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 5,413 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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58/100
Plasma A beta levels are affected by age and by systemic and CNS vascular risk factors.
Why it matters
In unadjusted models, plasma β-amyloid 1-40 and 1-42 levels were associated with later Alzheimer disease in normal subjects, but in the fully adjusted model neither peptide nor their ratio was associated with incident Alzheimer disease. This means the initial association did not hold after accounting for other factors.
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58/100
The positron emission tomography (PET) radiotracer Pittsburgh Compound-B (PiB) binds with high affinity to beta-pleated sheet aggregates of the amyloid-beta (Abeta) peptide in vitro.
Why it matters
This post-mortem study found that PiB binding in Alzheimer's disease brain tissue is highly selective for insoluble fibrillar amyloid-beta deposits and not for neurofibrillary pathology. It does not test a treatment or cure, but helps clarify what PiB-PET imaging measures in the brain.
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The risk of dementia and Alzheimer's disease (AD) probably results from an interaction between genetic and environmental factors.
Why it matters
Carrying the APOE epsilon4 allele was an independent risk factor for dementia and Alzheimer's disease, and lifestyle factors like physical inactivity, alcohol drinking, smoking, and dietary fat increased risk especially among carriers. This concerns risk factors, not treatment or cure.
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To determine the frequency of Alzheimer's disease (AD) pathology in patients presenting with progressive focal cortical syndromes, notably posterior cortical atrophy (PCA), corticobasal syndrome (CBS), behavioural variant frontotemporal dementia (bvFTD), progressive non-fluent aphasia (PNFA) (or a mixed aphasia) and semantic dementia (SD); and to compare the age of onset, evolution and prognosis in patients with focal cortical presentations of AD versus more typical AD and those with non AD pathology.
Why it matters
This study of brain tissue found that Alzheimer's disease was a much more common cause of focal cortical syndromes than previously recognized, especially in posterior cortical atrophy, progressive non-fluent aphasia and corticobasal syndrome. It is about diagnosis and disease frequency, not about treating or preventing Alzheimer's disease.
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Adherence to the Mediterranean diet (MeDi) may affect not only risk for Alzheimer disease (AD) but also subsequent disease course: Higher adherence to the MeDi is associated with lower mortality in AD.
Why it matters
In this study of 192 people already diagnosed with Alzheimer's disease, higher adherence to the Mediterranean diet was associated with lower mortality risk, with those in the highest adherence tertile surviving longer than those in the lowest. It concerns survival after diagnosis and does not show that the Mediterranean diet cures or prevents Alzheimer's disease.
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This study confirms the association between genetic variants in SORL1 and AD.
Why it matters
In this multiethnic community cohort, several individual variants and haplotypes in the SORL1 gene were significantly associated with Alzheimer's disease, confirming a previously reported link. Different variants were associated with Alzheimer's disease in different ethnic groups, so the genetic findings varied by population.
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These post-hoc analyses support the beneficial effects of memantine on cognition observed in a previously reported clinical trial.
Why it matters
In this exploratory reanalysis of a 24-week trial, memantine added to donepezil improved scores on memory, language, and praxis compared with placebo in people with moderate to severe Alzheimer's disease. As a post-hoc analysis, these findings are exploratory and do not show that memantine cures or prevents the disease.
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The CSDD, and particularly its mood subscale, appears to be more sensitive than the HDRS, it's subscales or the NPI-M, for comparing drug to placebo in treating major depression in AD patients.
Why it matters
This study compared three depression rating scales used to measure treatment effects in a trial of sertraline for depression in people with Alzheimer disease. It found only a slight, not significant, advantage for one scale, and it is about how to measure depression outcomes in trials, not about treating Alzheimer disease itself.
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58/100
These observations suggest that brain amyloid deposition results in low CSF Abeta(42), and that amyloid imaging and CSF Abeta(42) may potentially serve as antecedent biomarkers of (preclinical) AD.
Why it matters
This study found that people with positive amyloid imaging had the lowest levels of amyloid-beta42 in cerebrospinal fluid, suggesting that brain amyloid deposits may lower these fluid levels. The authors propose that amyloid imaging and cerebrospinal fluid amyloid-beta42 could potentially serve as early biomarkers of preclinical Alzheimer's disease, though the study did not test treatments or cures.
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We report duplication of the APP locus on chromosome 21 in five families with autosomal dominant early-onset Alzheimer disease (ADEOAD) and cerebral amyloid angiopathy (CAA).
