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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Lewy body (LB) disorders, including Parkinson disease (PD), Parkinson disease dementia (PDD), and dementia with Lewy bodies (DLB), are the second most common type of neurodegenerative dementia.
Why it matters
This review reports that Lewy body disorders show lower mean cortical amyloid ligand binding than Alzheimer disease, with some DLB and PDD cases showing increased binding, and that amyloid deposition may predict future dementia in Parkinson disease. It is a review of imaging findings and does not establish any treatment, cure, or prevention.
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Several studies have shown that cognitive intervention may be beneficial for people with Alzheimer disease (AD), but literature reviews conducted so far, have yielded mixed and inconclusive results.
Why it matters
This review of four randomized trials found that cognitive intervention improved only global cognitive functioning as measured by the Mini-Mental State Examination, with no effects in other domains. The authors say these results should be interpreted carefully and need confirmation in more high-quality research.
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50/100
Diabetes mellitus (DM) is considered to be a risk factor for dementia including Alzheimer's disease (AD).
Why it matters
This study of postmortem human brains found that genes involved in noninsulin-dependent diabetes and obesity were significantly altered in Alzheimer's disease brains and in an Alzheimer's disease mouse model. It indicates that altered expression of diabetes-related genes in Alzheimer's disease brains is a result of Alzheimer's pathology, which may be exacerbated by peripheral insulin resistance or diabetes.
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(18)F-AZD4694 showed reversible binding kinetics similar to (11)C-PiB, reaching an apparent steady state at 50 min after injection.
Why it matters
This head-to-head comparison found that the amyloid PET tracer 18F-AZD4694 had binding kinetics and low white matter binding similar to the benchmark tracer 11C-PiB in the same participants. It is a comparison of imaging tracers for detecting amyloid, not a test of any treatment, cure, or prevention.
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White matter hyperintensities contribute to the presentation of AD and, in the context of significant amyloid deposition, may provide a second hit necessary for the clinical manifestation of the disease.
Why it matters
This study found that amyloid positivity and increased white matter hyperintensity volume independently predicted an Alzheimer's disease diagnosis, and that white matter hyperintensities may provide a second hit needed for the clinical manifestation of the disease. Because risk factors for white matter hyperintensities are modifiable, the authors suggest this points to possible intervention and prevention strategies, though this was not tested.
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Tensions exist between abstract ethical principles regarding decision-making "standards" and their translation into research decisions.
Why it matters
This interview study of 40 proxy decision makers found that half agreed with both deciding based on how their relative would have decided and deciding based on their relative's best interests. It examines how proxies make enrollment decisions for Alzheimer disease research rather than testing any treatment.
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Deposition of amyloid β protein (Aβ) to form neuritic plaques in the brain is the pathological hallmark of Alzheimer's disease (AD).
Why it matters
This study reports that specifically inhibiting GSK3β reduces BACE1 expression and Alzheimer-associated phenotypes, but it does not state whether this was tested in humans or animals. It suggests a possible treatment approach, but no clinical treatment, cure, or prevention is established.
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More open debates of practical experiences from different trial centres and sponsors are essential for optimizing trial designs and improving conditions for participants.
Why it matters
This study looked at the practical experiences of staff and participants in amyloid immunotherapy trials, not at whether the treatment works. It found that these trials demand much more effort from patients and caregivers than older cholinesterase inhibitor trials.
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50/100
APOE4 is the greatest risk factor for Alzheimer disease (AD) and synergistic effects with amyloid-β peptide (Aβ) suggest interactions among apoE isoforms and different forms of Aβ accumulation.
Why it matters
In this new mouse model, introducing human APOE delayed amyloid deposition, and APOE4 mice had more compact plaques and higher total amyloid levels. These are animal findings only and do not establish any treatment or prevention for people.
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Increased connectivity after 1 year of DBS is observed, which is in contrast to the decreased connectivity observed over the course of AD.
