Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Download bibliography of all 5,209 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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Mutation carriers had significantly increased hippocampal and whole-brain atrophy rates compared with controls and these differences increased with time.
Why it matters
In nine people carrying mutations that cause familial Alzheimer's disease, shrinkage of the hippocampus and whole brain was faster than in healthy controls, and these differences appeared years before diagnosis. This suggests that MRI measures of brain shrinkage could help track disease progression before symptoms begin, though the study was small.
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These responder analyses may assist clinicians in evaluating the impact of memantine in a relevant clinical scenario, i.e., in patients with AD previously stabilized on a cholinesterase inhibitor.
Why it matters
In this responder analysis of a 24-week trial, memantine produced higher response rates than placebo for improving or stabilizing symptoms in people with moderate to severe Alzheimer's disease already taking donepezil. This concerns symptom improvement and stabilization, not curing or preventing the disease.
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During follow-up, 57 (42%) patients with MCI developed Alzheimer's disease, 21 (15%) developed other forms of dementia, and 56 (41%) remained cognitively stable for 5.2 years (range 4.0-6.8).
Why it matters
In patients with mild cognitive impairment, a combination of CSF T-tau and Abeta42 predicted progression to Alzheimer's disease with 95% sensitivity and 83% specificity, and pathological levels raised the risk substantially. These are early-detection biomarkers, not a treatment or cure.
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Although statin use might be less frequent in those with prevalent dementia, we found no association between statin use and subsequent onset of dementia or AD.
Why it matters
In this study, statin use was associated with lower prevalence of dementia at the initial assessment, but statin use at baseline did not predict who developed dementia or Alzheimer's disease three years later. The authors concluded there was no association between statin use and subsequent onset of dementia or Alzheimer's disease.
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The APOE epsilon4 allele acts as a potent risk factor for AD by accelerating onset.
Why it matters
In 3308 elderly residents of Cache County, the APOE ε4 allele accelerated the age at onset of Alzheimer's disease but did not meaningfully change the estimated 100-year lifetime incidence, which was 72%. This describes how APOE ε4 affects timing rather than whether a person develops the disease, and it does not test any treatment, cure, or prevention.
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59/100
These data support the use of rates of change from serial MRI studies in addition to standard clinical/psychometric measures as surrogate markers of disease progression in AD.
Why it matters
Among 160 subjects, rates of brain atrophy on serial MRI were greater in people who converted from normal to mild cognitive impairment or Alzheimer's disease and in faster progressors. This links imaging measures to disease progression and provides no information on treating, curing or preventing Alzheimer's disease.
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Stroke is associated with AD among elderly individuals.
Why it matters
In this longitudinal study of 1,766 Medicare recipients without dementia, a history of stroke was associated with a higher risk of Alzheimer's disease, and risk increased further when hypertension, diabetes, or heart disease were also present. This shows stroke and vascular risk factors are linked to Alzheimer's disease risk, but does not show that preventing stroke cures or prevents Alzheimer's disease.
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To accurately predict the development of Alzheimer's disease (AD) at its predementia stage would be a major breakthrough from both therapeutic and research standpoints.
Why it matters
This review states that hippocampal and entorhinal cortex atrophy are the most specific and sensitive structural imaging features of early Alzheimer's disease, and that people with mild cognitive impairment show significant hippocampal atrophy compared with normal controls. It notes that only longitudinal studies can assess whether initial atrophy measurements predict progression, and it does not offer a treatment or cure.
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Patients with frontotemporal dementia (FTD) with no known diagnosis of ALS or family history of ALS were clinically and electrophysiologically assessed for the presence of ALS.
Why it matters
Among 36 people with frontotemporal dementia (FTD) who had no known ALS and no family history of it, five met criteria for definite ALS when examined clinically and with EMG nerve-muscle testing, and two more had EMG signs of denervation in one limb. Another five had prominent muscle twitching (fasciculations) and six had trouble swallowing, all with normal EMG, and one of the twitching patients progressed to definite ALS within a year. This small study is about FTD and ALS rather than Alzheimer's disease, and it did not test any treatment.
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59/100
A new diagnostic indicator of FDG PET scan abnormality, based on age-adjusted t statistics and an automated voxel-based procedure, is presented and validated in a large data set comprising 110 normal controls and 395 patients with probable Alzheimer's disease (AD) that were studied in eight participating centers.
