Alzheimer’s Disease: Past, Present, and Future
Open accessAbstract
Although dementia has been described in ancient texts over many centuries (e.g., “Be kind to your father, even if his mind fail him.” – Old Testament: Sirach 3:12), our knowledge of its underlying causes is little more than a century old. Alzheimer published his now famous case study only 110 years ago, and our modern understanding of the disease that bears his name, and its neuropsychological consequences, really only began to accelerate in the 1980s. Since then we have witnessed an explosion of basic and translational research into the causes, characterizations, and possible treatments for Alzheimer’s disease (AD) and other dementias. We review this lineage of work beginning with Alzheimer’s own writings and drawings, then jump to the modern era beginning in the 1970s and early 1980s and provide a sampling of neuropsychological and other contextual work from each ensuing decade. During the 1980s our field began its foundational studies of profiling the neuropsychological deficits associated with AD and its differentiation from other dementias (e.g., cortical vs. subcortical dementias). The 1990s continued these efforts and began to identify the specific cognitive mechanisms affected by various neuropathologic substrates. The 2000s ushered in a focus on the study of prodromal stages of neurodegenerative disease before the full-blown dementia syndrome (i.e., mild cognitive impairment). The current decade has seen the rise of imaging and other biomarkers to characterize preclinical disease before the development of significant cognitive decline. Finally, we suggest future directions and predictions for dementia-related research and potential therapeutic interventions. (JINS, 2017, 23, 818–831)
AI snapshot
Written from the paper’s full text.
TL;DR
This narrative review traces the neuropsychological and neuropathological understanding of Alzheimer’s disease from Alzheimer’s 1907 case report through the 1980s, 1990s, 2000s, and 2010s. It highlights episodic memory as the earliest deficit, the rise of MCI and preclinical biomarker research, and a shift away from the amyloid cascade toward agnostic biomarker frameworks and precision medicine.
Key findings
- Historical milestones include Alzheimer’s 1907 description of Auguste Deter and the plaques/tangles he observed, Katzman’s 1976 reframing of AD as a major public health issue, and later DSM/ICD and NIA-AA diagnostic criteria.
- The neuropsychological profile of AD centers on early episodic memory impairment, semantic knowledge loss, and later executive, attention, and visuospatial deficits; diagnostic accuracy was high for CVLT learning/delayed recall (sensitivity 95–98%, specificity 88–89%), category fluency (96%/88%), and Trail-Making Part B (85%/83%), with category fluency plus delayed recall classifying 96% of AD patients and 93% of controls.
- APOE ε4 was present in 50–60% of AD patients versus 20–25% of healthy older adults, conferring about three-fold risk with one copy and eight-fold risk with two; MCI publications rose from fewer than 50 in 1999 to nearly 900 in 2007, but conventional MCI criteria showed false-positive susceptibility, with about one-third of ADNI MCI participants performing normally on extensive testing and showing low progression.
- Biomarker findings challenge the amyloid cascade: neurodegeneration in isolation was 2.5 times more common than amyloidosis alone, the A/T/N system avoids temporal ordering assumptions, and AD pathology prevalence plateaus around age 90 while dementia and other pathologies continue to increase.
Methods
- Design: narrative/historical review, not a primary study, covering Alzheimer’s writings and the modern era from the 1970s–1980s through the 2010s.
- Data or sample: no new sample; the authors provide “a sampling” of neuropsychological and contextual work from each decade, including studies such as ADNI and other longitudinal cohorts.
- Main analysis: qualitative synthesis of the literature, diagnostic criteria, biomarker models, and future predictions for dementia research and treatment.
Limitations
- The paper does not state limitations of its own review; evident from the text, it is a narrative review that explicitly offers “a sampling” rather than a systematic or exhaustive search, with no formal meta-analysis.
- Evident from the text: coverage is focused on the neuropsychology of AD and selected related dementias, with limited discussion of treatment development beyond broad future directions.
- The paper discusses substantive limitations of conventional MCI criteria and the amyloid cascade hypothesis, but these are critiques of those frameworks, not stated limitations of the review itself.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
0 of 98 cited sources checked · 0 supported · 0 flagged
- Premisecitation
Alzheimer's 1907 description of Auguste Deter is almost certainly the first neuropsychological characterization of Alzheimer's disease.
“Alzheimer’s description of her symptoms is almost certainly the first neuropsychological characterization of the disease:”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Alzheimer, 1907
Not checked in the free run.
- Premisecitation
Semantic encoding is less effective in improving the episodic memory performance of patients with Alzheimer's disease than normal elderly individuals.
“Semantic encoding was found to be less effective in improving the episodic memory performance of patients with AD than normal elderly individuals (Buschke, Sliwinski, Kuslansky, & Lipton, 1997).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Buschke, Sliwinski, Kuslansky, & Lipton, 1997
Not checked in the free run.
- Premisecitation
Various dementing disorders are associated with patterns of relatively preserved and impaired cognitive abilities that vary depending upon the etiology and neuropathology of the underlying disease.
“various dementing disorders are associated with patterns of relatively preserved and impaired cognitive abilities that vary depending upon the etiology and neuropathology of the underlying disease.”
Quote in the paperNot a substantial claim - Premisecitation
As Alzheimer's disease neuropathology spreads beyond medial temporal lobe structures to adjacent temporal, parietal, and frontal association cortices, several higher order cognitive abilities become affected.
“Studies also showed that, as the neuropathology of AD spreads beyond MTL structures to adjacent temporal, parietal, and frontal association cortices, several higher order cognitive abilities became affected.”
Quote in the paperNot a substantial claim - Interpretationcitation
The memory deficit in early Alzheimer's disease reflects an inability to effectively encode and store new information.
“The memory deficit was shown to reflect an inability to effectively encode and store new information since patients with very early AD were particularly impaired on measures of delayed recall”
Quote in the paperSubstantial claim
- Premisecitation
Deficits in executive functions develop in the course of Alzheimer's disease.
“Deficits in “executive” functions responsible for concurrent mental manipulation of information, concept formation, problem solving, and cue-directed behavior were found to develop in the course of AD”
Quote in the paperNot a substantial claim0 of 3 sources checked- cites Bondi, Monsch, Butters, Salmon, & Paulsen, 1993
Not checked in the free run.
- cites Lefleche & Albert, 1995
Not checked in the free run.
- cites Perry & Hodges, 1999
Not checked in the free run.
- Interpretationcitation
Alzheimer's disease results in a true loss of semantic knowledge rather than only an impaired ability to retrieve information from intact semantic memory stores.
“These findings demonstrated that AD results in a true loss of semantic knowledge (i.e., general knowledge and the meanings of words) rather than only an impaired ability to retrieve information from intact semantic memory stores”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Salmon, Heindel, & Lange, 1999
Not checked in the free run.
- Premisecitation
Extensive Alzheimer's disease pathology occurs earliest in medial temporal lobe structures important for episodic memory.
“neuropathologic studies that showed extensive AD pathology occurs earliest in medial temporal lobe (MTL) structures (e.g., hippocampus, entorhinal cortex) important for episodic memory (Hyman et al., 1984).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Hyman et al., 1984
Not checked in the free run.
- Premisecitation
Episodic memory impairment (amnesia) is usually the earliest and most salient aspect of the Alzheimer's disease dementia syndrome.
“Several studies at this time showed that episodic memory impairment (i.e., amnesia) is usually the earliest and most salient aspect of the AD dementia syndrome.”
Quote in the paperNot a substantial claim - Premisecitation
The degree of Alzheimer's disease pathology in the brain was significantly correlated with performance on standardized cognitive tests shortly before death.
“One of the most important studies during this period showed that the degree of AD pathology in the brain was significantly correlated with performance on standardized cognitive tests shortly before death (Blessed, Tomlinson, & Roth, 1968).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Blessed, Tomlinson, & Roth, 1968
Not checked in the free run.
- Premiseown data
When Alzheimer examined Auguste Deter's brain, he observed neuritic plaques, neurofibrillary tangles, and amyloid angiopathy that became the hallmarks of Alzheimer's disease.
“When he did so, he observed the neuritic plaques, neurofibrillary tangles, and amyloid angiopathy that were to become the hallmarks of the disease that now bears his name”
Quote in the paperNot a substantial claim - Premisecitation
Patients with Alzheimer's disease more often produce intrusion errors on verbal and non-verbal memory tests.
“patients with AD more often produced intrusion errors (i.e., previously learned information is produced during the attempt to recall new material) on both verbal and non-verbal memory tests”
Quote in the paperSubstantial claim0 of 2 sources checked- cites Butters, Granholm, Salmon, Grant, & Wolfe, 1987
Not checked in the free run.
- cites Jacobs, Salmon, Tröster, & Butters, 1990
Not checked in the free run.
- Premisecitation
The pattern of memory deficits in Alzheimer's disease differs from subcortical dementia, in which patients have difficulty learning new information but retain what was learned and improve with retrieval aids.
“This pattern of memory deficits was shown to differ from the pattern exhibited by patients with subcortical dementia who had difficulty learning new information, but retained what was learned well and showed improved performance with retrieval aids”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Cummings, 1990
Not checked in the free run.
- Interpretationnone given
Executive dysfunction and attention deficits play a less prominent role in the Alzheimer's disease dementia syndrome than in the subcortical dementia syndrome associated with fronto-striatal dysfunction.
“Executive dysfunction and deficits in attention played a less prominent role in the AD dementia syndrome than in the subcortical dementia syndrome associated with fronto-striatal dysfunction.”
Quote in the paperNot a substantial claim - Interpretationcitation
The pattern of cognitive deficits typically associated with Alzheimer's disease is characterized by prominent deficits in episodic and semantic memory, with additional, although somewhat less prominent, deficits in executive functions, visuospatial abilities, and attention.
“This study also illustrated that the pattern of cognitive deficits typically associated with AD is characterized by prominent deficits in episodic and semantic memory, with additional, although somewhat less prominent, deficits in executive functions, visuospatial abilities, and attention.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Salmon et al., 2002
Not checked in the free run.
- Premisecitation
Patients with the frontal variant of Alzheimer's disease had a significantly higher burden of neurofibrillary tangles, but not neuritic plaques, in the frontal cortex than a matched group of patients with typical clinical presentation of Alzheimer's disease.
