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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For example, focal temporal lobe dysfunction is associated with a pure amnestic syndrome, very slow decline, with atrophy and neurofibrillary tangles limited largely to the medial temporal region including the entorhinal cortex.
Why it matters
Alzheimer's disease is not one uniform condition: different brain regions affected produce different symptoms, ages of onset, and rates of decline. Genotypic differences, such as absence of apolipoprotein E e4, may underlie some of these subtypes.
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Florbetapir F18 has been approved by the Food and Drug Administration for in vivo assessment of amyloid pathology in patients undergoing evaluation for Alzheimer disease (AD).
Why it matters
After receiving florbetapir F18 amyloid imaging results, diagnosis changed in 54.6% of patients undergoing evaluation for cognitive decline, and diagnostic confidence increased by an average of 21.6%. Intended treatment with cholinesterase inhibitors or memantine increased in patients with positive scans and decreased in those with negative scans.
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Although amyloid-beta (Aβ) peptide deposition into insoluble plaques is a pathological hallmark of Alzheimer disease; soluble oligomeric Aβ has been hypothesized to more directly underlie impaired learning and memory in dementia of the Alzheimer type.
Why it matters
A new single-molecule assay measured soluble amyloid beta oligomers, which are hypothesized to underlie impaired learning and memory in Alzheimer's dementia. This is a test-development study and does not by itself provide a treatment or cure.
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PiB and florbetapir retention ratios were strongly associated in the same individuals, and this relationship was consistent across several data analysis methods, despite scan-rescan intervals of more than a year.
Why it matters
In 32 ADNI participants scanned with both PiB and florbetapir amyloid PET, results from the two tracers were strongly associated across several analysis methods. The authors show that cutoffs for amyloid positive or negative status can be converted between the two tracers.
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Amyloid plaques and hyperphosphorylated tau in cortical brain biopsies are reflected by low CSF Aβ42 and high CSF tau and p-tau levels, respectively.
Why it matters
In patients who had brain biopsies, those with amyloid plaques or tau in the tissue tended to have lower Aβ42 and higher tau and p-tau 181 in their spinal fluid. This supports using spinal fluid markers to reflect brain changes, which aids diagnosis but does not treat or prevent the disease.
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Performing exome sequencing in 14 autosomal dominant early-onset Alzheimer disease (ADEOAD) index cases without mutation on known genes (amyloid precursor protein (APP), presenilin1 (PSEN1) and presenilin2 (PSEN2)), we found that in five patients, the SORL1 gene harbored unknown nonsense (n=1) or missense (n=4) mutations.
Why it matters
In people with autosomal dominant early-onset Alzheimer's disease without mutations in known genes, several potentially pathogenic SORL1 mutations were found and were absent from controls. This genetic finding links SORL1 to a rare inherited form of the disease but does not by itself provide a treatment or cure.
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Short-term nutritional supplements enable an improvement in Alzheimer patients' nutritional status, but it remains to be seen whether they will be sufficient to improve long-term nutritional status.
Why it matters
A 3-week nutritional supplement programme improved nutritional status scores in undernourished patients with mild probable Alzheimer's disease, and the improvement persisted at 90 days. This addresses nutrition, not the treatment, cure, or prevention of Alzheimer's disease itself.
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We explored resting-state metabolic connectivity in prodromal Alzheimer's disease (pAD) patients and in healthy controls (CTR), through a voxel-wise interregional correlation analysis of 18F-fluorodeoxyglucose (FDG)-positron emission tomography (PET) by means of statistical parametric mapping.
Why it matters
Patients with prodromal Alzheimer's disease showed less metabolic connectivity than controls in both hypometabolic and nonhypometabolic areas, including the hippocampi and dorsolateral prefrontal cortex. This reduced connectivity suggests that metabolic disconnection may occur before remote hypometabolism, an early sign of synaptic degeneration.
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Fornix FA both cross-sectionally correlated with and longitudinally predicted memory decline and progression to AD.
