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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In its earliest clinical phase, Alzheimer's disease characteristically produces a remarkably pure impairment of memory.
Why it matters
This article argues that the earliest clinical phase of Alzheimer's disease mainly affects memory, and that this may begin with subtle changes in how synapses in the hippocampus work, before nerve cells are lost. It suggests the synaptic problems are caused by small, diffusible clumps (oligomers) of amyloid beta protein.
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Starting in 1991, participants were assessed with the Cognitive Abilities Screening Instrument (CASI) and diagnosed with dementia (including subtype) based on published criteria.
Why it matters
In an autopsy sample of 211 Japanese-American men, this study investigated the relationship between cerebral amyloid angiopathy, dementia, and cognitive function. It is a pathology study of associations and does not test any treatment or prevention.
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The results of this preliminary case-control study suggest that estradiol levels may decline significantly in women in whom AD develops.
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To determine the prevalence of early-onset Alzheimer disease (EOAD) and of autosomal dominant forms of EOAD (ADEOAD), we performed a population-based study in the city of Rouen (426,710 residents).
Why it matters
In Rouen (426,710 residents), this 1999 population study found early-onset Alzheimer's disease, defined as onset before age 61, at 41.2 per 100,000 persons at risk, and a strictly defined inherited form (at least three early-onset cases across three generations) at 5.3 per 100,000. In 34 French families with that inherited form, the authors found PSEN1 mutations in 19 (56%), including four variants "not reported elsewhere". These figures describe how common the disease was and which gene was involved in a selected group of families; they are not personal risk estimates, and the study tested no treatment.
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Using parametric methods, no evidence for linkage to the region spanned by the chromosome 12 markers could be detected if familial AD is assumed to arise from the same genetic locus in all 53 families.
Why it matters
In 53 families with multiple members affected by Alzheimer's disease, this study found no evidence for linkage to chromosome 12 markers when assuming all families share the same genetic locus. However, significant evidence for linkage appeared when allowing for locus heterogeneity, supporting the idea that more than one gene may be involved.
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To assess the relationship between dementia, neuronal loss, and neuropathological findings in Alzheimer's disease (AD), we counted the number of neurons, senile plaques, and neurofibrillary tangles in a high-order association cortex.
Why it matters
Counting cells in one region of the brain's outer layer (the superior temporal sulcus) in 34 people with Alzheimer's and 17 people without dementia, this 1997 study found that more than half of the neurons were lost in Alzheimer's. Neuron loss and tangles both rose with how long and how severe the illness was, and the neuron loss was many times greater than the number of tangles. Plaque counts and amyloid burden did not track neuron loss, tangles or disease duration. The authors say this suggests neuron loss contributes directly to the memory and thinking problems, but the study measured links, not cause, and tested no treatment.
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A candidate gene for the chromosome 1 Alzheimer's disease (AD) locus was identified (STM2).
Why it matters
Researchers identified a candidate gene (STM2) for the familial form of Alzheimer's disease linked to chromosome 1, and found a point mutation in it in affected people from Volga German families. The gene closely resembles a chromosome 14 Alzheimer's gene, which the authors say strongly supports the idea that mutations in both genes cause disease.
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These findings support previous contentions that a "preclinical phase" of detectable cognitive deficits can precede the clinical diagnosis of probable AD by many years, and they also support the hypothesis that problems with secondary verbal memory are among the first signs of AD.
Why it matters
In this 13-year prospective study, most screening neuropsychological measures were individually related to later Alzheimer's disease diagnosis, but only measures of verbal memory and immediate auditory attention span remained significantly related in stepwise regression. The results suggest cognitive changes can be detected years before clinical diagnosis, which may help identify people early, but the study reports no treatment or cure.
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Clinicians accurately predicted AD pathological findings or their absence in most cases.
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Gene dosage of the apolipoprotein E (APOE) epsilon 4 allele is a major risk factor for familial Alzheimer disease (AD) of late onset (after age 60).
Why it matters
This study found that the APOE epsilon2 allele appears to protect against late-onset Alzheimer's disease, while the epsilon4 allele increases risk, with the two versions acting in opposite directions. It supports the idea that apolipoprotein E is directly involved in the disease, but it does not test any treatment or prevention.
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This study measured the annual rate of cognitive change in patients with Alzheimer's disease and determined the effects of clinical variables on that rate.
Why it matters
This longitudinal study measured the annual rate of cognitive change in 111 patients with Alzheimer's disease and compared two cognitive scales. It describes measurement and predictors of decline but does not test any treatment, cure, or prevention.
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This statistical prediction is recommended for use in combination with clinical judgment to certify DAT patients for Medicare hospice coverage.
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False-positive (FP) plasma results may lead to overtreatment and false-negative (FN) results to missed or delayed disease-modifying therapies.
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Alzheimer's disease (AD) is a major cause of dementia and cognitive decline.
Why it matters
Using longitudinal imaging from over 1000 measurements in the DELCODE study, loss of episodic memory network deactivation was linked to amyloid and tau positivity and appeared before cognitive decline. The authors conclude that synaptic dysfunction and neurodegeneration are independent drivers of cognitive decline, providing a rationale for targeting synaptic dysfunction, but no treatment is tested.
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Overall, the available evidence suggests that natural compounds confer multitarget neuroprotective effects that directly engage with key pathological mechanisms underlying AD.