“These patients had a significantly higher burden of neurofibrillary tangles, but not neuritic plaques, in the frontal cortex than a matched group of patients with a typical clinical presentation of AD.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Johnson, Head, Kim, Starr, & Cotman, 1999
Not checked in the free run.
- Premisecitation
A frontal variant of Alzheimer's disease was identified in a subgroup of patients with autopsy-confirmed Alzheimer's disease who initially presented with disproportionately severe deficits on neuropsychological tests of frontal lobe functioning.
“A frontal variant of AD was identified in a subgroup of patients with autopsy-confirmed AD who initially presented with disproportionately severe deficits on neuropsychological tests of frontal lobe functioning (Johnson, Head, Kim, Starr, & Cotman, 1999).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Johnson, Head, Kim, Starr, & Cotman, 1999
Not checked in the free run.
- Premisecitation
Mutations on three genes (amyloid precursor protein on chromosome 21, presenilin 1 on chromosome 14, and presenilin 2 on chromosome 1) were identified in large families with autosomal dominant early-onset Alzheimer's disease.
“Mutations on three separate genes were identified in large families that displayed an autosomal dominant inheritance pattern of an early-onset form of AD (i.e., onset generally before the age of 60): the amyloid precursor protein gene on chromosome 21, the presenilin 1 gene on chromosome 14, and the presenilin 2 gene on chromosome 1”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Bird, 1999
Not checked in the free run.
- Premisecitation
Logopenic primary progressive aphasia is most often associated with Alzheimer's disease pathology disproportionately distributed in language-related cortical areas.
“PPA-L is most often associated with AD pathology disproportionately distributed in language-related cortical areas (Mesulam et al., 2008).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Mesulam et al., 2008
Not checked in the free run.
- Premisecitation
The APOE ε4 allele is a far more common genetic risk factor for sporadic, late-onset Alzheimer's disease.
“A far more common genetic risk factor for sporadic, late-onset AD was identified as the type ε4 allele of the gene for apolipoprotein E (APOE), a low density lipoprotein cholesterol carrier (Strittmatter et al., 1993).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Strittmatter et al., 1993
Not checked in the free run.
- Premiseown data
APOE ε4 status and measures of delayed recall were significant independent predictors of subsequent progression to Alzheimer's disease.
“Cox proportional hazards analysis showed that APOE ε4 status and measures of delayed recall were significant independent predictors of subsequent progression to AD”
Quote in the paperSubstantial claim0 of 3 sources checked- cites Bondi et al., 1995
Not checked in the free run.
- cites Petersen et al., 1995
Not checked in the free run.
- cites Reed et al., 1994
Not checked in the free run.
- Premisecitation
The APOE ε4 allele is present in 50 to 60% of patients with Alzheimer's disease compared to 20 to 25% of healthy older adults, regardless of family history of dementia.
“the APOE ε4 allele was found to be present in 50 to 60% of patients with AD (compared to 20 to 25% of healthy older adults), regardless of whether or not they have a family history of dementia (Strittmatter, et al., 1993).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Strittmatter, et al., 1993
Not checked in the free run.
- Interpretationcitation
The conventional operationalization of mild cognitive impairment for clinical trials and large-scale natural history studies is highly susceptible to false positive diagnostic errors.
“Unfortunately, this method appears to be highly susceptible to false positive diagnostic errors”
Quote in the paperSubstantial claim0 of 3 sources checked- cites Bondi et al., 2014 source
Not checked in the free run.
- cites Clark et al., 2013
Not checked in the free run.
- cites Edmonds, Delano-Wood, Clark, et al., 2015
Not checked in the free run.
- Premisecitation
An actuarial neuropsychological diagnostic method identifies mild cognitive impairment based on scores on multiple objective neuropsychological tests assessing a range of cognitive domains without reference to subjective complaints or clinical judgment.
“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.”
Quote in the paperSubstantial claim0 of 2 sources checked- cites Jak et al., 2009
Not checked in the free run.
- cites Bondi et al., 2014 source
Not checked in the free run.
- Premisenone given
Cerebrospinal fluid levels of Aβ and tau protein are indicative of Alzheimer's disease pathology in the brain.
“Several investigators refined the ability to detect and measure cerebrospinal fluid levels of Aβ (the main constituent of the plaque) and tau protein (a constituent of the neurofibrillary tangle) that were indicative of AD pathology in the brain.”
Quote in the paperSubstantial claim - Premisecitation
Neurodegeneration (measured by tau biomarkers or neuroimaging measures of atrophy) can occur before amyloidosis in individuals with prodromal Alzheimer's disease.
“Several studies, for example, have shown that neurodegeneration (measured by tau biomarkers or neuroimaging measures of atrophy) can occur before amyloidosis in individuals with prodromal AD”
Quote in the paperSubstantial claim0 of 3 sources checked- cites Braak, Zetterberg, Del Tredici, & Blennow, 2013
Not checked in the free run.
- cites Knopman et al., 2013
Not checked in the free run.
- cites Ryan et al., 2013
Not checked in the free run.
- Premisecitation
Neuroimaging measures of hippocampal, cortical, and general brain atrophy detect early neurodegenerative changes associated with Alzheimer's disease.
“Neuroimaging measures of hippocampal, cortical, and general brain atrophy were developed and applied to detect early neurodegenerative changes associated with AD”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Frisoni, Fox, Jack, Scheltens, & Thompson, 2010
Not checked in the free run.
- Interpretationcitation
There is increasing evidence that calls the amyloid cascade hypothesis into question, especially with regard to its invariant temporal sequence of pathological events.
“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, 2014).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Drachman, 2014
Not checked in the free run.
- Interpretationreasoning
The agnosticism of the A/T/N system concurs with the notion of a simple tallying of biomarker risks as previously suggested by Edmonds, Delano-Wood, Galasko, et al. (2015).
“This “agnosticism” concurs with the notion of a simple tallying of biomarker risks as previously suggested by Edmonds, Delano-Wood, Galasko, et al. (2015).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Edmonds, Delano-Wood, Galasko, et al. (2015)
Not checked in the free run.
- Interpretationreasoning
Taken together, these findings strongly suggest that the neurodegeneration of Alzheimer's disease may not depend upon prior amyloidosis.
“Taken together, these findings strongly suggest that the neurodegeneration of AD may not depend upon prior amyloidosis (Knopman et al., 2013, but cf. Jack, Knopman, et al., 2016).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites Knopman et al., 2013
Not checked in the free run.
- cites Jack, Knopman, et al., 2016
Not checked in the free run.
- Premisecitation
Cognitively normal individuals who later progressed to mild cognitive impairment or Alzheimer's disease, and had only one abnormal biomarker at baseline, were most likely to have neurodegeneration (P-tau positivity) as that abnormal biomarker rather than either amyloidosis alone or subtle cognitive deficit alone.
“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.e., P-tau positivity) as that abnormal biomarker rather than either amyloidosis alone or subtle cognitive deficit alone.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Edmonds, Delano-Wood, Galasko, et al., 2015
Not checked in the free run.
- Premisecitation
Biomarker development in most individuals with preclinical/prodromal Alzheimer's disease does not follow the temporal order proposed by the amyloid cascade hypothesis.
“Our prior work (Edmonds, Delano-Wood, Galasko, et al., 2015) in this area confirms that biomarker development in most individuals with preclinical/prodromal AD does not follow the temporal order proposed by the amyloid cascade hypothesis.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Edmonds, Delano-Wood, Galasko, et al., 2015
Not checked in the free run.
- Premisecitation
Jack, Bennett, and colleagues (2016) proposed the A/T/N system, a descriptive classification scheme for Alzheimer's disease biomarkers that is agnostic to the temporal ordering of mechanisms underlying Alzheimer's disease pathogenesis.
“Jack, Bennett, and colleagues (2016) 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.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Jack, Bennett, and colleagues (2016)
Not checked in the free run.
- Premisecitation
Neurodegeneration in isolation was 2.5 times more common than amyloidosis alone.
“In fact, neurodegeneration in isolation was 2.5 times more common than amyloidosis alone.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Edmonds, Delano-Wood, Galasko, et al., 2015
Not checked in the free run.
- Interpretationreasoning
The shift away from the amyloid cascade model toward a more equipotential conceptualization of AD biomarker risks fits well with the continuum hypothesis proposed by Braak and colleagues.
“Such a dramatic shift away from the strictures of the amyloid cascade model toward a more equipotential conceptualization of AD biomarker risks espoused by our tally system and by the A/T/N classification system fits well with a continuum hypothesis proposed by Braak and colleagues.”
Quote in the paperNot a substantial claim - Premisecitation
Tangle pathology spreads to the medial temporal lobe through specific projections from the locus coeruleus.
“Tangle pathology then spreads (possibly through cell-to-cell propagation; Iba et al., 2015) to MTL through specific projections from the locus coeruleus.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Iba et al., 2015
Not checked in the free run.
- Premisecitation
The original Braak staging theory proposed that progression of neurofibrillary tangle pathology proceeds along well-defined predilection sites beginning in the medial temporal lobe and then expands to adjacent association cortices and beyond.
“An original Braak staging theory proposed that progression of neurofibrillary tangle pathology proceeds along well-defined predilection sites beginning in the MTL and then expands to adjacent association cortices and beyond (Braak & Braak, 1991).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Braak & Braak, 1991
Not checked in the free run.
- Premisecitation
A growing number of studies have shown that cognitive measures can be as sensitive as physical biomarkers in predicting progression to dementia.
“a growing number of studies have shown that cognitive measures can be as sensitive as physical biomarkers in predicting progression to dementia”
Quote in the paperSubstantial claim0 of 3 sources checked- cites Gomar et al., 2014
Not checked in the free run.
- cites Heister et al., 2011
Not checked in the free run.
- cites Jedynak et al., 2012
Not checked in the free run.
- Interpretationreasoning
Pathological heterogeneity leads to neuropsychological heterogeneity, making dementia characterization and differential diagnosis more difficult.
“Such pathological heterogeneity leads to neuropsychological heterogeneity, making dementia characterization and differential diagnosis more difficult.”
Quote in the paperSubstantial claim - Interpretationnone given
Biomarker staging systems that are agnostic to the temporal order of their occurrence, such as a tally system or the A/T/N system, have been adopted.
