, et al.

We have shown that cognitively normal individuals who later progressed to MCI or AD, and had only one abnormal biomarker at baseline, were most likely to have neurodegeneration i. In fact, neurodegeneration in isolation was 2. Jack, Bennett, and colleagues have recently acknowledged these and similar findings and proposed a more descriptive classification scheme for AD biomarkers that is agnostic to the temporal ordering of mechanisms underlying AD pathogenesis.

Amyloid plaque pathology, in contrast, accumulates more diffusely across neocortex. This theory was recently updated to suggest that the pathogenic process actually starts with the formation of pretangle material in the lower brainstem with the first visible pathologic changes occurring in the locus coeruleus Braak et al. Tangle pathology then spreads possibly through cell-to-cell propagation; Iba et al. It is postulated that this begins well before amyloidosis. Braak and Del Tredici proposed that the initial tau pathology in locus coeruleus and its axonal projections may not result in outright neuronal death, but may restrict neuronal function.

Critics of the continuum theory argue that tau aggregation confined to brainstem structures and MTL, in the context of little to no amyloid deposition, should be considered an independent pathological process that is not integral to the developmental continuum of sporadic AD. In this view, the pathological diagnosis of AD requires the presence of amyloid pathology. Braak and Del Tredici counter this argument by suggesting that amyloid plaques may develop after neurofibrillary tangle pathology develops in sites associated with AD e.

This is evident in the adoption of biomarker staging systems that are agnostic to the temporal order of their occurrence e. This new understanding of AD may drive fundamental shifts in biomarker strategies, drug discovery, and therapeutics.

Neuropsychology has played a critical role in characterizing the cognitive changes associated with AD and related dementing disorders. Recent advances in AD biomarker development will alter this role. Increasingly, diagnosticians and investigators will be asked to use an array of available biomarkers to identify the neuropathologic determinants underlying cognitive changes within a given individual, and to detect neuropathology in its earliest stages before the onset of significant cognitive change.

That is not to say, however, that neuropsychology will cease to play an important role in dementia assessment and research. These functions will likely be enhanced by integrating biomarker information into assessments. Such pathological heterogeneity leads to neuropsychological heterogeneity, making dementia characterization and differential diagnosis more difficult.

Nelson et al. Panel a is the schematic representation of the prevailing view of Alzheimer neuropathology by age, whereas panel b depicts distinct brain diseases other than AD that may contribute to cognitive impairment in late life adapted from Nelson et al. In the future, a precision medicine approach will allow multiple biomarkers to target distinct pathologies to show which pathologies are present, a genetic analysis will allow polygenic risk for various disorders to be assessed, and neuropsychological assessment will identify distinct patterns of deficits that reflect the differential impact of distinct pathologies on the dementia syndrome.

Movement toward this goal is illustrated in a recent study which showed that individuals diagnosed as amnestic MCI in the ADNI cohort had great heterogeneity in the pattern of cognitive deficits they exhibited and that their deficits coincided well with specific regions of cortical thinning on neuroimaging see Figure 7 ; Edmonds et al.

These results demonstrate the potential utility of a combination of neuropsychological assessment and neuroimaging biomarkers to help explain a heterogeneous presentation of prodromal AD. Regional cortical thickness maps of the left and right lateral and medial pial surfaces for each neuropsychological MCI subtype relative to normal control NC participants Edmonds et al.

Their maps show no areas of cortical thinning relative to the NC group, suggesting they are false-positive diagnostic errors. Neuropathological heterogeneity in AD could also have important implications for future therapeutic approaches to the disease. In an equipotential model of AD, other aspects of AD related pathology may already exist, continue to develop, and adversely affect cognition even if amyloid pathology is removed.

If patients in anti-amyloid trials are positive for significant levels of amyloid, the anti-amyloid agent engages and clears amyloid, yet there is no clinical or cognitive benefit, it is reasonable to presume that pathology other than amyloid needs to be targeted. Since tau pathology is more firmly associated with clinical and cognitive decline than is amyloid pathology, and may accumulate in susceptible regions earlier than that of amyloid, tau-altering pharmacologic interventions would seem worthwhile.

Specific therapeutics may also be needed for other underlying pathologies e. Such a framework would also be accommodative of the specter of multiple biomarker abnormalities occurring concurrently. By joining forces across disciplines and assembling the most certain and important facts, investigators can launch new initiatives not previously imagined.

Salmon serves as a consultant for Bristol-Myers Squibb. Bondi serves as a consultant for Novartis and Eisai and receives royalties from Oxford University Press. The other authors report no disclosures. National Center for Biotechnology Information , U. J Int Neuropsychol Soc. Author manuscript; available in PMC Feb Mark W. Bondi , 1, 2 Emily C. Edmonds , 1, 2 and David P. Salmon 3. Emily C. David P. Author information Copyright and License information Disclaimer.

Correspondence and reprint requests to: Mark W. Copyright notice. The publisher's final edited version of this article is available at J Int Neuropsychol Soc. See other articles in PMC that cite the published article. Abstract Although dementia has been described in ancient texts over many centuries e.

Open in a separate window. Photographs of Alois Alzheimer left and his patient Auguste Deter right. Footnotes The other authors report no disclosures. Journal of Neurology, Neurosurgery, and Psychiatry. Diagnostic and Statistical Manual of Mental Disorders. Task force on nomenclature and statistics. The New England Journal of Medicine. Alzheimer disease. The association between quantitative measures of dementia and of senile changes in the cerebral grey matter of elderly subjects.

British Journal of Psychiatry. Neuropsychological criteria for mild cognitive impairment improves diagnostic precision, biomarker associations, and prediction of progression. Utility of a modified version of the Wisconsin Card Sorting Test in the detection of dementia of the Alzheimer type. Clinical Neuropsychologist. Psychology and Aging. Neuropathological staging of Alzheimer-related changes.

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Alzheimer's Disease 2021: Hot Topics in Disease Prevention and Clinical Trials

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Alzheimer's Disease: Research Advances and Medical Reality National Bureau of Economic Research Working Paper. #, April 29 Alzheimer's. The publisher's final edited version of this article is available drawn by Alzheimer from his paper entitled “Über eigenartige. Contributors, NIA-AA Research Framework: Toward a biological definition of Alzheimer's disease. Alzheimers Dement. 14, – ().