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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In this study, we have assessed the expression and splicing status of genes involved in the pathogenesis or affecting the risk of Alzheimer's disease (AD) in the postmortem inferior temporal cortex samples obtained from 60 subjects with varying degree of AD-related neurofibrillary pathology.
Why it matters
This study examined expression and splicing of Alzheimer's risk genes in postmortem brain tissue and in biopsies from patients with normal pressure hydrocephalus. It is a gene expression study and does not report a treatment or cure.
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Genetic analysis of familial forms of Alzheimer's disease (AD) causally links the proteolytic processing of the amyloid precursor protein (APP) and AD.
Why it matters
Using a mouse model, this study found misfolded and aggregated amyloid inside neurons in perinuclear compartments at intermediate times. This is animal work and does not yet show how intracellular amyloid leads to plaques in people or how to treat it.
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Late-onset Alzheimer's disease (LOAD) is a devastating neurodegenerative disease with no effective treatment or cure.
Why it matters
This review lists over 20 gene regions, plus rare variants in APP, TREM2 and PLD3, that contribute to late-onset Alzheimer's disease risk. It notes there is still no effective treatment or cure, so these genetic findings are leads for research rather than therapies.
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We have synthesized a family of rhein-huprine hybrids to hit several key targets for Alzheimer's disease.
Why it matters
A family of rhein-huprine hybrids inhibited several targets in vitro and protected against amyloid-beta-induced synaptic dysfunction in mouse brain slices. This is early laboratory work and does not establish a disease-modifying treatment for patients.
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43/100
The construct of mild cognitive impairment (MCI) has been proposed to identify patients at risk of developing Alzheimer's disease (AD) in the pre-clinical stage.
Why it matters
This review of neuropsychological markers found that measures of delayed recall are the best predictors of conversion from mild cognitive impairment to Alzheimer's disease, and that most people with mild cognitive impairment remain stable or return to normal. It notes that multi-domain amnestic mild cognitive impairment patients are the best candidates for clinical trials but not for treatment with disease-modifying drugs.
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Impairment in instrumental activities of daily living (IADL) heralds the transition from mild cognitive impairment (MCI) to dementia and is a major source of burden for both the patient and caregiver.
Why it matters
This study followed clinically normal elderly, mild cognitive impairment, and mild Alzheimer's dementia participants to see how regional cortical thinning and cerebrospinal fluid biomarkers relate to daily functioning. It concerns predicting functional decline, not treating, curing, or preventing Alzheimer's disease.
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There is much interest in early intervention for the prevention or postponement of dementia in Alzheimer's disease (AD).
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43/100
We used resting-state functional magnetic resonance imaging to measure the amplitude of low-frequency fluctuations (ALFF) of intrinsic brain activity in 23 patients with moderate Alzheimer's disease (AD) and 27 age- and gender-matched healthy controls.
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Glycosylation is one of the most common, and the most complex, forms of post-translational modification of proteins.
Why it matters
This review highlights that defects in protein glycosylation have been observed in Alzheimer's patients and discusses how glycosylation relates to tangles and plaques. It is a review of a topic that has not been thoroughly investigated and does not report a treatment.
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Before amyloid formation, peptides cleaved from the amyloid precursor protein (APP) exist as soluble oligomers.
Why it matters
This paper argues that clinical trials have largely aimed at removing insoluble beta amyloid in senile plaques and have not reduced soluble oligomer load, and that even treatments expected to remove soluble oligomers have not consistently done so. It concludes that failure to improve cognition has often been attributed to failure of the amyloid hypothesis or irreversible changes, not that a successful therapy has been found.
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The association between an AD-like signature using the established biomarkers Aβ42, T-tau, and P-tau with increased levels of NFL provides in vivo evidence of an association between AD and subcortical axonal degeneration in this uniquely large dataset of CSF samples tested for dementia biomarkers.