“This is evident in the adoption of biomarker staging systems that are agnostic to the temporal order of their occurrence (e.g., a tally system or the A/T/N system),”
Quote in the paperSubstantial claim - Interpretationreasoning
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.
“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.”
Quote in the paperSubstantial claim - Premisecitation
The recent singular focus on anti-amyloid treatments has led to disappointing results.
“Given the shift away from the amyloid cascade model toward a more equipotential conceptualization of AD, it is not surprising that the recent singular focus on anti-amyloid treatments has led to disappointing results (Cummings, Morstorf, & Zhong, 2014).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Cummings, Morstorf, & Zhong, 2014
Not checked in the free run.
- Interpretationcitation
A combination of neuropsychological assessment and neuroimaging biomarkers has potential utility to help explain a heterogeneous presentation of prodromal AD.
“These results demonstrate the potential utility of a combination of neuropsychological assessment and neuroimaging biomarkers to help explain a heterogeneous presentation of prodromal AD.”
Quote in the paperSubstantial claim - Premisecitation
The prevalence of dementia and other pathologies, such as cerebrovascular disease or hippocampal sclerosis, continues to increase with age.
“however, the prevalence of dementia and other pathologies, such as cerebrovascular disease or hippocampal sclerosis (arteriolosclerosis more generally), continue to increase with age (see Figure 6).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Nelson and colleagues (2011)
Not checked in the free run.
- Interpretationreasoning
The dogma that "amyloidosis is AD" is giving way to a broader conceptualization of the disease.
“As we move toward the end of the current decade, it is clear that the dogma that “amyloidosis is AD” is giving way to a broader conceptualization of the disease.”
Quote in the paperSubstantial claim - Interpretationcitation
As age increases, there is increasing heterogeneity in the neuropathology underlying what is clinically diagnosed as "AD dementia."
“It has also become clear that, as age increases, there is increasing heterogeneity in the neuropathology underlying what is clinically diagnosed as “AD dementia.””
Quote in the paperSubstantial claim0 of 1 sources checked- cites Nelson and colleagues (2011)
Not checked in the free run.
- Premisecitation
The cognitive deficits of amnestic MCI individuals in ADNI coincided well with specific regions of cortical thinning on neuroimaging.
“and that their deficits coincided well with specific regions of cortical thinning on neuroimaging (see Figure 7; Edmonds et al., 2016).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Edmonds et al., 2016
Not checked in the free run.
- Interpretationreasoning
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.
“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.”
Quote in the paperSubstantial claim - Premisecitation
Individuals diagnosed as amnestic MCI in the ADNI cohort had great heterogeneity in the pattern of cognitive deficits they exhibited.
“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”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Edmonds et al., 2016
Not checked in the free run.
- Interpretationreasoning
In some cases, "AD dementia" appears only following the addition of other pathologies to a sub-threshold level of AD pathology.
“This observation suggests that, in some cases, “AD dementia” appears only following the addition of other pathologies to a sub-threshold level of AD pathology.”
Quote in the paperSubstantial claim
- Classified as probably not a substantial claim. 13
- May combine two claims. 24
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationSenile and presenile Alzheimer's disease are histopathologically identical.
“Robert Katzman summarized data showing that senile and presenile AD were histopathologically identical”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Katzman, 1976
Not checked in the free run.
May combine two claims.
PremisecitationA deficit in language abilities (aphasia) is observed relatively early in the course of Alzheimer's disease, with deficits in confrontation naming, verbal fluency (particularly semantic categories), semantic categorization, and reduced ability to recall over-learned facts.
“A deficit in language abilities (i.e., aphasia) was observed relatively early in the course of AD, with deficits in confrontation naming, verbal fluency (particularly from semantic categories), semantic categorization, and a reduced ability to recall over-learned facts”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites Hodges & Patterson, 1995
Not checked in the free run.
- cites Nebes, 1989
Not checked in the free run.
May combine two claims.
PremisecitationAttention deficits occur in Alzheimer's disease and are usually evident on dual-processing tasks, tasks requiring disengagement and shifting of attention, and working memory tasks depending on control of attentional resources.
“Attention deficits were also found to occur and were usually evident on dual-processing tasks, tasks that require the disengagement and shifting of attention, and working memory tasks that depend upon the control of attentional resources”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites Parasuraman & Haxby, 1993
Not checked in the free run.
- cites Perry & Hodges, 1999
Not checked in the free run.
May combine two claims.
PremisecitationPatients with subcortical dementia or fronto-temporal dementia retain semantic knowledge well, but have difficulty in systematic retrieval from semantic memory stores.
“Patients with subcortical dementia or fronto-temporal dementia, in contrast, retained semantic knowledge well, but had difficulty in systematic retrieval from semantic memory stores”
Quote in the paperSubstantial claim0 of 2 sources checked- cites Rosser & Hodges, 1994
Not checked in the free run.
- cites Rascovsky, Salmon, Hansen, Thal, & Galasko, 2007
Not checked in the free run.
May combine two claims.
PremisecitationPatients with posterior cortical atrophy usually have prominent visual agnosia (sometimes including prosopagnosia) and constructional apraxia, and exhibit many or all features of Balint's syndrome.
“Patients with PCA usually have prominent visual agnosia (sometimes including prosopagnosia) and constructional apraxia, and exhibit many or all of the features of Balint’s syndrome”
Quote in the paperNot a substantial claim0 of 3 sources checked- cites Caine, 2004
Not checked in the free run.
- cites Mendez et al., 2002
Not checked in the free run.
- cites Renner et al., 2004
Not checked in the free run.
May combine two claims.
PremisecitationThe best-fitting combination of category fluency and delayed recall accurately classified 96% of patients with Alzheimer's disease and 93% of control subjects.
“The best-fitting combination of category fluency and delayed recall accurately classified 96% of the patients with AD and 93% of the control subjects”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Salmon et al., 2002
Not checked in the free run.
May combine two claims.
PremisecitationIn a study comparing mild Alzheimer's disease and matched normal controls, CVLT learning and delayed recall measures had sensitivity 95-98% and specificity 88-89%; category fluency had sensitivity 96% and specificity 88%; Trail-Making Part B had sensitivity 85% and specificity 83%.
“Results showed excellent sensitivity and specificity for learning and delayed recall measures from the California Verbal Learning Test (CVLT) (sensitivity: 95–98%, specificity: 88–89%), category fluency (sensitivity: 96%, specificity: 88%), and Trail-Making Part B (sensitivity: 85%, specificity: 83%).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Salmon et al., 2002
Not checked in the free run.
May combine two claims.
PremisecitationVisuospatial deficits occur in patients with Alzheimer's disease, but are usually less salient than other cognitive deficits in the early stages.
“Several studies showed that visuospatial deficits occurred in patients with AD (for review, see Cronin-Golomb & Amick, 2001), but these deficits were usually less salient than other cognitive deficits in the early stages of the disease”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites Cronin-Golomb & Amick, 2001
Not checked in the free run.
- cites Storandt Botwinick, Danziger, Berg, Hughes, 1984
Not checked in the free run.
May combine two claims.
PremisecitationWorking memory deficits in Alzheimer's disease are relatively mild and primarily characterized by disruption of the central executive with relative sparing of immediate memory.
“Deficits in working memory were relatively mild and primarily characterized by disruption of the “central executive” with relative sparing of immediate memory”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites Baddeley, Bressi, Della Sala, Logie, Spinnler, 1991
Not checked in the free run.
- cites Collette, Van der Linden, Bechet, Salmon, 1999
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationPosterior cortical atrophy occurs when there is disproportionate atrophy and deposition of neurofibrillary tangles and neuritic plaques in the occipital cortex and posterior parietal cortex relative to other cortical association areas.
“Posterior cortical atrophy (PCA) occurs when there is disproportionate atrophy and deposition of neurofibrillary tangles and neuritic plaques in the occipital cortex and posterior parietal cortex relative to other cortical association areas”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites Hof, Vogt, Bouras, & Morrison, 1997
Not checked in the free run.
- cites Renner et al., 2004
Not checked in the free run.
May combine two claims.
PremisecitationPosterior cortical atrophy is associated with posterior cortical hypometabolism with particular involvement of the dorsal visual stream, and with a posterior distribution of amyloid deposition revealed by Pittsburgh compound-B PET imaging.
“PCA is associated with posterior cortical hypometabolism with particular involvement of the dorsal visual stream (Nestor, Caine, Fryer, Clarke, & Hodges, 2003), and with a posterior distribution of amyloid deposition revealed by positron emission tomography (PET) imaging using Pittsburgh compound-B ([11C]-PIB) (Tenovuo, Kemppainen, Aalto, Nagren, & Rinne, 2008).”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites Nestor, Caine, Fryer, Clarke, & Hodges, 2003
Not checked in the free run.
- cites Tenovuo, Kemppainen, Aalto, Nagren, & Rinne, 2008
Not checked in the free run.
May combine two claims.
PremisecitationIn non-demented elderly, APOE ε4+ subjects performed significantly worse than ε4− subjects on measures of delayed recall, but not on tests of other cognitive abilities, despite no significant group differences in age, education, or global cognitive status.
“Although the groups did not differ significantly in age, education, or global cognitive status, the ε4+ subjects performed significantly worse than the ε4− subjects on measures of delayed recall, but not on tests of other cognitive abilities.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Bondi, Salmon, Galasko, Thomas, and Thal (1999)
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationMild cognitive impairment is defined as a condition in which individuals experience memory loss to a greater extent than expected for age, yet do not meet criteria for dementia.
“MCI was defined as a condition in which individuals experience memory loss to a greater extent than one would expect for age, yet do not meet criteria for dementia.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Petersen et al., 1999
Not checked in the free run.
May combine two claims.
InterpretationreasoningPoor recall is an early sensitive neuropsychological marker of Alzheimer's disease and not a cognitive phenotype of the ε4 genotype.
“suggesting that poor recall is an early sensitive neuropsychological marker of AD and not a cognitive phenotype of the ε4 genotype”
Quote in the paperSubstantial claim0 of 3 sources checked- cites Bondi et al., 1995
Not checked in the free run.
- cites Petersen et al., 1995
Not checked in the free run.
- cites Reed et al., 1994
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationMild cognitive impairment classification was broadened to include amnestic/non-amnestic subtypes and single/multiple domain conditions.