Why it matters
In five patients with mild Alzheimer disease, one year of deep brain stimulation of the fornix increased brain glucose metabolism, and higher metabolism was linked to better clinical outcomes. This was a small open-label phase I trial, so it cannot show that the treatment works.
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50/100
We aim to clarify the mechanisms of acupuncture in treating mild cognitive impairment (MCI) and Alzheimer disease (AD) by using functional magnetic resonance imaging (fMRI).
Why it matters
This small imaging study of 36 people found that brain activity differed between Alzheimer's disease, mild cognitive impairment, and healthy older adults during rest and acupuncture. It only describes brain activity patterns and does not show that acupuncture improves memory or treats the disease.
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Brain connectivity studies have revealed that highly connected 'hub' regions are particularly vulnerable to Alzheimer pathology: they show marked amyloid-β deposition at an early stage.
Why it matters
A computer model suggested that highly connected brain hub regions have the highest activity and that this activity could explain their vulnerability to Alzheimer pathology. This is a simulation, not a study in people, so it does not establish a treatment or prevention.
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Arch Neurol. 2008;65(7):963-967.) for the Mini-Mental State Examination in detecting cognitive dysfunction in a bilingual sample of highly educated ethnically diverse individuals.
Why it matters
This analysis looked at whether the Mini-Mental State Examination detects cognitive dysfunction accurately in highly educated, ethnically diverse people. It used existing data from 7,093 individuals with 16 or more years of education, so it concerns diagnosis rather than treatment, cure or prevention.
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Alzheimer's disease [AD] is the most common cause of dementia in North America.
Why it matters
This review argues that Alzheimer's disease involves problems with how the brain uses glucose and responds to insulin and insulin-like growth factor, alongside amyloid and tau changes. It proposes that treatments targeting insulin and IGF resistance and deficiency in the brain should be developed and tested, but no treatment is proven here.
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We conclude that Aβ deposition is associated with a pattern of cortical thickness reduction consistent with AD prior to the development of cognitive impairment.
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The greatest advantage of the RSD proposed in this article is its ability to critically address the question on a DM effect.
Why it matters
This paper proposes a new trial design for studying whether a treatment modifies the course of Alzheimer's disease. It is a methodological proposal and reports no treatment results.
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Histologic studies show that the amygdala is affected by Alzheimer disease (AD) pathology, and its medial aspect is the most involved.
Why it matters
In 19 Alzheimer disease patients compared with 19 healthy controls, both amygdala volumes were significantly smaller and surface mapping showed local tissue loss in specific nuclei. This describes structural brain differences in Alzheimer's disease and does not offer a treatment, cure or prevention.
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White matter hyperintensity volume predicts 1-year cognitive decline in a relatively healthy convenience sample that was similar to clinical trial samples, and therefore should be considered as a covariate of interest at baseline and longitudinally in future AD treatment trials.
Why it matters
In 804 participants followed for one year, higher baseline white matter hyperintensity volume was associated with greater subsequent cognitive decline. This is an observational study and does not show that treating white matter disease prevents or cures Alzheimer's.
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The results of this study suggest that hyperinsulinemia and hyperglycemia caused by insulin resistance accelerate NP formation in combination with the effects of APOE epsilon4.
Why it matters
In this autopsy study of 135 residents, higher levels of 2-hour post-load plasma glucose, fasting insulin, and insulin resistance were associated with increased risk for neuritic plaques, but there was no relationship with neurofibrillary tangles. The authors suggest that hyperinsulinemia and hyperglycemia caused by insulin resistance accelerate neuritic plaque formation, but this does not show that treating insulin resistance prevents Alzheimer disease.
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We confirm in a completely independent data set that CR1, CLU, and PICALM are AD susceptibility loci in European ancestry populations.
Why it matters
In 7,070 people with Alzheimer's and 8,169 cognitively normal older people from 12 studies, this analysis confirmed in a separate data set that common variants in the CR1, CLU and PICALM genes are linked to Alzheimer's in white participants, with small effects (odds ratios of 0.89 to 1.14), but none were significantly linked in the African American, Israeli-Arab or Caribbean Hispanic groups. The PICALM link depended on APOE: the authors report that PICALM "confer[s] risk predominantly in APOE ε4-positive subjects" and that the two genes interact. These are statistical associations, not causes or a personal risk test, and the study tested no treatment.