Why it matters
In routine clinical samples, established Alzheimer's disease biomarkers (Aβ42, T-tau, P-tau) correlated with neurofilament light, a marker of subcortical axonal injury, and a group with an Alzheimer's biomarker pattern often had high neurofilament light levels. This suggests that Alzheimer's pathology frequently occurs alongside subcortical axonal damage, which may matter for how the disease is assessed, but the study does not test any treatment or prevention.
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Behavioral and psychological problems are often observed in patients with dementia such as that associated with Alzheimer disease, and these noncognitive symptoms place an extremely heavy burden on the family and caregivers.
Why it matters
In APP-transgenic mice, peripheral lipopolysaccharide triggered behavioral changes and brain inflammatory responses, with increased blood-brain barrier vulnerability. This is animal research and does not show a treatment, cure, or prevention for people.
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There is considerable interest in designing therapeutic studies of individuals at risk of Alzheimer disease (AD) to prevent the onset of symptoms.
Why it matters
In cognitively normal older adults, higher baseline amyloid load on PET correlated with a faster rate of hippocampal shrinkage over about 18 months, even though amyloid-positive and amyloid-negative people did not differ in brain, ventricle or hippocampal volumes at the start. This supports using brain atrophy rates as an outcome measure in trials aimed at preventing Alzheimer's symptoms, but it is an observational imaging study, not a test of any treatment.
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43/100
Significantly increased levels of oxidized nucleic acids, proteins, and lipids have been described in the brains of subjects with Alzheimer disease (AD) and mild cognitive impairment (MCI) as well as young adults with Down syndrome, compared to age-matched controls.
Why it matters
This review notes that oxidized molecules are found in the brains of people with Alzheimer disease and mild cognitive impairment, suggesting oxidative stress occurs early. Several antioxidants and related agents have shown protective effects in cells and animals, but their effectiveness in human trials has not been established.
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Alzheimer disease (AD) is associated with the accumulation in the brain of extracellular neuritic plaques composed mainly of β-amyloid (Aβ) and of intracellular neurofibrillary tangles composed of hyperphosphorylated forms of the microtubule-associated protein tau.
Why it matters
This work links Alzheimer disease to increased function and connectivity between the endoplasmic reticulum and mitochondria, alongside the known amyloid plaques and tau tangles. It is a speculative mechanism based on prior cell findings, not a treatment or cure.
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The human brain contains about 100 billion neurons forming an intricate network of innumerable connections, which continuously adapt and rewire themselves following inputs from external and internal environments as well as the physiological synaptic, dendritic and axonal sculpture during brain maturation and throughout the life span.
Why it matters
This review argues that Alzheimer's disease targets functionally connected neuronal networks and their synaptic terminals, affecting brain connectivity before neuronal loss and atrophy. It suggests that mapping these dynamic interactions could aid early diagnosis and monitoring and open avenues to innovative treatments, but it presents no trial results.
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43/100
Alzheimer's disease (AD) is the most common cause of dementia and a progressive neurodegeneration that appears to result from multiple pathogenic mechanisms (including protein misfolding/aggregation, involved in both amyloid β-dependent senile plaques and tau-dependent neurofibrillary tangles), metabolic and mitochondrial dysfunction, excitoxicity, calcium handling impairment, glial cell dysfunction, neuroinflammation, and oxidative stress.
Why it matters
This review argues that oxidative stress appears to be a major determinant of Alzheimer's disease and is present from early stages, with oxidized proteins found in both mild cognitive impairment and Alzheimer's disease. It concludes that a single-target therapy will likely be difficult to achieve, so oxidative stress is proposed as one of the main targets to investigate.
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Third, we benchmarked the results of our virtual reality episodic memory test against a classical memory test and a subjective daily memory complaint scale.
Why it matters
In a virtual reality episodic memory test, Alzheimer's disease patients performed worse than those with amnestic mild cognitive impairment, who in turn performed worse than healthy aged groups. The authors say these cognitive differences may provide additional insight into the early diagnosis and rehabilitation of pathological aging.