“This classification scheme was subsequently broadened to include “amnestic MCI” or “non-amnestic MCI” subtypes, and “single domain” or “multiple domain” conditions to indicate the number of cognitive domains affected”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites Petersen, 2004
Not checked in the free run.
- cites Winblad et al., 2004
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationThe original clinical criteria for mild cognitive impairment were: subjective memory complaint, objective memory impairment for age, relatively preserved general cognition, essentially intact activities of daily living, and not demented.
“The specific clinical criteria for MCI they originally put forth were: (1) subjective memory complaint, (2) objective memory impairment for age, (3) relatively preserved general cognition, (4) essentially intact activities of daily living, and (5) not demented (Petersen et al., 1999).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Petersen et al., 1999
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationFamilial Alzheimer's disease forms are rare and account for only approximately 1 to 2% of all cases of the disease.
“These forms of familial AD are rare and account for only approximately 1 to 2% of all cases of the disease.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Bird, 1999
Not checked in the free run.
May combine two claims.
PremisecitationA subset of patients with primary progressive aphasia have Alzheimer's disease pathology; these patients usually present with logopenic primary progressive aphasia, characterized by hesitant, grammatically correct speech and spared language comprehension.
“A subset of patients with primary progressive aphasia (PPA) was found to have AD pathology. These patients usually presented with logopenic PPA (PPA-L), which is characterized by hesitant, grammatically correct speech and spared language comprehension (Gorno-Tempini et al., 2004).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Gorno-Tempini et al., 2004
Not checked in the free run.
May combine two claims.
PremisecitationThe APOE ε4 allele is not deterministic, but confers an approximately three-fold risk of developing Alzheimer's disease if one copy is present, and an eight-fold risk if two copies are present.
“Unlike the genes associated with early-onset familial AD, the APOE ε4 allele is not deterministic, but confers an approximately three-fold risk of developing AD if one copy of the ε4 allele is present, and an eight-fold risk if two copies are present (Katzman & Kawas, 1994).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Katzman & Kawas, 1994
Not checked in the free run.
May combine two claims.
InterpretationreasoningAll these biomarkers have greatly increased the accuracy with which Alzheimer's disease pathology in the brain can be detected before the onset of cognitive symptoms, and improved the ability to differentiate Alzheimer's disease from other pathologies that lead to dementia.
“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.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationNeurodegeneration in the face of normal amyloid levels was evident in 23% of the original sample of Jack et al. (2010) and in an even higher percentage in Edmonds, Delano-Wood, Galasko, et al. (2015).
“Neurodegeneration in the face of normal amyloid levels was evident in 23% of the original sample of Jack et al. (2010) (and in an even higher percentage in Edmonds, Delano-Wood, Galasko, et al., 2015).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites Jack et al., 2010
Not checked in the free run.
- cites Edmonds, Delano-Wood, Galasko, et al., 2015
Not checked in the free run.
May combine two claims.
PremisecitationThe actuarial method produced greater diagnostic stability than the conventional method (individuals classified as mild cognitive impairment did not revert to normal cognition after 1 year) and revealed stronger relationships between cognition, biomarkers, and rates of progression to dementia.
“This actuarial method was shown to produce greater diagnostic stability than the conventional method (i.e., individuals classified as MCI did not revert to “normal” cognition after 1 year; Jak et al., 2009), and revealed stronger relationships between cognition, biomarkers, and rates of progression to dementia in patients classified as MCI in this way (Bondi et al., 2014).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites Jak et al., 2009
Not checked in the free run.
- cites Bondi et al., 2014 source
Not checked in the free run.
May combine two claims.
PremisecitationIn ADNI participants classified as mild cognitive impairment by conventional criteria, approximately one-third performed within normal limits on more extensive cognitive testing and showed a low rate of progression to dementia.
“Despite their MCI diagnosis, approximately one-third of these participants performed within normal limits on this more extensive cognitive testing and showed a low rate of progression to dementia.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Edmonds, Delano-Wood, Clark, et al. (2015)
Not checked in the free run.
May combine two claims.
PremisecitationIn 1999 fewer than 50 papers were published on mild cognitive impairment, whereas by 2007 this number approached 900 peer-reviewed studies in that year alone.
“in 1999 fewer than 50 papers were published in the medical literature on the topic of MCI, whereas by 2007, this number approached 900 peer-reviewed studies in that year alone”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Petersen and colleagues (2009)
Not checked in the free run.
May combine two claims.
PremisecitationPittsburgh compound-B ([11C]-PIB) binds to Aβ and can be used with PET imaging to reveal deposition of amyloid in the brain.
“Klunk and colleagues (see Mathis et al., 2003) developed Pittsburgh compound-B ([11C]-PIB), an agent that binds to Aβ, for use with PET imaging to reveal deposition of amyloid in the brain.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Mathis et al., 2003
Not checked in the free run.
May combine two claims.
PremisecitationAxonal injury and tau lesions in late-myelinating regions have been shown to predate amyloid deposition in prodromal Alzheimer's disease.
“Axonal injury (Ryan et al., 2013) and tau lesions in late-myelinating regions (Braak et al., 2011) have been shown to predate amyloid deposition in prodromal AD.”
Quote in the paperSubstantial claim0 of 2 sources checked- cites Ryan et al., 2013
Not checked in the free run.
- cites Braak et al., 2011
Not checked in the free run.
May combine two claims.
PremisecitationMild cognitive impairment subtypes correspond to various etiologies, with amnestic mild cognitive impairment most indicative of Alzheimer's disease and non-amnestic mild cognitive impairment suggesting other neurodegenerative conditions such as frontotemporal lobar degeneration or dementia with Lewy bodies.
“It was proposed that these MCI subtypes correspond to various etiologies, with “amnestic MCI” being most indicative of AD and “non-amnestic MCI” suggesting other neurodegenerative conditions such as FTLD or DLB”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites Petersen & Morris, 2005
Not checked in the free run.
- cites Smith & Bondi, 2013
Not checked in the free run.
Classified as probably not a substantial claim.
PremisecitationInitial tau pathology in the locus coeruleus and its axonal projections may not result in outright neuronal death but may restrict neuronal function.
“Braak and Del Tredici (2015) 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.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Braak and Del Tredici (2015)
Not checked in the free run.
Classified as probably not a substantial claim.
PremisecitationThe A/T/N system makes no assumptions about temporal ordering of biomarkers or their putative causal relationships.
“This new model, known as the A/T/N system (“A” refers to Aβ, “T” to tau, and “N” to neurodegeneration), makes no assumptions about temporal ordering of biomarkers or their putative causal relationships.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Jack, Bennett, and colleagues (2016)
Not checked in the free run.
Classified as probably not a substantial claim.
PremisecitationThe absence of Aβ deposits is not an adequate rationale for excluding tau-only cases from the developmental spectrum of the AD-related process.
“therefore, the “absence of Aβ deposits is not an adequate rationale for excluding tau-only cases from the developmental spectrum of the AD-related process.””
Quote in the paperSubstantial claim0 of 1 sources checked- cites Braak and Del Tredici (2014)
Not checked in the free run.
Classified as probably not a substantial claim.
PremisecitationAmyloid plaques may develop after neurofibrillary tangle pathology develops in sites associated with AD, such as the medial temporal lobe.
“Braak and Del Tredici (2014) counter this argument by suggesting that amyloid plaques may develop after neurofibrillary tangle pathology develops in sites associated with AD (e.g., MTL);”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Braak and Del Tredici (2014)
Not checked in the free run.
May combine two claims.
PremisecitationThe pathogenic process starts with the formation of pretangle material in the lower brainstem, with the first visible pathologic changes occurring in the locus coeruleus.
“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., 2011).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Braak et al., 2011
Not checked in the free run.
Classified as probably not a substantial claim.
PremisecitationThe pathogenic process begins well before amyloidosis.
“It is postulated that this begins well before amyloidosis.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Braak et al., 2011
Not checked in the free run.
Probably not a substantial claim: may not pass S4 (based).
Premisenone givenNew evidence has been accepted that brainstem tauopathy and its propagation to the medial temporal lobe may occur before amyloidosis associated with late-onset sporadic AD.
“and with the acceptance of new evidence that brainstem tauopathy and its propagation to the MTL may occur before amyloidosis associated with late-onset sporadic AD.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationRequiring a minimum threshold level of amyloid deposition for a neuropathologic diagnosis of AD may be justified only when applied in cases with clinically evident dementia, but not when applied to non-demented individuals.
“They further argue that requiring a minimum threshold level of amyloid deposition for a neuropathologic diagnosis of AD (as in the PART criteria) may be justified only when applied in cases with clinically evident dementia, but not when applied to non-demented individuals.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Braak and Del Tredici (2014)
Not checked in the free run.
May combine two claims.
PremisecitationThe prevalence of AD pathology increases with age but reaches a plateau at approximately age 90.
“Nelson and colleagues (2011) showed that the prevalence of AD pathology increases with age but reaches a plateau at approximately age 90;”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Nelson and colleagues (2011)
Not checked in the free run.
The paper relies on this without support.
Tau pathology is more firmly associated with clinical and cognitive decline than is amyloid pathology.
“Since tau pathology is more firmly associated with clinical and cognitive decline than is amyloid pathology,”
The paper relies on this without support.
Tau pathology may accumulate in susceptible regions earlier than amyloid pathology.
“and may accumulate in susceptible regions earlier than that of amyloid,”
The paper relies on this without support.
Amyloid plaque pathology accumulates more diffusely across neocortex.
“Amyloid plaque pathology, in contrast, accumulates more diffusely across neocortex.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Additional pathogenic mechanisms possibly overlapping with Aβ plaques and NFT formation include inflammation, oxidative damage, iron deregulation, cholesterol metabolism, blood-brain barrier dysfunction, or α-synuclein toxicity.