Why it matters
This study found duplication of the APP locus in five families with autosomal dominant early-onset Alzheimer's disease and cerebral amyloid angiopathy, with brains showing abundant amyloid-beta deposits in tissue and vessels. It identifies a genetic cause of a rare inherited form of the disease rather than a treatment, cure or prevention.
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Donepezil treatment slows the progression of hippocampal atrophy, suggesting a neuroprotective effect of donepezil in Alzheimer's disease.
Why it matters
In this cohort study, patients with Alzheimer's disease who took donepezil had a smaller annual rate of hippocampal volume loss than those who never took anti-Alzheimer drugs. This suggests donepezil may slow one measure of disease progression, but it does not show that donepezil cures or prevents Alzheimer's disease.
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Formation of senile plaques composed of amyloid beta peptide, a pathological hallmark of Alzheimer disease, in human brains precedes disease onset by many years.
Why it matters
In amyloid precursor protein transgenic mice, an intravenously given fluorine-containing compound labeled brain plaques that could be seen with MRI, offering a way to image amyloid without radiation exposure. This is animal work and does not show that this approach diagnoses or treats Alzheimer's disease in people.
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Nearly all persons had at least some AD pathology.
Why it matters
Researchers examined the brains of 180 Catholic clergy from the Religious Orders Study after death and compared them with each person's last clinical diagnosis: 60 had no cognitive impairment, 37 had mild cognitive impairment (MCI) and 83 had dementia. Nearly everyone had some Alzheimer's pathology, and on Braak stage and CERAD and NIA-Reagan criteria the MCI group fell between the other two groups; the authors say this suggests MCI "may be the earliest clinical manifestation of common age-related neurologic diseases." It is an autopsy association study in one specialised group: it does not show that MCI always leads to dementia, and it does not test any treatment or prevention.
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Recent functional imaging studies have revealed coactivation in a distributed network of cortical regions that characterizes the resting state, or default mode, of the human brain.
Why it matters
Compared functional MRI scans of 13 people with mild Alzheimer's and 13 age-matched older controls. The Alzheimer's group showed lower resting activity in the posterior cingulate and hippocampus, and the authors suggest activity in this brain network may prove a biomarker for early Alzheimer's.
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Parkinson's disease is a common neurodegenerative disorder primarily characterized by rigidity, tremor and bradykinesia.
Why it matters
This cross-sectional imaging study found that Parkinson's disease patients with dementia had reduced grey matter volume in several brain regions compared with controls, while those without dementia showed reduced volume in the frontal lobe. It describes brain atrophy patterns in Parkinson's disease and does not test any treatment, cure, or prevention for Alzheimer's disease.
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The p-tau proteins in CSF come closest to fulfilling the criteria of a biological marker of AD.
Why it matters
In 206 memory-clinic patients and controls, this 2004 study found that three forms of phosphorylated tau in spinal fluid (p-tau231, p-tau181 and p-tau199) were on average higher in people clinically diagnosed with Alzheimer's than in non-demented controls or people with frontotemporal, Lewy body or vascular dementia. Used alone, p-tau231 and p-tau181 each ruled out more than 75% of the non-Alzheimer's group when set to detect at least 85% of Alzheimer's cases, and combining all three markers did not improve on a single marker. It is a one-time diagnostic comparison based on clinical diagnoses and does not test any treatment.
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58/100
Previous studies reported substantial contributions of neurofibrillary tangles (NFT), amyloid deposits, and neuronal loss to the development of dementia.
Why it matters
In a clinicopathologic study of 22 elderly cases, the authors report — in the paper's title — that "tangle and neuron numbers, but not amyloid load, predict cognitive status." The study responded to earlier work that had "measured densities, rather than absolute numbers" of these brain changes and had given "conflicting results"; it used stereologic counts instead. The results data are not included in our record, and as a small, after-death association study it cannot show what causes memory loss or how to treat it.
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The association between the apoE epsilon4 allele and Alzheimer disease does not seem to be mediated by vascular factors.
Why it matters
In 1,449 people from eastern Finland followed for an average of 21 years, carrying the APOE ε4 gene variant (odds ratio 2.1), having raised total cholesterol in midlife (2.8) and having high systolic blood pressure in midlife (2.6) were each linked to Alzheimer's in later life, even after accounting for one another. The authors concluded that the risk from these "treatable factors" appears greater than the risk from ε4, but the three estimates have wide, overlapping confidence intervals. This was an observational study, so it does not show that lowering cholesterol or blood pressure prevents Alzheimer's.