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We compared proteomic profiles of CSF from individuals with FAD who were mutation carriers (MCs) and related noncarriers (NCs).
Why it matters
This study used unbiased proteomics to compare cerebrospinal fluid proteins in carriers of familial Alzheimer disease mutations with related noncarriers. It is a biomarker discovery study and does not test any treatment, cure or prevention.
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Alzheimer's disease (AD) is the leading cause of dementia, accounting for 60-70% of all cases [Hebert et al., 2003, 1].
Why it matters
This paper explains that amyloid pathology begins 10 to 20 years before dementia symptoms and that PET imaging can detect it in cognitively normal people, which could help select high-risk participants for trials. It is about using imaging as a research and detection tool, not about a treatment that prevents or cures Alzheimer's disease.
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Cerebral amyloid angiopathy (CAA) may result from focal to widespread amyloid-β protein (Aβ) deposition within leptomeningeal and intracortical cerebral blood vessels.
Why it matters
This review describes how cerebral amyloid angiopathy can cause vascular lesions that may lead to dementia and may contribute to dementia by impeding clearance of solutes and transport of nutrients across the blood brain barrier. It notes that severe cerebral amyloid angiopathy is an independent risk factor for cognitive decline, and suggests that pericapillary amyloid-β represents early impairment of the perivascular drainage pathway.
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The current drug treatment for Alzheimer's disease (AD) is only partially and temporary effective.
Why it matters
In this small proof-of-concept study, eight patients with probable Alzheimer disease who received repetitive transcranial magnetic stimulation combined with cognitive training showed average improvement on cognitive scales after 6 weeks and 4.5 months. The sample was very small and there was no control group, so this is preliminary and does not establish a treatment.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by brain deposition of senile (neuritic) plaques containing amyloid-β, neurofibrillary tangles, synaptic loss, neuroinflammation, and overexpression of arachidonic acid (AA, 20:4n-6) metabolizing enzymes.
Why it matters
In postmortem prefrontal cortex from 10 Alzheimer's patients and 9 non-Alzheimer's controls, mean total brain lipid, phospholipid, cholesterol, and triglyceride concentrations did not differ significantly between the groups. A significant 73% decrease in one lipid measure was found, but this is a small postmortem study and does not establish a treatment or cure.
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In the human brain the monoaminooxidase-B enzyme or MAO-B is highly abundant in astrocytes.
Why it matters
In brain sections from Alzheimer patients, binding of [11C]-L-deprenyl was higher in the temporal lobes and white matter and coincided with more activated astrocytes. The authors describe it as a promising imaging biomarker of increased MAO-B activity, not a treatment, cure or prevention.
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Alzheimer's disease (AD) is the most common form of dementia.
Why it matters
This review states that inflammation appears to be involved in Alzheimer's disease and that neuroinflammation plays a critical role in its pathogenesis. It summarizes markers of inflammation and does not show that anti-inflammatory treatment cures or prevents 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.
- Nonpharmacological therapies in Alzheimer's disease: a systematic review of efficacy
- Magnetic resonance imaging biomarkers for the early diagnosis of Alzheimer's disease: a machine learning approach
- Evaluation of a calibrated (18)F-FDG PET score as a biomarker for progression in Alzheimer disease and mild cognitive impairment
- Exome analysis of 22,319 individuals links extremely rare copy-number variants and 22q11.21 dosage to Alzheimer risk
- Association Between Olfactory Dysfunction and Amnestic Mild Cognitive Impairment and Alzheimer Disease Dementia
- Effect of simvastatin on CSF Alzheimer disease biomarkers in cognitively normal adults
- Is tau in the absence of amyloid on the Alzheimer's continuum?: A study of discordant PET positivity
- 2024 Alzheimer's disease facts and figures
- Hospitalization in community-dwelling persons with Alzheimer's disease: frequency and causes
- The Alzheimer's disease risk factors apolipoprotein E and TREM2 are linked in a receptor signaling pathway