“A number of additional pathogenic mechanisms have been described, possibly overlapping with Aβ plaques and NFT formation or induced by them, including inflammation, oxidative damage, iron deregulation, and cholesterol metabolism blood-brain barrier (BBB) dysfunction or α-synuclein toxicity.9-13”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [9]
Cites
Folstein, M. F., Folstein, S. E., & McHugh, P. R. (1975) · Journal of Psychiatric Research · doi:10.1016/0022-3956(75)90026-6 · Cited by 88,282 · see citing works
McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D., & Stadlan, E. M. (1984) · Neurology · doi:10.1212/wnl.34.7.939 · Cited by 27,915 · see citing works
Hirono, N., Mori, E., Ikejiri, Y., Imamura, T., Shimomura, T., Hashimoto, M., Yamashita, H., & Ikeda, M. (1997) · PubMed · Cited by 21,010 · see citing works
Kok, J. S., Berg, I. J., & Scherder, E. J. A. (2013) · Dementia and Geriatric Cognitive Disorders Extra · doi:10.1159/000353441 · Cited by 20,589 · see citing works
Older Adults' Reasons for Using Technology while Aging in Place
Peek, S. T. M., Luijkx, K. G., Rijnaard, M. D., Nieboer, M. E., van der Voort, C. S., Aarts, S., van Hoof, J., Vrijhoef, H. J., & Wouters, E. (2015) · Gerontology · doi:10.1159/000430949 · Cited by 19,803 · see citing works
Sensitivity and False Alarm Rate of a Fall Sensor in Long-Term Fall Detection in the Elderly
Kangas, M., Korpelainen, R., Vikman, I., Nyberg, L., & Jämsä, T. J. (2014) · Gerontology · doi:10.1159/000362720 · Cited by 19,003 · see citing works
McKhann, G. M., Knopman, D. S., Chertkow, H., Hyman, B. T., Jack, C. R., Kawas, C. H., Klunk, W. E., Koroshetz, W. J., Manly, J. J., Mayeux, R., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.005 · Cited by 18,657 · see citing works
Neuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123 · cited 1× · see citing works
“An original Braak staging theory proposed that progression of neurofibrillary tangle pathology proceeds along well-defined predilection sites beginning in the MTL and then expands to adjacent association cortices and beyond (Braak & Braak, 1991).”
BackgroundAmyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D. (2013) · Neurodegenerative Diseases · doi:10.1159/000337230 · Cited by 10,359 · see citing works
Albert, M. S., DeKosky, S. T., Dickson, D., Dubois, B., Feldman, H. H., Fox, N. C., Gamst, A., Holtzman, D. M., Jagust, W. J., Petersen, R. C., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.008 · Cited by 10,152 · cited 2× · see citing works
“In 2011, the National Institute on Aging and Alzheimer’s Association (NIA-AA) published updated diagnostic guidelines for MCI (Albert et al., 2011) and introduced research criteria for “preclinical” AD (Sperling et al., 2011).”
BackgroundMild Cognitive Impairment: Clinical Characterization and Outcome
Petersen, R. C., Smith, G. E., Waring, S. C., Ivnik, R. J., Tangalos, E. G., & Kokmen, E. (1999) · Archives of Neurology · doi:10.1001/archneur.56.3.303 · Cited by 8,980 · see citing works
Mild cognitive impairment as a diagnostic entity
Petersen, R. C. (2004) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.2004.01388.x · Cited by 7,864 · see citing works
Sperling, R. A., Aisen, P. S., Beckett, L. A., Bennett, D. A., Craft, S., Fagan, A. M., Iwatsubo, T., Jack, C. R., Kaye, J., Montine, T. J., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.003 · Cited by 7,155 · see citing works
Sensitivity of revised diagnostic criteria for the behavioural variant of frontotemporal dementia
Rascovsky, K., Hodges, J. R., Knopman, D., Mendez, M. F., Kramer, J. H., Neuhaus, J., van Swieten, J. C., Seelaar, H., Dopper, E. G. P., Onyike, C. U., et al. (2011) · Brain · doi:10.1093/brain/awr179 · Cited by 5,221 · see citing works
Self-citationClassification of primary progressive aphasia and its variants
Gorno-Tempini, M. L., Hillis, A. E., Weintraub, S., Kertesz, A., Mendez, M., Cappa, S. F., Ogar, J. M., Rohrer, J. D., Black, S., Boeve, B. F., et al. (2011) · Neurology · doi:10.1212/wnl.0b013e31821103e6 · Cited by 5,141 · see citing works
Winblad, B., Palmer, K., Kivipelto, M., Jelic, V., Fratiglioni, L., Wahlund, L. ‐., Nordberg, A., Bäckman, L., Albert, M., Almkvist, O., et al. (2004) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.2004.01380.x · Cited by 4,946 · see citing works
Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade
Jack, C. R., Knopman, D. S., Jagust, W. J., Shaw, L. M., Aisen, P. S., Weiner, M. W., Petersen, R. C., & Trojanowski, J. Q. (2010) · The Lancet Neurology · doi:10.1016/s1474-4422(09)70299-6 · Cited by 4,806 · see citing works
Diagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB Consortium
McKeith, I. G., Boeve, B. F., Dickson, D. W., Halliday, G., Taylor, J.-P., Weintraub, D., Aarsland, D., Galvin, J., Attems, J., Ballard, C. G., et al. (2017) · Neurology · doi:10.1212/wnl.0000000000004058 · Cited by 4,476 · see citing works
Self-citationJack, C. R., Knopman, D. S., Jagust, W. J., Petersen, R. C., Weiner, M. W., Aisen, P. S., Shaw, L. M., Vemuri, P., Wiste, H. J., Weigand, S. D., et al. (2013) · The Lancet Neurology · doi:10.1016/s1474-4422(12)70291-0 · Cited by 4,396 · see citing works
Strittmatter, W. J., Saunders, A. M., Schmechel, D., Pericak-Vance, M., Enghild, J., Salvesen, G. S., & Roses, A. D. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.5.1977 · Cited by 4,268 · see citing works
Blessed, G., Tomlinson, B. E., & Roth, M. (1968) · British Journal of Psychiatry · doi:10.1192/bjp.114.512.797 · Cited by 4,117 · see citing works
Clinical and biomarker changes in dominantly inherited Alzheimer's disease
Bateman, R. J., Xiong, C., Benzinger, T. L. S., Fagan, A. M., Goate, A., Fox, N. C., Marcus, D. S., Cairns, N. J., Xie, X., Blazey, T. M., et al. (2012) · New England Journal of Medicine · doi:10.1056/nejmoa1202753 · Cited by 3,814 · see citing works
Jessen, F., Amariglio, R. E., van Boxtel, M., Breteler, M., Ceccaldi, M., Chételat, G., Dubois, B., Dufouil, C., Ellis, K. A., van der Flier, W. M., et al. (2014) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2014.01.001 · Cited by 3,014 · see citing works
Appelhof, B., Bakker, C., den IJssel, J. C. L. V. D., Zwijsen, S. A., Smalbrugge, M., Verhey, F. R. J., de Vugt, M. E., Zuidema, S. U., & Koopmans, R. T. C. M. (2017) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000477087 · Cited by 2,773 · see citing works
Albert, M., DeKosky, S. T., Dickson, D. W., Dubois, B., Feldman, H., Fox, N. C., Gamst, A. C., Holtzman, D. M., Jagust, W. J., Petersen, R. C., et al. (2013) · FOCUS The Journal of Lifelong Learning in Psychiatry · doi:10.1176/appi.focus.11.1.96 · Cited by 2,630 · see citing works
Alzheimer's disease: cell-specific pathology isolates the hippocampal formation.