Why it matters
In this small study of 23 people with mild cognitive impairment, fornix imaging measures predicted memory decline and progression to Alzheimer's dementia, while hippocampal volume did not. This is a small study about prediction, not about treating, curing, or preventing the disease.
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Late-onset Alzheimer's disease (AD) is 50-70% heritable with complex genetic underpinnings.
Why it matters
In clinically normal older people, a polygenic score based on up to 26 common genetic variants was associated with thinner cortex in Alzheimer's-vulnerable regions, even after accounting for APOE genotype and CSF amyloid-beta1-42. This suggests genetic risk, imaging, and CSF markers might together help predict future cognitive decline, but it does not provide a treatment or prevention.
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Mild cognitive impairment (MCI) is considered as a transition phase between normal aging and Alzheimer's disease (AD).
Why it matters
In this prospective study, a molecular signature of three metabolites predicted progression to Alzheimer's disease, with 2,4-dihydroxybutanoic acid as the major contributor, and the findings primarily implicate hypoxia, oxidative stress and membrane lipid remodeling. This concerns markers of progression, not treatment or prevention.
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52/100
Since the introduction of amyloid imaging nearly 10 years ago, this technique has gained widespread use and acceptance.
Why it matters
This review discusses how amyloid imaging can be used in developing and evaluating drugs for Alzheimer's disease, including screening trial participants and measuring outcomes. It is a discussion of a biomarker method and does not itself show that any treatment, cure or prevention works.
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Lipids are key regulators of brain function and have been increasingly implicated in neurodegenerative disorders including Alzheimer disease (AD).
Why it matters
This study profiled lipids in brain tissue from late-onset Alzheimer's patients and from three transgenic familial Alzheimer's mouse models, finding an elevation of a signaling pool of diacylglycerol in affected regions while the cerebellum lacked major lipid changes. It is a descriptive lipidomic comparison and reports no treatment, cure or prevention.
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It is established that chronic spirochetal infection can cause slowly progressive dementia, brain atrophy and amyloid deposition in late neurosyphilis.
Why it matters
This review analyzed existing literature and reported a statistically significant association between spirochetes and Alzheimer's disease. It is an analysis of published data, not a trial, so it does not show that treating infection would prevent or cure the disease.
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Central auditory dysfunction is a precursor to AD.
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Older persons with Mild Cognitive Impairment (MCI) feature neurobiological Alzheimer's Disease (AD) in 50% to 70% of the cases and develop dementia within the next 5 to 7 years.
Why it matters
This review found that episodic memory and semantic fluency are the most reliable neuropsychological markers of progression from mild cognitive impairment to Alzheimer's disease, and that hippocampal atrophy and whole brain atrophy have strong evidence as structural markers. The findings are about tracking disease progression and do not report on treating, curing, or preventing Alzheimer's disease.
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Neither PPA phenotyping nor imaging alone is a reliable predictor of pathology.
Why it matters
Among patients with two forms of primary progressive aphasia, many had pathology or biomarkers consistent with Alzheimer's disease, and combining neuropsychological testing with MRI atrophy patterns improved identification. This is about predicting underlying pathology, not about treating or preventing Alzheimer's disease.
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Here, we review progress by the Penn Biomarker Core in the Alzheimer's Disease Neuroimaging Initiative (ADNI) toward developing a pathological cerebrospinal fluid (CSF) and plasma biomarker signature for mild Alzheimer's disease (AD) as well as a biomarker profile that predicts conversion of mild cognitive impairment (MCI) and/or normal control subjects to AD.
Why it matters
This review describes how a cerebrospinal fluid signature combining Abeta1-42 and total tau distinguished mild Alzheimer's disease and appeared to predict conversion from mild cognitive impairment to Alzheimer's disease. It also presents a model in which amyloid biomarkers become abnormal first, followed by neurodegenerative biomarkers and then clinical symptoms.
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52/100
Subjects with mild cognitive impairment (MCI) have an increased risk to develop Alzheimer's disease (AD).