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A safe and effective medicine, huperzine Alpha remarkably improves the cognition, behavior, ADL,and mood of AD patients.
Why it matters
In this 12-week trial of 202 patients with mild to moderate Alzheimer's disease, huperzine Alpha improved scores on cognition, daily living, and behavior scales compared with placebo. It is a short-term symptomatic treatment study and does not show whether the drug changes the underlying disease or prevents it.
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58/100
Compared with individuals with the APOEepsilon3/epsilon3, the odds of having AD were significantly increased among those with 1 or more copies of the epsilon4 allele; the odds ratio (OR) for the epsilon3/epsilon4 genotype was 2.6 (95% confidence interval [CI], 1.8-3.7), and the OR for the epsilon4/epsilon4 genotype was 10.5 (95% CI, 5.1-21.8).
Why it matters
Among African American participants, carrying one or more copies of the APOE ε4 allele was linked to higher odds of Alzheimer disease, while the ε2/ε3 genotype was linked to lower odds. These risks decreased substantially after age 68, and the findings are about genetic association, not a treatment or cure.
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58/100
Individuals with an isolated pathologic diagnosis of AD, hippocampal sclerosis, frontotemporal degeneration, and neurofibrillary tangle--only degeneration usually had substantial hippocampal atrophy, while those with changes of typical aging did not.
Why it matters
In this study, hippocampal atrophy on antemortem MRI was a fairly sensitive marker of the pathologic stage of Alzheimer's disease and consequent cognitive status, though it was not specific for Alzheimer's disease. Individuals with isolated pathologic diagnoses of Alzheimer's disease, hippocampal sclerosis, frontotemporal degeneration, and neurofibrillary tangle-only degeneration usually had substantial hippocampal atrophy, while those with changes of typical aging did not.
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Rapid progress in deciphering the biological mechanism of Alzheimer's disease (AD) has arisen from the application of molecular and cell biology to this complex disorder of the limbic and association cortices.
Why it matters
This review describes how inherited forms of Alzheimer's disease involve increased production or deposition of amyloid beta-protein, and how identifying the enzymes presenilin/gamma-secretase and beta-secretase provides targets for drug screening. It does not report a treatment or cure, but summarizes biological findings that could guide future therapeutic development.
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Vaccinations with amyloid-beta peptide (A beta) can dramatically reduce amyloid deposition in a transgenic mouse model of Alzheimer's disease.
Why it matters
In a mouse model of Alzheimer's, vaccination with amyloid-beta protected the mice from learning and memory deficits and partially reduced amyloid buildup. This is an early animal study, so it does not yet show whether such a vaccine would prevent or treat Alzheimer's in people.
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This study evaluated efficacy and safety of donepezil hydrochloride (donepezil) at 5 mg/day in patients with mild to moderately severe Alzheimer's disease for 24 weeks in a double-blind, placebo-controlled comparative trial.
Why it matters
This 24-week, double-blind, placebo-controlled trial found that donepezil 5 mg/day improved cognitive and global function compared with placebo in 228 evaluable patients with mild to moderately severe Alzheimer's disease. This supports donepezil as a symptomatic treatment, but it does not show that the drug cures or prevents Alzheimer's disease.
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Why it matters
Examines RAGE and its role in amyloid-beta peptide neurotoxicity in Alzheimer's disease.
From across this topic
10 of the 5,374 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.
- Atherosclerosis and Alzheimer--diseases with a common cause? Inflammation, oxysterols, vasculature
- Long-read sequencing reveals hidden structural complexity within Alzheimers disease-associated GWAS loci
- HIV Neuroinfection and Alzheimer's Disease: Similarities and Potential Links?
- Alzheimer's disease drug development pipeline: 2023
- The Clinical and Economic Burden of Newly Diagnosed Alzheimer’s Disease in a Medicare Advantage Population
- Is the amyloid hypothesis of Alzheimer's disease therapeutically relevant?
- Comparison of CSF markers and semi-quantitative amyloid PET in Alzheimer's disease diagnosis and in cognitive impairment prognosis using the ADNI-2 database
- Changes in Daily Functioning in Association With Tau and Amyloid Among Unimpaired Older Adults With and Without Elevated Amyloid
- The development and convergence of co-pathologies in Alzheimer's disease
- Genome-Wide Association and Mechanistic Studies Indicate That Immune Response Contributes to Alzheimer's Disease Development