Hyman, B. T., Van Hoesen, G. W., Damasio, A. R., & Barnes, C. L. (1984) · Science · doi:10.1126/science.6474172 · Cited by 2,268 · see citing works
Stages of the Pathologic Process in Alzheimer Disease: Age Categories From 1 to 100 Years
Braak, H., Thal, D. R., Ghebremedhin, E., & Del Tredici, K. (2011) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0b013e318232a379 · Cited by 2,194 · see citing works
The clinical use of structural MRI in Alzheimer disease
Frisoni, G. B., Fox, N. C., Jack, C. R., Scheltens, P., & Thompson, P. M. (2010) · Nature Reviews Neurology · doi:10.1038/nrneurol.2009.215 · Cited by 2,113 · see citing works
Qualitative Assessment of Verbal Fluency Performance in Frontotemporal Dementia
van den Berg, E., Jiskoot, L. C., Grosveld, M. J. H., Swieten, J. C. V., & Papma, J. M. (2017) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000477538 · Cited by 2,061 · see citing works
Squire, L. R. (1986) · Elsevier eBooks · doi:10.1016/b978-0-12-268330-5.50013-5 · Cited by 1,932 · see citing works
A/T/N: An unbiased descriptive classification scheme for Alzheimer disease biomarkers
Jack, C. R., Bennett, D. A., Blennow, K., Carrillo, M. C., Feldman, H. H., Frisoni, G. B., Hampel, H., Jagust, W. J., Johnson, K. A., Knopman, D. S., et al. (2016) · Neurology · doi:10.1212/wnl.0000000000002923 · Cited by 1,864 · see citing works
Vitamin E and Donepezil for the Treatment of Mild Cognitive Impairment
Petersen, R. C., Thomas, R. G., Grundman, M., Bennett, D., Doody, R., Ferris, S., Galasko, D., Jin, S., Kaye, J., Levey, A., et al. (2005) · New England Journal of Medicine · doi:10.1056/nejmoa050151 · Cited by 1,844 · see citing works
Alzheimer’s disease drug-development pipeline: Few candidates, frequent failures
Cummings, J. L., Morstorf, T., & Zhong, K. (2014) · Alzheimer's Research & Therapy · doi:10.1186/alzrt269 · Cited by 1,744 · see citing works
Cognition and anatomy in three variants of primary progressive aphasia
Gorno‐Tempini, M. L., Dronkers, N. F., Rankin, K. P., Ogar, J. M., Phengrasamy, L., Rosen, H. J., Johnson, J. K., Weiner, M. W., & Miller, B. L. (2004) · Annals of Neurology · doi:10.1002/ana.10825 · Cited by 1,608 · see citing works
Schmechel, D. E., Saunders, A. M., Strittmatter, W. J., Crain, B. J., Hulette, C. M., Joo, S. H., Pericak-Vance, M. A., Goldgaber, D., & Roses, A. D. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.20.9649 · Cited by 1,525 · see citing works
Primary age-related tauopathy (PART): a common pathology associated with human aging
Crary, J. F., Trojanowski, J. Q., Schneider, J. A., Abisambra, J. F., Abner, E. L., Alafuzoff, I., Arnold, S. E., Attems, J., Beach, T. G., Bigio, E. H., et al. (2014) · Acta Neuropathologica · doi:10.1007/s00401-014-1349-0 · Cited by 1,467 · see citing works
An english translation of alzheimer’s 1907 paper, “über eine eigenartige erkankung der hirnrinde”
Stelzmann, R. A., Norman Schnitzlein, H., & Reed Murtagh, F. (1995) · Clinical Anatomy · doi:10.1002/ca.980080612 · Cited by 1,455 · see citing works
Mild Cognitive Impairment: Ten Years Later
Petersen, R. C., Roberts, R. O., Knopman, D. S., Boeve, B. F., Geda, Y. E., Ivnik, R. J., Smith, G. E., & Jack, C. R. (2009) · Archives of Neurology · doi:10.1001/archneurol.2009.266 · Cited by 1,447 · see citing works
Attention and executive deficits in Alzheimer's disease: A critical review
Perry, R. J. (1999) · Brain · doi:10.1093/brain/122.3.383 · Cited by 1,180 · see citing works
The Alzheimer's Disease Neuroimaging Initiative: A review of papers published since its inception
Weiner, M. W., Veitch, D. P., Aisen, P. S. S., Beckett, L. A., Cairns, N. J., Green, R. C., Harvey, D. J., Jack, C. R., Jagust, W. J., Liu, E., et al. (2013) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2013.05.1769 · Cited by 1,011 · see citing works
Synthesis and Evaluation of 11C-Labeled 6-Substituted 2-Arylbenzothiazoles as Amyloid Imaging Agents
Mathis, C. A., Wang, Y., Holt, D. P., Huang, G.-F., Debnath, M. L., & Klunk, W. E. (2003) · Journal of Medicinal Chemistry · doi:10.1021/jm030026b · Cited by 976 · see citing works
Mild Cognitive Impairment as a Clinical Entity and Treatment Target
Petersen, R. C., & Morris, J. C. (2005) · Archives of Neurology · doi:10.1001/archneur.62.7.1160 · Cited by 935 · see citing works
The `subcortical dementia' of progressive supranuclear palsy
Albert, M. L., Feldman, R. G., & Willis, A. L. (1974) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp.37.2.121 · Cited by 871 · see citing works
(1992) · Annals of Internal Medicine · doi:10.7326/0003-4819-117-4-351_2 · Cited by 858 · see citing works
Quantification of Five Neuropsychological Approaches to Defining Mild Cognitive Impairment
Jak, A. J., Bondi, M. W., Delano-Wood, L., Wierenga, C., Corey-Bloom, J., Salmon, D. P., & Delis, D. C. (2009) · The American Journal of Geriatric Psychiatry · doi:10.1097/jgp.0b013e31819431d5 · Cited by 823 · see citing works
Self-citationPetersen, R. C. (1995) · JAMA · doi:10.1001/jama.1995.03520400044042 · Cited by 783 · see citing works
Bondi, M. W., Initiative, F. T. A. D. N., Edmonds, E. C., Jak, A. J., Clark, L. R., Delano-Wood, L., McDonald, C. R., Nation, D. A., Libon, D. J., Au, R., et al. (2014) · Journal of Alzheimer's Disease · doi:10.3233/jad-140276 · Cited by 750 · see citing works
Self-citationüber eigenartige Krankheitsfälle des späteren Alters
Alzheimer, A. (1911) · Zeitschrift für die gesamte Neurologie und Psychiatrie · doi:10.1007/bf02866241 · Cited by 712 · see citing works
THE DECLINE OF WORKING MEMORY IN ALZHEIMER'S DISEASE
Baddeley, A., Bressi, S., Sala, S. D., Logie, R. H., & Spinnler, H. R. (1991) · Brain · doi:10.1093/brain/114.6.2521 · Cited by 699 · see citing works
Three dimensions of the amyloid hypothesis: time, space and 'wingmen'
Musiek, E. S., & Holtzman, D. M. (2015) · Nature Neuroscience · doi:10.1038/nn.4018 · Cited by 697 · see citing works
Snowdon, D. A. (1996) · JAMA · doi:10.1001/jama.1996.03530310034029 · Cited by 696 · see citing works
Hodges, J. R. (1995) · Neuropsychologia · doi:10.1016/0028-3932(94)00127-b · Cited by 644 · see citing works
Semantic memory impairment in Alzheimer's disease: Failure of access or degraded knowledge?
Hodges, J. R., Salmon, D. P., & Butters, N. (1992) · Neuropsychologia · doi:10.1016/0028-3932(92)90104-t · Cited by 627 · see citing works
Self-citationThe Prevalence and Malignancy of Alzheimer Disease
Katzman, R. (1976) · Archives of Neurology · doi:10.1001/archneur.1976.00500040001001 · Cited by 623 · see citing works
Rathore, S., Habes, M., Iftikhar, M. A., Shacklett, A., & Davatzikos, C. (2017) · NeuroImage · doi:10.1016/j.neuroimage.2017.03.057 · Cited by 622 · see citing works
Comparing predictors of conversion and decline in mild cognitive impairment
Landau, S. M., Harvey, D., Madison, C. M., Reiman, E. M., Foster, N. L., Aisen, P. S., Petersen, R. C., Shaw, L. M., Trojanowski, J. Q., Jack, C. R., et al. (2010) · Neurology · doi:10.1212/wnl.0b013e3181e8e8b8 · Cited by 616 · see citing works
Episodic and Semantic Memory: A Comparison of Amnesic and Demented Patients
Butters, N., Granholm, E. L., Salmon, D. P., Grant, I., & Wolfe, J. (1987) · Journal of Clinical and Experimental Neuropsychology · doi:10.1080/01688638708410764 · Cited by 596 · see citing works
Self-citationSEMANTIC MEMORY LOSS IN DEMENTIA OF ALZHEIMER'S TYPE
Chertkow, H. M., & Bub, D. N. (1990) · Brain · doi:10.1093/brain/113.2.397 · Cited by 571 · see citing works
Quantitative and qualitative analyses of clock drawings in Alzheimer's and Huntington's disease
Rouleau, I., Salmon, D. P., Butters, N., Kennedy, C. M., & McGuire, K. (1992) · Brain and Cognition · doi:10.1016/0278-2626(92)90112-y · Cited by 556 · see citing works
Self-citationThe preclinical phase of the pathological process underlying sporadic Alzheimer’s disease
Braak, H., & Del Tredici, K. (2015) · Brain · doi:10.1093/brain/awv236 · Cited by 540 · see citing works
Prevalence and Malignancy of Alzheimer Disease
Lijtmaer, H., Fuld, P. A., & Katzman, R. (1976) · Archives of Neurology · doi:10.1001/archneur.1976.00500040088017 · Cited by 517 · see citing works
Alzheimer and frontotemporal pathology in subsets of primary progressive aphasia
Mesulam, M., Wicklund, A., Johnson, N., Rogalski, E., Léger, G. C., Rademaker, A., Weintraub, S., & Bigio, E. H. (2008) · Annals of Neurology · doi:10.1002/ana.21388 · Cited by 513 · see citing works
Neuropsychological Assessment of Dementia
Salmon, D. P., & Bondi, M. W. (2008) · Annual Review of Psychology · doi:10.1146/annurev.psych.57.102904.190024 · Cited by 449 · see citing works
Self-citationSheline, Y. I., Morris, J. C., Snyder, A. Z., Price, J. L., Yan, Z., D’Angelo, G., Liu, C., Dixit, S., Benzinger, T. L. S., Fagan, A. M., et al. (2010) · Journal of Neuroscience · doi:10.1523/jneurosci.3987-10.2010 · Cited by 430 · see citing works
Semantic memory in Alzheimer's disease.
Nebes, R. D. (1989) · Psychological Bulletin · doi:10.1037/0033-2909.106.3.377 · Cited by 423 · see citing works
Clinical and Pathological Evidence for a Frontal Variant of Alzheimer Disease
Johnson, J. K., Head, E., Kim, R., Starr, A., & Cotman, C. W. (1999) · Archives of Neurology · doi:10.1001/archneur.56.10.1233 · Cited by 414 · see citing works
Nelson, P. T., Head, E., Schmitt, F. A., Davis, P. R., Neltner, J. H., Jicha, G. A., Abner, E. L., Smith, C. D., Van Eldik, L. J., Kryscio, R. J., et al. (2011) · Acta Neuropathologica · doi:10.1007/s00401-011-0826-y · Cited by 365 · see citing works
Posterior Cortical Atrophy: Clinical Characteristics and Differences Compared to Alzheimer’s Disease
Mendez, M. F., Ghajarania, M., & Perryman, K. M. (2002) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000058331 · Cited by 364 · see citing works
Psychiatric Aspects of Neurological Disease
Daly, D. D. (1976) · American Journal of Psychiatry · doi:10.1176/ajp.133.4.463-a · Cited by 330 · see citing works
Small, B. J., Fratiglioni, L., Viitanen, M., Winblad, B., & Bäckman, L. (2000) · Archives of Neurology · doi:10.1001/archneur.57.6.839 · Cited by 329 · see citing works
Psychometric Differentiation of Mild Senile Dementia of the Alzheimer Type
Storandt, M., Botwinick, J., Danziger, W. L., Berg, L., & Hughes, C. P. (1984) · Archives of Neurology · doi:10.1001/archneur.1984.04050170043013 · Cited by 325 · see citing works
Delis, D. C., Massman, P. J., Butters, N., Salmon, D. P., Cermak, L. S., & Kramer, J. H. (1991) · Psychological Assessment · doi:10.1037/1040-3590.3.1.19 · Cited by 312 · see citing works
Self-citationProgressive posterior cortical dysfunction
Renner, J. A., Burns, J. M., Hou, C. E., McKeel, D. W., Storandt, M., & Morris, J. C. (2004) · Neurology · doi:10.1212/01.wnl.0000140290.80962.bf · Cited by 311 · see citing works
Suspected non-Alzheimer disease pathophysiology — concept and controversy
Jack, C. R., Knopman, D. S., Chételat, G., Dickson, D. W., Fagan, A. M., Frisoni, G. B., Jagust, W. J., Mormino, E. C., Petersen, R. C., Sperling, R. A., et al. (2016) · Nature Reviews Neurology · doi:10.1038/nrneurol.2015.251 · Cited by 299 · see citing works
Rosser, A. E., & Hodges, J. R. (1994) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp.57.11.1389 · Cited by 298 · see citing works
Executive function deficits in mild Alzheimer's disease.