Why it matters
In this small study, a computer method using MRI patterns predicted which people with mild cognitive impairment would convert to Alzheimer's disease with 75% accuracy, with the most predictive areas being the anterior cingulate gyrus and orbitofrontal cortex. This is a prediction method only and does not test any treatment, cure, or prevention.
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CSF biomarkers amyloid beta 1-42 (Abeta(42)), total tau (tau), and tau phosphorylated at threonine 181 (p-tau-181) are useful diagnostic markers for Alzheimer disease (AD).
Why it matters
This study tested whether cerebrospinal fluid biomarkers amyloid beta 1-42, total tau, and tau phosphorylated at threonine 181 predict the rate of further cognitive decline in patients who already have Alzheimer disease. It is a prediction study and does not test any treatment, cure, or prevention.
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Hippocampal volume change over time, measured with MRI, has huge potential as a marker for Alzheimer's disease.
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Subtyping PPA helps to predict AD versus frontotemporal lobar degeneration pathology at the group level.
Why it matters
In 23 consecutive autopsies of people with primary progressive aphasia, a dementia that starts with language problems, all six with the agrammatic form had frontotemporal lobar degeneration, and seven of the eleven with the logopenic form had Alzheimer's disease. The authors conclude that subtyping "helps to predict" the underlying disease "at the group level", but that "no clinical predictor is completely reliable in individual patients"; APOE4 did not predict Alzheimer's pathology in this group. It is a small diagnosis-and-pathology study, not about treating or preventing Alzheimer's.
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Vascular cognitive impairment risk factors include stroke, hypertension, diabetes and atherosclerosis.
Why it matters
This review describes how vascular risk factors such as stroke, hypertension, diabetes and atherosclerosis interact with Alzheimer's disease, noting that the risk of AD is increased in people with adult-onset diabetes, hypertension, atherosclerotic disease and atrial fibrillation. In experiments, small strokes combined with high brain amyloid led to growing damage, more cognitive impairment and more neuroinflammation than either alone. The picture is that blood vessel damage and Alzheimer's changes add together in producing dementia.
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The therapeutic imperative for Alzheimer disease (AD) and Parkinson disease (PD) calls for discovery and validation of biomarkers.
Why it matters
This study found a panel of 8 cerebrospinal fluid proteins that identified Parkinson disease well and Alzheimer disease moderately well. It is about diagnosis, not about treating, curing or preventing Alzheimer's.
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A temporoparietal pattern of atrophy on MRI in patients with progressive fluent aphasia and relatively preserved processing speed is suggestive of underlying Alzheimer disease pathology rather than frontotemporal lobar degeneration with ubiquitin-only immunoreactive changes.
Why it matters
Among people with progressive aphasia, those with Alzheimer's pathology had better processing speed than those with FTLD-U pathology, and their brain atrophy spared the hippocampus. This helps distinguish these underlying pathologies, which matters for diagnosis, but it does not test any treatment.
From across this topic
9 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 9. The same 9 appear here every time.
- Cannabidiol and Alzheimer Disease: A Comprehensive Review and In Silico Insights Into Molecular Interactions
- A multiancestry polygenic risk score for Alzheimer's disease is associated with cognitive decline and neuropathological hallmarks in diverse populations
- Rofecoxib: no effect on Alzheimer's disease in a 1-year, randomized, blinded, controlled study
- N400 evidence of abnormal responses to speech in Alzheimer's disease
- Recent advances in neuroimaging of Alzheimer's disease and related dementias
- Brain differences in infants at differential genetic risk for late-onset Alzheimer disease: a cross-sectional imaging study
- Rates of Alzheimer disease biomarker positivity stratified by by sex and race in a specialty memory clinic
- There Is No Direct Causal Relationship Between Coronary Artery Disease and Alzheimer Disease: A Bidirectional Mendelian Randomization Study
- Increased CSF APPs-α levels in patients with Alzheimer disease treated with acitretin