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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Unlike the CSF biomarkers evaluated, changes in serial structural MRI are correlated with concurrent change on general cognitive and functional indices in impaired subjects, track with clinical disease stage, and are influenced by APOE genotype.
Why it matters
In this study comparing annual change in MRI and CSF biomarkers across cognitively normal, amnestic mild cognitive impairment, and Alzheimer's disease groups, there was no significant average annual change in either CSF biomarker in any group except total-tau in cognitively normal people. In contrast, annual increase in ventricular volume increased in the order Alzheimer's disease greater than mild cognitive impairment greater than cognitively normal, and it correlated with worsening cognition in the impaired groups.
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This enlarged study confirms earlier findings that statin therapy in early old age, but not in late age, may be associated with a lower risk of AD.
Why it matters
In this cohort, statin use was associated with lower Alzheimer disease risk in people younger than 80, but this association diminished with age and was not significant in those 80 and older. The interaction with APOE ε4 was not significant, and this observational study does not prove statins prevent the disease.
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A subgroup of patients with Alzheimer disease with extreme levels of CSF biomarkers exhibits worse clinical outcomes over time, including faster progression of cognitive deficits, no response to ChEI treatment, and a higher mortality.
Why it matters
Among people already diagnosed with Alzheimer's disease, a pattern of spinal fluid markers with very high T-tau and P-tau was linked to worse thinking at the start, faster decline, poorer response to cholinesterase inhibitor treatment, and shorter survival. This is about predicting outcomes in existing disease, not about treating or preventing it.
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The results suggest that APOE epsilon4 and heavy drinking and heavy smoking lower the age of onset for AD in an additive fashion.
Why it matters
In this cross-sectional study of Alzheimer's patients, having an APOE epsilon4 allele, a history of heavy drinking or a history of heavy smoking was each linked to an earlier age of onset by 2-3 years, and having all three was linked to onset nearly 10 years earlier. It describes associations with age of onset and does not test a treatment, cure or prevention.
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Mutations in presenilin 2 are rare causes of early onset familial Alzheimer's disease.
Why it matters
This analysis of 146 affected cases in 11 Volga German families, plus 18 autopsies, examined the phenotypes and genotypes associated with presenilin 2 mutations, including the N141I mutation. It describes a rare inherited form of early onset familial Alzheimer's disease and does not report a treatment or cure.
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55/100
Low CSF Abeta(1-42) (surrogate for Abeta amyloid load) is more closely linked to the presence of APOE epsilon4 than to clinical status.
Why it matters
In cognitively normal people, those with mild cognitive impairment, and those with Alzheimer's disease, low levels of amyloid beta in spinal fluid were more closely tied to carrying the APOE epsilon4 gene than to the person's clinical diagnosis. This suggests APOE epsilon4 is linked to amyloid buildup early, but the study does not test any treatment or show that acting on this changes disease course.
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Why it matters
A phase 2, double-blind, placebo-controlled, ascending-dose study used 11C-PiB PET scans to assess change in fibrillar amyloid-beta load in patients with Alzheimer's disease treated with bapineuzumab.
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Brain atrophy and altered CSF levels of amyloid beta (Abeta(42)) and the microtubule-associated protein tau are potent biomarkers of Alzheimer's disease (AD)-related pathology.
Why it matters
This longitudinal study examined how cerebrospinal fluid biomarkers relate to brain atrophy in normal controls, mild cognitive impairment, and Alzheimer's disease. It is a biomarker and imaging study and does not test any treatment, cure, or prevention.
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The strong correlation between hippocampal atrophy and beta-amyloid (Abeta) burden in the Pittsburgh compound B-positive healthy control group suggests that Abeta deposition in the inferior temporal neocortex is related to hippocampal synaptic and neuronal degeneration.
Why it matters
In healthy controls with elevated amyloid on PET, amyloid burden in the inferior temporal region correlated with hippocampal atrophy, but no such correlation was found in the mild cognitive impairment or Alzheimer disease groups. The authors suggest amyloid deposition in that region is related to hippocampal degeneration, but this is an observational imaging finding with no treatment tested.
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55/100
Apathy is a persistent behavioural feature in PD with a high incidence and prevalence over time.
Why it matters
This four-year study found that apathy was common and persistent in Parkinson's disease, with dementia at baseline and faster motor decline as risk factors. It is about a behavioral feature of Parkinson's disease and does not test any treatment, cure, or prevention for Alzheimer's disease.
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55/100
The brain changes associated with AD may already begin developing early in middle age, especially among APOE epsilon 4 carriers.
Why it matters
In this autopsy study of a general population, amyloid plaques and tau tangles appeared from around age 30 and were more common in APOE epsilon 4 carriers, especially at ages 50 to 59. It describes when these brain changes begin and who is more likely to have them, but it does not test any treatment or prevention.
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55/100
MRI evidence of small subacute infarcts is present in a substantial proportion of living patients with advanced cerebral amyloid angiopathy (CAA).
Why it matters
Among people with probable cerebral amyloid angiopathy, 15% had small subacute infarcts on MRI, and those with infarcts had more hemorrhages than those without. This is about a related blood vessel condition, not about treating, curing, or preventing Alzheimer's disease.
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55/100
Uncontrolled diabetes increases the risk of Alzheimer's disease and VaD.
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Intracellular trafficking and proteolytic processing of amyloid precursor protein (APP) have been the focus of numerous investigations over the past two decades.
Why it matters
This review describes how amyloid precursor protein is trafficked and processed to produce amyloid-beta, the peptide central to the amyloid cascade hypothesis of Alzheimer's disease. It summarizes scientific understanding but does not report a new treatment or prevention.
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Increased cardiorespiratory fitness is associated with reduced brain atrophy in Alzheimer disease (AD).