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Alzheimer's disease (AD), the most common cause of dementia among the elderly, may either represent the far end of a continuum that begins with age-related memory decline or a distinct pathobiological process.
Why it matters
This review argues that transgenic mice expressing amyloid precursor protein should be seen as models of accelerated brain aging or asymptomatic Alzheimer's disease, so intervention studies in them relate to primary prevention. It also points to roles for soluble beta-amyloid oligomers and soluble tau in disease processes, but these are animal-model findings.
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Insulin resistance (IR) is the main pathological condition underlying vascular disorders, such as diabetes and cardiovascular disease, which are well established risk factors for cognitive decline and Alzheimer disease (AD).
Why it matters
In 50 non-diabetic, cognitively intact women aged 50 to 65, greater insulin resistance was linked to smaller right and total hippocampal volume and worse memory performance, regardless of APOE epsilon4 status. This suggests insulin resistance may be a marker of dementia risk but does not test any treatment or prevention.
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Clinical, cognitive, and CSF markers consistent with AD may precede detection of cerebral amyloid beta using amyloid imaging agents such as PiB that primarily label fibrillar amyloid beta plaques.
Why it matters
This case report followed a man from normal cognition to very mild Alzheimer's dementia: his memory began to decline at about age 88, a PiB amyloid PET scan at 88½ was negative, and his spinal fluid at 89½ showed low amyloid-β42 and high tau. At autopsy after his death at 91 he had frequent diffuse amyloid plaques meeting one set of criteria for definite Alzheimer's, but only sparse neuritic plaques and tangles. It is a documented example of an amyloid scan coming back negative in a patient with clinical, cognitive and spinal-fluid markers of Alzheimer's.
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Mutations in the amyloid precursor protein (APP), presenilin 1 (PSEN1), and presenilin 2 (PSEN2) genes lead to increased Abeta levels before symptoms arise.
Why it matters
This imaging study looked at amyloid deposition in people carrying autosomal dominant Alzheimer mutations compared with healthy controls and people with sporadic Alzheimer's disease. It supports the idea that amyloid builds up before symptoms in familial Alzheimer's disease, but it does not test or provide any treatment.
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This effect is independent of baseline neuropsychological and MRI predictors.
Why it matters
In this small study of 75 people, higher baseline CSF p-tau levels independently predicted faster hippocampal atrophy over time. This is a marker of disease progression, not a treatment, cure or prevention for Alzheimer's 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.
- Effective dosage and mode of exercise for enhancing cognitive function in Alzheimer's disease and dementia: a systematic review and Bayesian Model-Based Network Meta-analysis of RCTs
- Characterization of pathogenic SORL1 genetic variants for association with Alzheimer's disease: a clinical interpretation strategy
- Regional white matter integrity differentiates between vascular dementia and Alzheimer disease
- TREM2 variants: new keys to decipher Alzheimer disease pathogenesis
- Exploratory Tau Biomarker Results From a Multiple Ascending-Dose Study of BIIB080 in Alzheimer Disease: A Randomized Clinical Trial
- Alzheimer's and dementia: Diagnosis, assessment, and disease monitoring global, regional, and national burden of Alzheimer's disease and other dementias (ADODs) and their risk factors, 1990–2021: A systematic analysis for the Global Burden of Disease study 2021
- Mechanisms of synaptic dysfunction in Alzheimer's disease
- The National Alzheimer's Coordinating Center (NACC) Database: The Uniform Data Set
- Independent and reproducible hippocampal radiomic biomarkers for multisite Alzheimer's disease: diagnosis, longitudinal progress and biological basis
- Optimizing power to track brain degeneration in Alzheimer's disease and mild cognitive impairment with tensor-based morphometry: an ADNI study of 515 subjects