Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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The common inhalation anesthetic isoflurane has previously been reported to enhance the aggregation and cytotoxicity of the Alzheimer disease-associated amyloid beta protein (Abeta), the principal peptide component of cerebral beta-amyloid deposits.
Why it matters
In human neuroglioma cells, the anesthetic isoflurane caused apoptosis and increased amyloid beta levels. This is cell-based work and does not establish that isoflurane causes or worsens Alzheimer's disease in patients.
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This is the first demonstration of gender differences in brain ferritin iron levels.
Why it matters
This imaging study in healthy adults found age-related changes in brain ferritin iron and lower ferritin iron in women than men in several brain regions. It suggests brain iron accumulation may be a risk factor that could be modified, but it does not test any treatment, cure, or prevention for Alzheimer's disease.
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Mild cognitive impairment (MCI) is generally referred to the transitional zone between normal cognitive function and early dementia or clinically probable Alzheimer's disease (AD).
Why it matters
This study found increased protein oxidation in the hippocampus of people with mild cognitive impairment and identified specific oxidized proteins involved in energy metabolism, synaptic plasticity, and cell proliferation. The authors conclude protein oxidation plays a significant role in the development of Alzheimer's disease from mild cognitive impairment, but this does not provide a treatment or cure.
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Sequential processing of amyloid precursor protein (APP) by membrane-bound proteases, BACE1 and gamma-secretase, plays a crucial role in the pathogenesis of Alzheimer disease.
Why it matters
This laboratory work identified beta subunits of voltage-gated sodium channels as new targets of the same enzymes (BACE1 and gamma-secretase) that cut amyloid precursor protein. It is early, cell-based research and does not test any treatment or show a benefit for patients.
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Evidence suggests that Alzheimer disease (AD) begins as a disorder of synaptic function, caused in part by increased levels of amyloid beta-peptide 1-42 (Abeta42).
Why it matters
In a mouse model, brief treatment with the phosphodiesterase 4 inhibitor rolipram improved synaptic and cognitive deficits, and the benefit lasted beyond the treatment period. This is an animal study, so it does not establish rolipram as a treatment, cure, or prevention for Alzheimer's disease in humans.
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Using positron emission tomography and [(11)C](R)-PK11195, a marker of "peripheral benzodiazepine sites" that is upregulated on activated microglia during progressive tissue pathology, we show increased binding of [(11)C](R)-PK11195 in frontotemporal lobar degeneration in the typically affected frontotemporal brain regions.
Why it matters
Using PET and [(11)C](R)-PK11195, increased binding was found in frontotemporal lobar degeneration in typically affected brain regions, implying an active glial response reflecting progressive neuronal degeneration. This is an imaging study in frontotemporal dementia and does not report a treatment or cure.
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Epidemiologic studies indicate that elderly women are at higher risk for Alzheimer disease compared to men.
Why it matters
In this large autopsy series, women had more affected brain regions and more extensive senile plaque deposits than men at early tangle stages, especially women carrying the APOE4 allele. It describes differences in brain lesions and does not provide a treatment, cure or prevention.
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Insulin is best known for its action on peripheral insulin target tissues such as the adipocyte, muscle and liver to regulate glucose homeostasis.
Why it matters
This review of experimental models describes how insulin signaling in the hippocampus and cortex may be involved in learning and memory, and notes that deterioration of insulin receptor signaling is associated with aging-related brain degeneration. It is based on animal and laboratory work and does not show that any insulin treatment helps people with Alzheimer's disease.
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Cytoplasmic deposition of alpha-synuclein aggregates is a common pathological feature of many neurodegenerative diseases.
Why it matters
In cells and neurons, the lysosomal degradation pathway can clear oligomeric alpha-synuclein but not mature fibrillar inclusion bodies, and blocking this pathway worsened alpha-synuclein toxicity. Enhancing lysosomal function is suggested as a possible way to halt or prevent Parkinson's disease and other Lewy body diseases.
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Inhibition of gamma-secretase, one of the enzymes responsible for the cleavage of the amyloid precursor protein (APP) to produce the pathogenic beta-amyloid (Abeta) peptides, is an attractive approach to the treatment of Alzheimer disease.
Why it matters
In mice, chronic treatment with the gamma-secretase inhibitor LY-411,575 reduced amyloid-beta production but also altered lymphopoiesis and intestinal cell differentiation. This was an animal study showing unintended biological consequences, so it is not yet known whether this approach would be safe or effective in people.