Lafleche, G., & Albert, M. (1995) · Neuropsychology · doi:10.1037/0894-4105.9.3.313 · Cited by 285 · see citing works
Edmonds, E. C., Delano‐Wood, L., Clark, L. R., Jak, A. J., Nation, D. A., McDonald, C. R., Libon, D. J., Au, R., Galasko, D., Salmon, D. P., et al. (2015) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2014.03.005 · Cited by 256 · see citing works
Self-citationHof, P. R., Vogt, B. A., Bouras, C., & Morrison, J. H. (1997) · Vision Research · doi:10.1016/s0042-6989(96)00240-4 · Cited by 246 · see citing works
Jedynak, B., Lang, A., Liu, B., Katz, E., Zhang, Y., Wyman, B. T., Raunig, D. L., Jedynak, C. P., Caffo, B. S., & Prince, J. L. (2012) · NeuroImage · doi:10.1016/j.neuroimage.2012.07.059 · Cited by 245 · see citing works
Early Diagnosis of Alzheimers Disease: Is MCI Too Late?
Petersen, R. C. (2009) · Current Alzheimer Research · doi:10.2174/156720509788929237 · Cited by 239 · see citing works
Episodic memory changes are associated with the APOE- epsilon 4 allele in nondemented older adults
Bondi, M. W., Salmon, D. P., Monsch, A. U., Galasko, D., Butters, N., Klauber, M. R., Thal, L. J., & Saitoh, T. (1995) · Neurology · doi:10.1212/wnl.45.12.2203 · Cited by 236 · see citing works
Self-citationBondi, M. W., Salmon, D. P., Galasko, D., Thomas, R. G., & Thal, L. J. (1999) · Psychology and Aging · doi:10.1037//0882-7974.14.2.295 · Cited by 235 · see citing works
Self-citationDrachman, D. A. (2014) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2013.11.003 · Cited by 224 · see citing works
Iba, M., McBride, J. D., Guo, J. L., Zhang, B., Trojanowski, J. Q., & Lee, V. M.-Y. (2015) · Acta Neuropathologica · doi:10.1007/s00401-015-1458-4 · Cited by 223 · see citing works
Diagnosis of early dementia by the Double Memory Test
Herman Buschke, L., Sliwinski, M. J., Kuslansky, G., & Lipton, R. B. (1997) · Neurology · doi:10.1212/wnl.48.4.989 · Cited by 222 · see citing works
Nestor, P. J. (2003) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp.74.11.1521 · Cited by 217 · see citing works
Ryan, N. S., Keihaninejad, S., Shakespeare, T. J., Lehmann, M., Crutch, S. J., Malone, I. B., Thornton, J. S., Mancini, L., Hyare, H., Yousry, T., et al. (2013) · Brain · doi:10.1093/brain/awt065 · Cited by 205 · see citing works
Predicting MCI outcome with clinically available MRI and CSF biomarkers
Heister, D. S., Brewer, J. B., Magda, S., Blennow, K., McEvoy, L. K., & Initiative, A. D. N. (2011) · Neurology · doi:10.1212/wnl.0b013e3182343314 · Cited by 201 · see citing works
Subtle Cognitive Decline and Biomarker Staging in Preclinical Alzheimer’s Disease
Edmonds, E. C., Initiative, A. D. N., Delano‐Wood, L., Galasko, D. R., Salmon, D. P., & Bondi, M. W. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-150128 · Cited by 195 · see citing works
Self-citationAlzheimer’s disease can be accurately diagnosed in very mildly impaired individuals
Salmon, D. P., Thomas, R. G., Pay, M. M., Booth, A., Hofstetter, C. R., Thal, L. J., & Katzman, R. (2002) · Neurology · doi:10.1212/wnl.59.7.1022 · Cited by 189 · see citing works
Self-citationBrain injury biomarkers are not dependent on β‐amyloid in normal elderly
Knopman, D. S., Jack, C. R., Wiste, H. J., Weigand, S. D., Vemuri, P., Lowe, V. J., Kantarci, K., Gunter, J. L., Senjem, M. L., Mielke, M. M., et al. (2013) · Annals of Neurology · doi:10.1002/ana.23816 · Cited by 183 · see citing works
Attention and brain function in Alzheimer's disease: A review.
Parasuraman, R., & Haxby, J. V. (1993) · Neuropsychology · doi:10.1037/0894-4105.7.3.242 · Cited by 174 · see citing works
Bondi, M. W., Salmon, D. P., Galasko, D. R., et al. (1999) · Psychology and Aging · doi:10.1037/0882-7974.14.2.295 · Cited by 170 · see citing works
Self-citationAre Empirically-Derived Subtypes of Mild Cognitive Impairment Consistent with Conventional Subtypes?
Clark, L. R., Delano-Wood, L., Libon, D. J., McDonald, C. R., Nation, D. A., Bangen, K. J., Jak, A. J., Au, R., Salmon, D. P., & Bondi, M. W. (2013) · Journal of the International Neuropsychological Society · doi:10.1017/s1355617713000313 · Cited by 167 · see citing works
Self-citationPreclinical cognitive markers of dementia of the Alzheimer type.
Bondi, M. W., Monsch, A. U., Galasko, D., Butters, N., Salmon, D. P., & Delis, D. C. (1994) · Neuropsychology · doi:10.1037/0894-4105.8.3.374 · Cited by 163 · see citing works
Self-citationRascovsky, K., Salmon, D., Hansen, L., Thal, L., & Galasko, D. (2007) · Neuropsychology · doi:10.1037/0894-4105.21.1.20 · Cited by 160 · see citing works
Self-citationPsychiatric aspects of neurological disease
Benson, D. F., & Blumer, D. P. (1975) · Grune & Stratton eBooks · Cited by 151 · see citing works
Wirth, M., Madison, C. M., Rabinovici, G. D., Oh, H., Landau, S. M., & Jagust, W. J. (2013) · The Journal of Neuroscience · doi:10.1523/jneurosci.4409-12.2013 · Cited by 151 · see citing works
Lower Cognitive Performance in Normal Older Adult Male Twins Carrying the Apolipoprotein E 4 Allele
Reed, T., Carmelli, D., Swan, G. E., Breitner, J. C. S., Welsh-Bohmer, K. A., Jarvik, G. P., Deeb, S., & Auwerx, J. H. (1994) · Archives of Neurology · doi:10.1001/archneur.1994.00540240033012 · Cited by 143 · see citing works
Braak, H., Zetterberg, H., Tredici, K. D., & Blennow, K. (2013) · Acta Neuropathologica · doi:10.1007/s00401-013-1139-0 · Cited by 141 · see citing works
Cortical vs Subcortical Dementia
Huber, S. J. (1986) · Archives of Neurology · doi:10.1001/archneur.1986.00520040072023 · Cited by 127 · see citing works
Salmon, D. P., Heindel, W. C., & Lange, K. L. (1999) · Journal of the International Neuropsychological Society · doi:10.1017/s1355617799577126 · Cited by 114 · see citing works
Self-citationSolomon, P., & Patch, V. D. (1974) · Medical Entomology and Zoology · Cited by 113 · see citing works
On the nature of the memory disorder in presenile dementia
Miller, E. (1971) · Neuropsychologia · doi:10.1016/0028-3932(71)90064-9 · Cited by 103 · see citing works
Braak, H., & Tredici, K. D. (2014) · Acta Neuropathologica · doi:10.1007/s00401-014-1356-1 · Cited by 99 · see citing works
Phonological loop and central executive functioningin Alzheimers disease
Collette, F. (1999) · Neuropsychologia · doi:10.1016/s0028-3932(98)00148-1 · Cited by 96 · see citing works
Differentiation of Alzheimer's Disease and Huntington's Disease With the Dementia Rating Scale
Salmon, D. P., Kwo-On-Yuen, P. F., Heindel, W. C., et al. (1989) · Archives of Neurology · doi:10.1001/archneur.1989.00520470060028 · Cited by 87 · see citing works
Self-citationRichard, E., Schmand, B. A., Eikelenboom, P., & Van Gool, W. A. (2013) · BMJ Open · doi:10.1136/bmjopen-2012-002541 · Cited by 84 · see citing works
Heterogeneous cortical atrophy patterns in MCI not captured by conventional diagnostic criteria
Edmonds, E. C., Eppig, J. S., Bondi, M. W., Leyden, K. M., Goodwin, B., Delano‐Wood, L., McDonald, C. R., & Initiative, A. D. N. (2016) · Neurology · doi:10.1212/wnl.0000000000003326 · Cited by 84 · see citing works
Self-citationShort- and long-term memory in patients with presenile dementia (Alzheimer's disease)
Miller, E. (1973) · Psychological Medicine · doi:10.1017/s003329170004856x · Cited by 81 · see citing works
Wilson, P. T., & Spitzer, R. L. (1968) · PubMed · Cited by 74 · see citing works
Mild Cognitive Impairment and Dementia: Definitions, Diagnosis, and Treatment
Duff, K. M. (2014) · Archives of Clinical Neuropsychology · doi:10.1093/arclin/acu034 · Cited by 70 · see citing works
Impaired Recall and the Memory Disturbance in Presenile Dementia
MILLER, B. (1975) · British Journal of Social and Clinical Psychology · doi:10.1111/j.2044-8260.1975.tb00151.x · Cited by 70 · see citing works
Gomar, J. J., Conejero‐Goldberg, C., Davies, P., Goldberg, T. E., & Initiative, A. D. N. (2014) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2013.11.009 · Cited by 67 · see citing works
Posterior Cortical Atrophy: A Review of the Literature
Caine, D. (2004) · Neurocase · doi:10.1080/13554790490892239 · Cited by 63 · see citing works
Bondi, M. W., Monsch, A. U., Butters, N., Salmon, D. P., & Paulsen, J. S. (1993) · The Clinical Neuropsychologist · doi:10.1080/13854049308401518 · Cited by 48 · see citing works
Self-citationIntrusion errors in the figural memory of patients with Alzheimer's and Huntington's disease
Jacobs, D. M., Salmon, D. P., Tröster, A. I., et al. (1990) · Archives of Clinical Neuropsychology · doi:10.1093/arclin/5.1.49 · Cited by 44 · see citing works
Self-citationMild Cognitive Impairment and Dementia: Definitions, Diagnosis, and Treatment
Smith, G. E., & Bondi, M. W. (2013) · Cited by 40 · see citing works
Self-citationPosterior Cortical Atrophy: A Rare Form of Dementia with in vivo Evidence of Amyloid-β Accumulation
Tenovuo, O. S., Kemppainen, N. M., Aalto, S., et al. (2008) · Journal of Alzheimer s Disease · doi:10.3233/jad-2008-15301 · Cited by 38 · see citing works
Psychopathology through a life span-genetic prism.
