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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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.
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The authors explored the possibility that estrogen loss associated with menopause may contribute to the development of Alzheimer's disease by using a case-control study nested within a prospective cohort study.
Why it matters
In this case-control study, the risk of Alzheimer's disease and related dementia was lower in estrogen users than nonusers, and risk decreased with higher estrogen dose and longer use. The authors suggest estrogen deficiency may contribute to Alzheimer's disease in older women, but this is observational and not a proven treatment.
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Apolipoprotein E is immunochemically localized to the senile plaques, vascular amyloid, and neurofibrillary tangles of Alzheimer disease.
Why it matters
In 30 people with late-onset Alzheimer's disease, each from a different affected family, half of their APOE gene copies were the type 4 form (allele frequency 0.50), compared with 0.16 in 91 age-matched unrelated controls (P = 0.014). In separate laboratory tests, apolipoprotein E in spinal fluid bound tightly to synthetic beta-amyloid, the main component of Alzheimer's plaques, and the protein was found in plaques and tangles. The authors only "suggested" a role for the E4 form in familial late-onset disease: this small study measured how common the allele was, not any individual's risk, and it tested no treatment.
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Why it matters
Reports that a mutation of the β-amyloid precursor protein found in familial Alzheimer's disease increases β-protein production.
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We evaluated a new magnetic resonance (MR)-based technique for performing volumetric measurements of temporal lobe structures.
Why it matters
This study found that MRI-based hippocampal volume measurements were smaller in patients with dementia of the Alzheimer type and could help tell them apart from cognitively normal elderly people. It is about diagnosis only and does not address treating, curing, or preventing Alzheimer's disease.
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Researchers examined brains obtained at autopsy from nondemented and demented individuals to study extracellular amyloid deposits and intraneuronal neurofibrillary changes.
Why it matters
Using brains examined after death, this study found that the spread of tangle-type changes inside nerve cells ("neurofibrillary tangles and neuropil threads") follows a set pattern that can be divided into six stages, while the spread and density of amyloid deposits were "of limited significance" for staging. In the last two stages (V-VI), virtually all of the brain's outer association areas were destroyed. It is a way to grade how far the changes have gone in brain tissue, not a test or a treatment.
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Thirty-six clinically diagnosed and pathologically confirmed Alzheimer's disease (AD) patients included 13 with cortical and subcortical Lewy bodies (LBs).
Why it matters
In 36 people whose Alzheimer's was confirmed at autopsy, 13 also had Lewy bodies; compared with "pure" Alzheimer's, this group had more nerve-cell loss in brainstem and basal-forebrain areas, lower cortical ChAT levels and fewer midfrontal tangles. In a matched comparison of 9 people per group, those with Lewy bodies had greater problems with attention, fluency and visuospatial skills and a significant increase in masked facies, but classic parkinsonian signs such as resting tremor and limb rigidity were not typical. The authors suggest this "Lewy body variant" may sometimes be recognisable before death, but this small 1990 autopsy series reports no diagnostic accuracy and tests no treatment.
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The researchers isolated and sequenced an apparently full-length complementary DNA clone coding for the A4 polypeptide.
Why it matters
Reports that the precursor of the Alzheimer's amyloid A4 protein resembles a cell-surface receptor. Working out what the precursor protein looks like is groundwork for understanding the disease, not a treatment.
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Early and accurate diagnosis of Alzheimer's disease (AD) has a major impact on the progress of research on dementia.
Why it matters
This report describes a workshop that identified research opportunities and clinical issues influencing progress on diagnosing Alzheimer's disease, especially in its earliest stages. It does not test a treatment or cure, but focuses on improving diagnosis to support research.
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Clinical criteria for the diagnosis of Alzheimer's disease include insidious onset and progressive impairment of memory and other cognitive functions.
Why it matters
These 1984 criteria describe how to diagnose probable, possible, and definite Alzheimer's disease clinically, noting that no laboratory test can determine the diagnosis and that other causes of dementia must be excluded. They are diagnostic guidance, not a treatment or prevention for the disease.
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Copy-number variants (CNVs) are major contributors to human disease.
Why it matters
This study found that rare copy-number variants in some Alzheimer's-associated genes and deletions at 22q11.21 increase Alzheimer's risk, while duplication at 22q11.21 decreases risk. It also found that SCARF2 overexpression increased amyloid-beta uptake, consistent with the duplication's protective effect.
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Dementia diagnosis increasingly relies on blood-based biomarkers, yet their performance in diverse populations remains insufficiently characterized.
Why it matters
In a Latin American cohort, plasma AT(N) biomarkers helped distinguish Alzheimer's disease from frontotemporal lobar degeneration, especially when combined with imaging and cognitive tests. This is a diagnostic study, not a treatment or cure.
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57/100
The APOE-ε4/ε4 genotype is the strongest genetic risk factor for sporadic Alzheimer's disease, though the relative risk is diminished in individuals with African ancestry.
Why it matters
A 19 base pair deletion near APOE was linked to lower Alzheimer's risk and later onset in African American APOE-ε4 carriers. This is a genetic finding about risk, not a treatment or prevention method.
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Dementia poses a significant global health challenge for both clinicians and patients, impacting millions of individuals worldwide, yet its early diagnosis remains underexplored.
Why it matters
This scoping review found that most studies using explainable AI for dementia detection and prognosis relied on public datasets without clinical validation. It addresses diagnostic technology, not treating, curing, or preventing the disease.
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.
- 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