Why it matters
Across eight centres, an automated, age-adjusted score of brain glucose PET scans separated 395 people with probable Alzheimer's disease from 110 healthy controls with 93% sensitivity and specificity for mild to moderate disease, and 84% sensitivity at 93% specificity for very mild disease (MMSE 24 or better). The patients were compared only with healthy people, not with other dementias, and diagnoses were clinical ("probable"). The authors conclude that the method "can be used potentially as a sensitive biomarker for early AD diagnosis", not that it is ready for routine use.
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Phosphorylation of tau protein at threonine 231 (using full-length tau, 441 amino acids, for the numbering scheme) (p-tau(231)) occurs specifically in postmortem brain tissue of patients with Alzheimer disease (AD) and can be sensitively detected in cerebrospinal fluid (CSF).
Why it matters
This cross-sectional multicenter study tested whether cerebrospinal fluid tau phosphorylated at threonine 231 could distinguish Alzheimer patients from controls and from people with other dementias, and compared it with total tau. It is a diagnostic comparison only and provides no treatment, cure, or prevention.
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In the first of five phases in the evolution of beta-amyloidosis Abeta deposits are found exclusively in the neocortex.
Why it matters
This study describes five phases in the evolution of beta-amyloidosis in the human brain, beginning in the neocortex and spreading hierarchically to allocortical regions, diencephalic nuclei, striatum, cholinergic nuclei, brainstem nuclei, and finally the cerebellum. The 17 clinically proven Alzheimer's disease cases exhibited phases 3, 4, or 5, while nine nondemented cases with Alzheimer's-related amyloid pathology showed phases 1, 2, or 3.
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CERAD was funded by the National Institute on Aging with a mandate to standardize assessment in Alzheimer's disease.
Why it matters
CERAD developed and evaluated standardized clinical, neuropsychological, and neuropathological assessments for Alzheimer's disease. These measures have been translated into multiple languages and used in clinical and epidemiological studies.
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59/100
Some well-known risk factors for AD were confirmed in this study and potential new risk factors were identified.
Why it matters
This longitudinal study found that older age, fewer years of education, occupational exposure to fumigants or defoliants, a history of migraines, and self-reported memory loss at baseline were associated with increased Alzheimer's disease risk. Vaccinations and occupational exposure to excessive noise were associated with reduced risk.
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A population-based longitudinal study in Sweden, the Kungsholmen Project A random sample of 370 nondemented persons, aged 75 years and older and not treated with B(12) and folate, was followed for 3 years to detect incident AD cases.
Why it matters
This population-based longitudinal study in Sweden suggests that vitamin B12 and folate may be involved in the development of Alzheimer's disease, with a clear association detected only when both vitamins were taken into account. The authors say monitoring serum B12 and folate in the elderly may be relevant for prevention, but this is an association from one study, not proof that these vitamins prevent Alzheimer's disease.
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Incidence of parkinsonism and PD increased with age, PD was the most common type of parkinsonism, and men had a risk of developing PD twice that of women.
Why it matters
This study measured how often parkinsonism and Parkinson's disease occurred in older Italians and found higher rates in men. It concerns Parkinson's disease, not the treatment, cure or prevention of Alzheimer's disease.
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This text examines how inflammation occurs in vulnerable regions of the Alzheimer's disease brain in response to stimuli like damaged neurons and insoluble deposits.
Why it matters
Addresses inflammation and its place in Alzheimer's disease. Inflammation is presented as a feature of the disease to investigate rather than as something treated here.
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We used magnetic resonance imaging (MRI) measurements to determine whether persons in the prodromal phase of Alzheimer's disease (AD) could be accurately identified before they developed clinically diagnosed dementia.
Why it matters
In this study, 79 subjects with mild memory difficulty received a baseline MRI and were followed for 3 years, during which 19 converted to a diagnosis of probable Alzheimer's disease; baseline MRI measures of the entorhinal cortex, banks of the superior temporal sulcus and anterior cingulate were most useful in discriminating who converted, with 93% accuracy, sensitivity 0.95 and specificity 0.90. This concerns predicting who will develop Alzheimer's disease using imaging, not treating, curing or preventing it.