Gottesman, I. I. (2001) · American Psychologist · doi:10.1037/0003-066x.56.11.867 · Cited by 38 · see citing works
Rue, A. L., Matsuyama, S. S., McPherson, S. E., Sherman, J., & Jarvik, L. F. (1992) · Journal of Clinical and Experimental Neuropsychology · doi:10.1080/01688639208402842 · Cited by 34 · see citing works
Tau Imaging in Alzheimer's Disease Diagnosis and Clinical Trials
Brosch, J. R., Farlow, M. R., Risacher, S. L., & Apostolova, L. G. (2016) · Neurotherapeutics · doi:10.1007/s13311-016-0490-y · Cited by 34 · see citing works
Handbook on the Neuropsychology of Aging and Dementia
Ravdin, L., Katzen, H., & Publishing, S. I. (2019) · Clinical handbooks in neuropsychology · doi:10.1007/978-3-319-93497-6 · Cited by 30 · see citing works
Norton, L., Bondi, M. W., Salmon, D. P., et al. (1997) · Journal of Clinical and Experimental Neuropsychology · doi:10.1080/01688639708403766 · Cited by 26 · see citing works
Self-citationRetrieval from long‐term memory in presenile dementia: Two tests of an hypothesis
Miller, E. (1978) · British Journal of Social and Clinical Psychology · doi:10.1111/j.2044-8260.1978.tb00256.x · Cited by 25 · see citing works
Alzheimer: The Life of a Physician and the Career of a Disease
Freeman, W. (2004) · American Journal of Psychiatry · doi:10.1176/appi.ajp.161.2.381 · Cited by 20 · see citing works
Dementia: a Survey of the syndrome of Dementia
Pearce, J. (1985) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp.48.2.196 · Cited by 19 · see citing works
Dementia: A survey of the syndrome of dementia
Mahendra, B. (1984) · Medical Entomology and Zoology · Cited by 17 · see citing works
Defining the Genetic Architecture of Alzheimer's Disease: Where Next?
Sims, R., & Williams, J. H. (2015) · Neurodegenerative Diseases · doi:10.1159/000440841 · Cited by 13 · see citing works
Flagged first, then by citations
Research works printed but not linked: 8
- Katzman, 1994, Alzheimer disease, 105
- Bird, 1999, Alzheimer disease, 57
- 1992, International Classification of Diseases
- Cronin-Golomb, 2001, Handbook of Neuropsychology. Aging and dementia, Vol. 6, 119
- 1968, Diagnostic and Statistical Manual of Mental Disorders
- Squire, 1987, Memory and brain
- Cummings, 1990, Subcortical dementia
- Alzheimer, 1907, über eine eigenartige Erkankung der Hirnrinde, Allgemeine Zeitschrift fur Psychiatrie under Psychisch-Gerichtliche Medizin, 64, 146
Cited by
Sorted by citations
Current and Future Treatments in Alzheimer Disease: An Update
Yiannopoulou, K. G., & Papageorgiou, S. G. (2020) · Journal of Central Nervous System Disease · doi:10.1177/1179573520907397 · Cited by 966 · see citing works
TGF-β Signaling in Cellular Senescence and Aging-Related Pathology
Tominaga, K., & Suzuki, H. I. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20205002 · Cited by 393 · see citing works
Böhle, M., Eitel, F., Weygandt, M., & Ritter, K. (2019) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2019.00194 · Cited by 291 · see citing works
Wang, W., Zhou, Q., Jiang, T., Li, S., Ye, J., Zheng, J., Wang, X., Liu, Y., Deng, M., Ke, D., et al. (2021) · Theranostics · doi:10.7150/thno.55680 · Cited by 242 · see citing works
Specific basal forebrain-cortical cholinergic circuits coordinate cognitive operations
Záborszky, L., Gombkoto, P., Varsanyi, P., Gielow, M. R., Poe, G., Role, L. W., Ananth, M., Rajebhosale, P., Talmage, D. A., Hasselmo, M. E., et al. (2018) · The Journal of Neuroscience · doi:10.1523/jneurosci.1676-18.2018 · Cited by 202 · see citing works
An update on the novel and approved drugs for Alzheimer disease
Alhazmi, H. A., & Albratty, M. (2022) · Saudi Pharmaceutical Journal · doi:10.1016/j.jsps.2022.10.004 · Cited by 122 · see citing works
“These oligomers form protobrils, which eventually lead to amyloid deposits (Bondi et al., 2017).”
A Primary Care Agenda for Brain Health: A Scientific Statement From the American Heart Association
Lazar, R. M., Howard, V. J., Kernan, W. N., Aparicio, H. J., Levine, D. A., Viera, A. J., Jordan, L. C., Nyenhuis, D. L., Possin, K. L., Sorond, F. A., et al. (2021) · Stroke · doi:10.1161/str.0000000000000367 · Cited by 109 · see citing works
Jiskoot, L. C., Poos, J. M., Vollebergh, M. E., Franzen, S., van Hemmen, J., Papma, J. M., van Swieten, J. C., Kessels, R. P. C., & van den Berg, E. (2021) · Journal of Neurology · doi:10.1007/s00415-020-10096-y · Cited by 42 · see citing works
Effect of glycyrrhizic acid on scopolamine-induced cognitive impairment in mice
Ban, J. Y., Park, H. K., & Kim, S. K. (2020) · International Neurourology Journal · doi:10.5213/inj.2040154.077 · Cited by 40 · see citing works
[Retracted] A Review of Bile Acid Metabolism and Signaling in Cognitive Dysfunction‐Related Diseases
Weng, Z.-B., Chen, Y.-R., Lv, J.-T., Wang, M.-X., Chen, Z.-Y., Zhou, W., Shen, X.-C., Zhan, L.-B., & Wang, F. (2022) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2022/4289383 · Cited by 32 · see citing works
RetractedPotential Impacts of Extreme Heat and Bushfires on Dementia
Farugia, T. L., Cuni-Lopez, C., & White, A. R. (2021) · Journal of Alzheimer’s Disease · doi:10.3233/jad-201388 · Cited by 29 · see citing works
Turcu, A. L., Companys-Alemany, J., Phillips, M. B., Patel, D. S., Griñán-Ferré, C., Loza, M. I., Brea, J. M., Pérez, B., Soto, D., Sureda, F. X., et al. (2022) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2022.114354 · Cited by 27 · see citing works
Current therapeutics for Alzheimer’s disease and clinical trials
Xiao, D., & Zhang, C. (2024) · Exploration of Neuroscience · doi:10.37349/en.2024.00048 · Cited by 30 · see citing works
Control of the temporal development of Alzheimer’s disease pathology by the MR1/MAIT cell axis
Wyatt-Johnson, S. K., Kersey, H. N., Codocedo, J. F., Newell, K. L., Landreth, G. E., Lamb, B. T., Oblak, A. L., & Brutkiewicz, R. R. (2023) · Journal of Neuroinflammation · doi:10.1186/s12974-023-02761-6 · Cited by 22 · see citing works
“Discussion Alzheimer’s disease is a devastating neurodegenerative disease that is growing as a worldwide epidemic, mainly affecting the elderly [1, 2].”
BackgroundRouhi, N., Chakeri, Z., Ghorbani Nejad, B., Rahimzadegan, M., Rafi Khezri, M., Kamali, H., & Nosrati, R. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e37533 · Cited by 20 · see citing works
Pathogenesis, Animal Models, and Drug Discovery of Alzheimer’s Disease
Xia, Z.-D., Ma, R.-X., Wen, J.-F., Zhai, Y.-F., Wang, Y.-Q., Wang, F.-Y., Liu, D., Zhao, X.-L., Sun, B., Jia, P., et al. (2023) · Journal of Alzheimer's Disease · doi:10.3233/jad-230326 · Cited by 19 · see citing works
Fitting Contralateral Neuroanatomical Asymmetry into the Amyloid Cascade Hypothesis
Arreola, F., Salazar, B., & Martinez, A. (2022) · Healthcare · doi:10.3390/healthcare10091643 · Cited by 3 · see citing works
Wei, H., Wu, C., Yuan, Y., & Lai, L. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1249682 · Cited by 3 · see citing works
- Authors
- Bondi, M. W., Edmonds, E. C., & Salmon, D. P.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Bondi, Mark W.
- Venue
- Journal of the International Neuropsychological Society
- Publisher
- Cambridge University Press (CUP)
- Published
- 2017-10
- Volume
- 23
- Issue
- 9-10
- Pages
- 818-831
- ISSN
- 1355-6177 (ISSN-L)
- 1469-7661
- PMC
- PMC5830188
- OpenAlex
- W2775724624
- Cited by
- 649
- References
- 129
- Citations by year
- 2026: 43 · 2025: 93 · 2024: 84 · 2023: 114 · 2022: 96 · 2021: 105 · 2020: 73 · 2019: 31 · 2018: 8 · 2017: 1
- FWCI
- 4.69
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of the International Neuropsychological Society (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- U.S. Department of Veterans Affairs (IK2 CX001415)
- National Institute on Aging (R01AG049810, P50AG005131, K24AG026431)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurology and Historical Studies
- Keywords
- Alzheimer's disease, dementia, neuropsychological deficits, dementia subtypes, mild cognitive impairment, preclinical biomarkers, neuroimaging, neuropathology, therapeutic interventions
- MeSH terms
- Alzheimer Disease, Humans, Neuropsychological Tests, History, 20th Century, History, 21st Century, Cognitive Dysfunction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-10.
Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-10.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