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48/100
Inheritance of the APOE epsilon4 allele is associated with increased risk of late posttraumatic seizures.
Why it matters
In 106 patients with moderate to severe traumatic brain injury, inheriting the APOE epsilon 4 allele was associated with a 2.41-fold higher relative risk of late posttraumatic seizures. The study did not find that epsilon 4 was associated with an unfavorable functional outcome overall.
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Patients with Alzheimer's disease have higher plasma homocysteine levels than controls, but it is uncertain whether higher plasma homocysteine levels are involved in the early pathogenesis of the disease.
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The most frequent human apolipoprotein (apo) E isoforms, E3 and E4, differentially affect Alzheimer's disease (AD) risk (E4 > E3) and age of onset (E4 < E3).
Why it matters
In mice engineered to make human amyloid-beta with either human apoE3 or apoE4, apoE3 "delayed the synaptic deficits until old age, whereas apoE4 was not protective at any of the ages analyzed." The loss of nerve-cell connections did not track plaques: in apoE4 mice it "preceded plaque formation", and old apoE3 and apoE4 mice had "comparable synaptic/cholinergic deficits" despite different plaque loads. This is animal research. The authors suggest only that the difference "could contribute" to apoE4's higher Alzheimer's risk, and it does not establish any treatment or prevention in people.
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Pathologic alterations in the microtubule-associated protein tau have been implicated in a number of neurodegenerative disorders, including Alzheimer's disease (AD), progressive supranuclear palsy (PSP), and frontotemporal dementia (FTD).
Why it matters
In fruit flies, overexpressing tau together with the fly GSK-3 homolog Shaggy worsened neurodegeneration and produced neurofibrillary pathology. This is an animal model study that may help identify future drug targets, but no treatment for patients was tested.
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3-4-(2-Fluoro-alpha-methyl-[1,1'-biphenyl]-4-acetyloxy)-3-methoxyphenyl]-2-propenoic acid 4-nitrooxy butyl ester (NCX-2216), a nitric oxide (NO)-releasing derivative of the cyclooxygenase-1-preferring nonsteroidal anti-inflammatory drug (NSAID) flurbiprofen, dramatically reduced both beta-amyloid (Abeta) loads and Congo red staining in doubly transgenic (Tg) amyloid precursor protein plus presenilin-1 mice when administered at 375 ppm in diet between 7 and 12 months of age.
Why it matters
In transgenic mice, an experimental nitric oxide-releasing anti-inflammatory drug reduced amyloid load and increased activated microglia, while celecoxib had no effect on amyloid deposition. This is animal research and does not show that any of these drugs treat or prevent Alzheimer's disease in people.
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The brain is the most cholesterol-rich organ in the human body.
Why it matters
This small study found elevated levels of 24S-hydroxycholesterol in the cerebrospinal fluid of people with Alzheimer's disease, which the authors interpret as increased cholesterol turnover in the brain during neurodegeneration. It is a small measurement study and does not test any treatment, cure, or prevention.
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Study of the hippocampal formation of 82 subjects, including 25 control subjects from 33 to 83 years of age, 34 subjects with Alzheimer disease (AD) from 65 to 89 years of age, and 23 subjects with Down syndrome (DS) from 33 to 72 years of age, revealed hippocampal vasculopathy with fibrosis and calcification (VFC) in 40% of control, 59% of AD, and 4% of DS subjects.
Why it matters
This autopsy study found vascular fibrosis and calcification in the hippocampus in some control, Alzheimer disease and Down syndrome subjects, with severe calcification linked to neuron loss in two Alzheimer cases. It describes blood vessel changes after death and provides no treatment, cure or prevention.
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The aim of this study was to evaluate the effects of two doses of anapsos in comparison with placebo on cognitive performance, brain bioelectrical activity pattern and cerebral hemodynamic parameters in patients with mild to moderate senile dementia of vascular type and Alzheimer type.
Why it matters
In this small 45-patient pilot study, the 360 mg/day dose of anapsos improved cognitive performance compared with placebo, including in the subset with Alzheimer's disease, but the 720 mg/day dose did not. These are preliminary results from a short four-week trial, so they do not establish that anapsos treats or prevents Alzheimer's disease.