Why it matters
In people with early-stage Alzheimer's disease, higher cardiorespiratory fitness was associated with greater whole brain and white matter volume after controlling for age. This is an observational association and does not show that improving fitness prevents or treats Alzheimer's disease.
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Alzheimer disease (AD) is the most common form of dementia worldwide.
Why it matters
This cross-sectional study used 3-dimensional mapping of MRI data from 24 patients with amnestic mild cognitive impairment and 25 with mild Alzheimer's disease to look at gray matter atrophy. It describes brain changes in the disease, not a treatment or cure.
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The efficacy of the inhibitors of acetylcholinesterase in Alzheimer's Disease (AD) is moderated and some patients do not respond to these treatments.
Why it matters
In this small trial, patients who received sulbutiamine followed by donepezil showed improved episodic memory and daily activities compared with those who received donepezil followed by placebo. The authors conclude sulbutiamine may be an add-on to anticholinesterase treatment in early and moderate Alzheimer's disease, but this is a small study and does not show a cure.
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Cerebrovascular compromise of the cholinergic pathways may be a factor that contributes more selectively than does total white matter lesion burden to response to cholinergic therapy in Alzheimer disease, particularly on frontal/executive tasks.
Why it matters
In Alzheimer's patients taking cholinesterase inhibitors, having more white matter changes in cholinergic pathways did not lead to worse overall thinking, function, or behavior after one year. In fact, those with more such changes improved on executive function and working memory tasks compared with those with fewer changes.
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For celecoxib, ADAPT data do not show the same level of risk as those of the APC trial.
Why it matters
In this randomized prevention trial, cardiovascular or cerebrovascular events occurred in 5.54% of celecoxib-treated, 8.25% of naproxen-treated and 5.68% of placebo-treated participants, and treatment was suspended after another trial reported increased cardiovascular risk with celecoxib. The trial reports safety events rather than showing that these anti-inflammatory drugs prevent Alzheimer's dementia.
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Alzheimer's disease (AD) reduces associative effects on false recognition in the Deese-Roediger-McDermott task, either due to impaired memory for gist or impaired use of gist in memory decisions.
Why it matters
This study found that Alzheimer's disease patients showed smaller effects of associative blocking and associative strength on false recognition compared to controls, consistent with gist memory impairments. It proposes that overdependence on degraded gist memory in Alzheimer's disease is caused by even larger impairments in item-specific recollections.
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Seizure incidence is increased in people starting with mild-to-moderate AD.
Why it matters
In this group of people with mild Alzheimer's disease followed over time, about 8% had a first unprovoked seizure within seven years, and younger age, African-American background, more severe dementia and focal epileptiform findings on EEG predicted seizures. This describes a complication of the disease and does not test any treatment, cure or prevention.
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Expectation/placebo-related mechanisms and specific effects of therapies show additive effects, such that a therapy is less effective if the placebo component is absent.
Why it matters
In Alzheimer patients, reduced frontal assessment scores and reduced prefrontal connectivity were tied to a smaller placebo component of an analgesic treatment, so a higher dose was needed for adequate pain relief. This concerns pain treatment in people who already have Alzheimer disease, not preventing or curing it.
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We investigated whether functional brain networks are abnormally organized in Alzheimer's disease (AD).
Why it matters
In 15 Alzheimer patients and 13 controls, this EEG study found a longer characteristic path length in the Alzheimer patients while the cluster coefficient showed no significant change, suggesting a loss of small-world network organization. It is a small study of brain network patterns and provides no information on treating, curing or preventing Alzheimer's disease.
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Declining body mass index (BMI) is associated with increased risk of incident Alzheimer disease (AD).
Why it matters
Among 918 older Catholic clergy without dementia, followed for an average of 5.5 years (151 developed Alzheimer's), people whose body mass index fell by about 1 unit a year had roughly a 35% higher risk of Alzheimer's than people whose weight held steady, and those with a lower BMI at the start also had somewhat higher risk; results were similar after excluding people diagnosed in the first 4 years. The authors suggest that weight loss "may reflect pathologic processes that contribute to the subsequent development of AD," meaning it may be an early sign rather than a cause. This is an observational study and does not show that gaining or keeping weight would prevent Alzheimer's.
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Epidemiological studies suggest that increased intake of the omega-3 (n-3) polyunsaturated fatty acid (PUFA) docosahexaenoic acid (DHA) is associated with reduced risk of Alzheimer's disease (AD).
Why it matters
In aged transgenic mice, diets enriched with the omega-3 fatty acid DHA reduced total amyloid beta by more than 70% and reduced plaque burden compared with low-DHA or control diets. This is an animal study and does not show that DHA prevents or treats Alzheimer's disease in people.
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.
- Levels of normal and abnormally phosphorylated tau in different cellular and regional compartments of Alzheimer disease and control brains
- Magnetic resonance imaging of hippocampal and amygdala volume in women with childhood abuse and borderline personality disorder
- Family Caregiver Burden and Neuropsychiatric Symptoms in Japanese Community‐Dwelling People With Alzheimer's Disease: A Cross‐Sectional Study Using a Web‐Based Questionnaire
- [Patients with mild cognitive impairment and a reduced CSF Aβ₁₋₄₂ protein progress rapidly to Alzheimer's disease]
- Cerebrospinal fluid biomarkers and rate of cognitive decline in very mild dementia of the Alzheimer type
- The Importance of Complement-Mediated Immune Signaling in Alzheimer's Disease Pathogenesis
- Relative risk of Alzheimer disease and age-at-onset distributions, based on APOE genotypes among elderly African Americans, Caucasians, and Hispanics in New York City
- Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature
- Drug repositioning and repurposing for Alzheimer disease
- Blood biomarkers for Alzheimer's disease in clinical practice and trials