Why it matters
This systematic review of 41 lab studies, 25 in animals and 16 in cells, found that natural compounds such as plant chemicals and herbal formulas consistently showed protective effects against Alzheimer's-related changes, including less oxidative stress, inflammation and amyloid-β clumping. The authors note that problems with absorption, standardization and proof of clinical benefit remain, and that well-controlled clinical trials are needed before these can be considered treatments.
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59/100
BackgroundAlzheimer's disease (AD) accounts for the majority of dementia-related disorders among aging populations.
Why it matters
This review found that task-based EEG shows consistent brain wave changes in people with mild cognitive impairment and Alzheimer's disease, such as reduced event-related potential amplitudes and disrupted connectivity. These EEG measures may help detect cognitive impairment early, but the review does not evaluate any treatment or cure.
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Meta-analyses of epidemiological studies have suggested that Alzheimer's disease (AD) may be linked with exposure to extremely low frequency (ELF) magnetic fields (MF).
Why it matters
This cohort study found no association between residential extremely low frequency magnetic fields from indoor transformer stations and Alzheimer's disease risk (hazard ratio 1.02). It is an observational study of exposure and risk, not a treatment, cure, or prevention trial.
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Microglia are resident immune cells of the brain and are implicated in the etiology of Alzheimer's disease (AD) and other diseases.
Why it matters
Analysing primary microglia from 189 human postmortem brains, this study found gene expression changes associated with multiple Alzheimer's disease phenotypes, including dementia severity and neuropathological lesions, plus changes in gene-gene coordination and disease subtypes. It furthers understanding of microglia in Alzheimer's disease biology and nominates candidate targets, but identifies no treatment, cure or prevention.
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The pTau217/Aβ42 ratio demonstrated the highest diagnostic accuracy, with an AUC of 0.927 (0.900-0.954).
Why it matters
A blood test measuring the ratio of two proteins, pTau217 and Aβ42, was better at detecting brain amyloid than measuring either protein alone. The authors say this ratio could be useful, but it needs to be validated in more and different clinical settings before it can be widely used.
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Higher structural stiffness of the carotid artery is associated with cognitive decline, whereas both structural and load‐dependent stiffness are associated with brain structural abnormalities common in Alzheimer disease‐related dementias.
Why it matters
This cohort study found that greater structural carotid artery stiffness was associated with greater longitudinal cognitive decline and structural brain abnormalities related to Alzheimer's disease and related dementias. It identifies a vascular risk factor but does not test a treatment, cure, or prevention.
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Early onset hallucinations were significantly more common in pLBD than pAD (OR 0.069 [95% CI 0.012-0.397], p = 0.003) or mixed AD+LBD (OR 0.09 [95% CI 0.010-0.771], p = 0.028) and there was a greater increase in the odds of hallucinations over time in pAD and AD+LBD than pLBD such that there was was no difference in the prevalence of late-onset hallucinations between pLBD, pAD or AD+LBD.
Why it matters
In this post-mortem cohort, hallucinations early in disease were more common in pure Lewy body disease than in pure Alzheimer's disease or mixed disease, and were linked to specific brain pathology. Later hallucinations increased in Alzheimer's and mixed disease, suggesting different underlying causes over time.
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AD was common in both AD-related syndromes (110/125 [88%]) and FTLD-related syndromes (45/198 [23%]).
Why it matters
This clinicopathological study measured three blood biomarkers (p-tau217, NfL, and GFAP) in 349 autopsied individuals, including people with syndromes usually linked to frontotemporal lobar degeneration. It examined whether these blood tests can detect Alzheimer's disease pathology in people whose clinical syndrome is not typical Alzheimer's, but the available summary does not report how well the biomarkers performed.
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Plasma tau phosphorylated at threonine 181 (p-tau181) and 217 (p-tau217) have demonstrated high accuracy for Alzheimer's disease (AD) diagnosis, defined by CSF/PET amyloid beta (Aβ) positivity, but most studies have been performed in research cohorts, limiting their generalizability.
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Increasing evidence points to a pivotal role of immune processes in the pathogenesis of Alzheimer disease, which is the most prevalent neurodegenerative and dementia-causing disease of our time.
Why it matters
This review states that immune processes appear to play a pivotal role in Alzheimer's disease, based on experimental, epidemiological, neuropathological and genetic evidence. It reports no treatment, cure or prevention and describes mechanisms rather than tested therapies.
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Amyloid, tau, neurodegeneration and neuroinflammation plasma biomarkers are modified in DLB, albeit with moderate diagnosis performance.
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.
- Association of plasma clusterin concentration with severity, pathology, and progression in Alzheimer disease
- The role of interleukin-1 in neuroinflammation and Alzheimer disease: an evolving perspective
- Hypercortisolemia and glucocorticoid receptor-signaling insufficiency in Alzheimer's disease initiation and development
- The Use of Tau PET to Stage Alzheimer Disease According to the Braak Staging Framework
- Associations between plasma complement C1q and cerebrospinal fluid biomarkers of Alzheimer's disease pathology in cognitively intact adults: The CABLE study
- 2014 Alzheimer's disease facts and figures
- Plasma proteomics reveals stage-dependent biological remodelling in Alzheimer's disease
- Associations of blood cell indices and anemia with risk of incident dementia: A prospective cohort study of 313,448 participants
- Roles of vascular and metabolic components in cognitive dysfunction of Alzheimer disease: short- and long-term modification by non-genetic risk factors
- An explainable and efficient deep learning framework for EEG-based diagnosis of Alzheimer's disease and frontotemporal dementia