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Recent research has identified some key players involved in the proteolytic processing of amyloid precursor protein (APP) to amyloid beta-peptide, the principal component of the amyloid plaques in Alzheimer patients.
Why it matters
This review discusses how amyloid precursor protein is processed and how its fragments may be involved in cell signaling. It describes basic biology and does not test any treatment or prevention.
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Hyperphosphorylation of the microtubule-associated protein tau is specifically found in those brain cells affected in several tauopathies.
Why it matters
This study built a lab test for tau phosphorylated at threonine 181 (p-tau181) in spinal fluid, standardised against a synthetic peptide. Average levels were higher in Alzheimer's patients (23.5 pM) and lower in frontotemporal dementia patients (8.6 pM) than in age-matched controls (15.9 pM), though the reported ranges overlap and the record gives no group sizes or diagnostic accuracy. It is a measurement study, not a test of any treatment or prevention.
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Predictive models may help differentiate MSA and PD premortem.
Why it matters
This study identified clinical features that best distinguish multiple system atrophy from Parkinson's disease using pathologically confirmed cases. It is about differential diagnosis between these two conditions, not about treating, curing or preventing Alzheimer's disease.
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Progressive supranuclear palsy (PSP) and cortocobasal degeneration (CBD) are often clinically confused with each other because they share a rapid disease progression, parkinsonism that responds poorly or transiently to levodopa therapy, and associated signs (e.g., ocular abnormalities, pyramidal signs and cognitive involvement).
Why it matters
This study examined clinical features that help distinguish postmortem-confirmed progressive supranuclear palsy from corticobasal degeneration. It is about improving diagnosis of these disorders, not treating, curing, or preventing Alzheimer's disease.
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The excessive generation and accumulation of 40- and 42-aa beta-amyloid peptides (Abeta40/Abeta42) in selectively vulnerable brain regions is a major neuropathological feature of Alzheimer's disease.
Why it matters
Using neurons and cell fractionation, this work found that distinct amyloid beta peptides are generated in the endoplasmic reticulum and the trans-Golgi network. This is basic cell biology about where amyloid is made and does not test a therapy.
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48/100
HIV produces a chronic viral infection of the central nervous system that elicits chronic glial activation and overexpression of glial cytokines that are also implicated in Alzheimer disease (AD) pathogenesis.
Why it matters
In people with HIV, those carrying the APOE E4 version were about twice as likely to have dementia and more likely to have peripheral neuropathy. This links a known Alzheimer's risk factor to neurologic symptoms in another condition, but it does not provide a treatment or prevention for Alzheimer's disease.
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48/100
The presynaptic protein alpha-synuclein has been implicated in the pathogenesis of Parkinson's disease.
Why it matters
In the rat optic system, alpha-synuclein bound to brain vesicles, and the A30P familial Parkinson's disease mutation abolished this binding. The authors propose that mutant alpha-synuclein may accumulate and form Lewy body filaments, but this is laboratory work and not a treatment.
From across this topic
10 of the 4,748 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.
- GBA Variants are associated with a distinct pattern of cognitive deficits in Parkinson's disease
- Early functional changes in lewy body dementia: roles of dynamics, locus coeruleus, and compensation
- Insights From TgF344-AD, a Double Transgenic Rat Model in Alzheimer’s Disease Research
- A Paravascular Pathway Facilitates CSF Flow Through the Brain Parenchyma and the Clearance of Interstitial Solutes, Including Amyloid β
- Benzoxazole Derivatives as Dual p38α Mitogen‐Activated Protein Kinase and Acetylcholinesterase Inhibitors: Design, Synthesis, and Evaluation for Alzheimer's Disease and Cancer Therapy
- Naturally Occurring Monoclonal Antibodies and Their Therapeutic Potential for Neurologic Diseases
- Activation of neuronal caspase-3 by intracellular accumulation of wild-type Alzheimer amyloid precursor protein
- Cyanidin-3-O-Glucoside Regulates the M1/M2 Polarization of Microglia via PPARγ and Aβ42 Phagocytosis Through TREM2 in an Alzheimer's Disease Model
- Quantitative analysis and clinico-pathological correlations of different dipeptide repeat protein pathologies in C9ORF72 mutation carriers
- The MIND diet association with lower microglial inflammation in the hippocampus: A Community‐Based Neuropathologic Study