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This study investigated cerebral glucose metabolism in very early Alzheimer's disease, before a clinical diagnosis of probable Alzheimer's disease is possible, using [18F]fluorodeoxyglucose positron emission tomography.
Why it matters
This PET study found a marked 21-22% metabolic reduction in the posterior cingulate cortex in very early Alzheimer's disease, before a clinical diagnosis was possible. It identifies an early brain change but does not test any treatment, cure or prevention.
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Why it matters
Reports that presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease increase secreted amyloid beta-protein, similar to that in Alzheimer's senile plaques, in vivo.
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Even in elderly subjects without dementia, the apolipoprotein E genotype is related to the degree of deposition of beta-amyloid protein in the cerebral cortex.
Why it matters
In 92 autopsied people aged 85 or older from a population cohort in Vantaa, Finland (out of 271 eligible), the ε4 form of the apolipoprotein E gene made up 30% of gene copies in those with Alzheimer's disease versus 8% in those without dementia. Even among those without dementia, APOE genotype was related to how much of the cortex was covered by amyloid plaques, the study's estimate of beta-amyloid deposition. This shows an association in the very old, not that ε4 causes amyloid or dementia, and the stored abstract gives no figures for the plaque result.
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The study reported the cloning of a novel gene (E5-1) encoded on chromosome 1 with sequence similarity to the S182 gene on chromosome 14q24.3.
Why it matters
Reports families with inherited (familial) Alzheimer's disease that carry missense mutations in a gene on chromosome 1 related to the Alzheimer's disease type 3 gene.
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We conducted a case-control study of clinically diagnosed Alzheimer's disease (AD) on 170 cases aged 52 to 96 years, and 170 controls matched for age, sex and, where possible, the general practice of origin.
Why it matters
This case-control study found significant odds ratios for a family history of dementia, probable Alzheimer's disease, or Down's syndrome, and for underactivity as a behavioral trait. It did not confirm previously reported associations with head injury, starvation, thyroid disease, analgesic abuse, antacid use, alcohol abuse, smoking, or being left-handed.
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The type, frequency, and extent of MR signal abnormalities in Alzheimer's disease and normal aging are a subject of controversy.
Why it matters
In an early 1.5 T MRI study of 12 people with Alzheimer's disease, 4 with multi-infarct dementia and 9 age-matched controls, small bright spots in the deep white matter appeared in about 60% of both the Alzheimer's patients and the controls and were unrelated to high blood pressure or other vascular risk factors. A more extensive smooth "halo" of brightness around the ventricles was more common in Alzheimer's patients (p = .024), and the authors suggest it "may be of diagnostic importance". This is a very small imaging comparison: it does not test a diagnostic rule, a treatment or any way of preventing the disease.
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Genetic risk for AD does not modify the association between hypertension and dementia.
Why it matters
In this cohort, midlife hypertension was significantly associated with dementia incidence across all genetic risk groups among White participants and among Black participants. The study examined how genetic risk for Alzheimer's disease modifies the link between midlife hypertension and dementia.
From across this topic
10 of the 5,172 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Progressive aphasia secondary to Alzheimer disease vs FTLD pathology
- Impact of vitamin A on aged people’s cognition and Alzheimer’s disease progression in an animal model
- Dissociable spatial topography of cortical atrophy in early‐onset and late‐onset Alzheimer's disease: A head‐to‐head comparison of the LEADS and ADNI cohorts
- The Danish Alzheimer intervention study: rationale, study design and baseline characteristics of the cohort
- A review on neuroimaging-based classification studies and associated feature extraction methods for Alzheimer's disease and its prodromal stages
- Bibliometric analysis of neuroinflammation and Alzheimer's disease
- Assessment of Plasma and Cerebrospinal Fluid Biomarkers in Patients with Alzheimer’s Disease and Other Dementias: A Center-Based Study
- Effect of apolipoprotein E on biomarkers of amyloid load and neuronal pathology in Alzheimer disease
- Performance of FDG PET for detection of Alzheimer's disease in two independent multicentre samples (NEST-DD and ADNI)
- Amyloidogenic processing of the Alzheimer beta-amyloid precursor protein depends on lipid rafts