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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40/100
There is much interest in understanding the mechanisms responsible for interactions among stress, aging, memory and Alzheimer's disease.
Why it matters
Using a rat model of early life stress, this study examined interactions between age, stress and insulin on cognition. This is animal work and does not show that any intervention prevents or treats Alzheimer's disease in people.
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Inflammation is believed to play a role in Alzheimer's disease (AD).
Why it matters
This study measured osteopontin levels in serum and cerebrospinal fluid of people with Alzheimer's disease, frontotemporal dementia and controls, and found higher levels in Alzheimer's disease cerebrospinal fluid that correlated with MMSE score. It is a biomarker study and does not test any treatment, cure or prevention.
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Synapse loss is an early and invariant feature of Alzheimer's disease (AD) and there is a strong correlation between the extent of synapse loss and the severity of dementia.
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Alzheimer's disease (AD) and Parkinson's disease (PD) are the most common causes of dementia and movement disorders in the elderly.
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40/100
Retinal ganglion cell loss is considered to be a cause of visual impairment in Alzheimer;s patients.
Why it matters
This study examined amyloid precursor protein processing and eye structure in Alzheimer's transgenic mice and found retinal changes. It is animal research and does not show a treatment, cure, or prevention for people.
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beta-Amyloid (Abeta) deposits are one of the major histopathological hallmarks of Alzheimer's disease (AD).
Why it matters
This postmortem brain tissue study found that the PET tracer [11C]PIB binds to amyloid deposits in Alzheimer's disease brain regions. It helps validate amyloid imaging as a way to detect amyloid in the brain, but it does not test any treatment, cure, or prevention.
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Oxidative stress has been shown to be a triggering event in the pathogenesis of Alzheimer's disease (AD).
Why it matters
This study found that markers of oxidative damage were increased in the blood of people with mild cognitive impairment and mild Alzheimer's disease compared to controls. The findings describe biological changes associated with disease progression but do not test any treatment or prevention.
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The five-predictor combination strongly predicted conversion to AD and was markedly superior to combining age and MMSE.
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40/100
These results agree with a persistent inflammatory status in AD, reinforcing the hypothesis of a progressive impairment of the immune response in this disorder and suggesting that monocytes may be good targets to study the progression from MCI to AD.
Why it matters
This study found that monocytes from people with Alzheimer's disease and mild cognitive impairment produced more of certain inflammatory cytokines and responded less to inflammatory challenges than controls. It supports a persistent inflammatory state and suggests monocytes as a possible target for studying progression, but does not test any treatment, cure or prevention.
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The complex etiology of Alzheimer's disease (AD) prompts scientists to develop multifunctional compounds to combat causes and symptoms of such neurodegeneration.
Why it matters
Researchers designed and tested coumarin compounds that inhibit both acetylcholinesterase and the beta-site amyloid precursor protein cleavage enzyme (BACE1) in the laboratory. These are early chemical findings and no treatment, cure or prevention in people is reported.
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40/100
A small, orally available natural product penetrates into the brain in vivo to rescue the memory impairment produced by soluble Abeta oligomers through a mechanism that restores hippocampal synaptic plasticity.
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40/100
Alzheimer's disease is the most common neurodegenerative disorder in the elderly.
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Human immunodeficiency virus-1 (HIV-1)-infected and immune-activated macrophages and microglia secrete neurotoxins.
Why it matters
This work concerns HIV-associated dementia and the role of the pro-inflammatory cytokines TNF-alpha and IL-1beta in neuronal death, not Alzheimer's disease. It provides no treatment, cure or prevention for Alzheimer's disease.
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40/100
Inhibitors of the enzyme acetylcholinesterase (AChE) are presently used as long-term symptomatic treatments for patients with Alzheimer disease (AD), as they enhance central levels of synaptic acetylcholine.
Why it matters
This review discusses whether cholinesterase inhibitors, currently used for symptomatic treatment, might also act as disease-modifying agents in Alzheimer's disease. It does not report a proven treatment, cure, or prevention.
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40/100
Potentially treatable neuropsychiatric symptoms are common in AD and represent a major source of distress among caregivers.
Why it matters
In 435 patients with probable Alzheimer's disease, behavioral and psychological symptoms were very common, with apathy the most common and persistent, and hallucinations more common in severe dementia. Caregivers rated moderate or severe distress for 10 of 12 symptom domains, and their total distress was strongly tied to the total symptom score rather than to the patient's cognition or function.
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Neuropathologically, Alzheimer-type abnormalities are demonstrated in patients with Down syndrome (DS), both demented and nondemented and more than a half of patients with DS above 50 years develop Alzheimer's disease (AD).
Why it matters
This review describes that more than half of people with Down syndrome above 50 develop Alzheimer's disease and that up to 84% of demented individuals with Down syndrome develop seizures, with late-onset epilepsy associated with Alzheimer's disease. It discusses risk factors and clinical associations but reports no treatment, cure or prevention.
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40/100
The cornu ammonis 1 region of the hippocampus (CA1) sector of hippocampus is vulnerable to both Alzheimer's disease (AD)-type neurofibrillary degeneration and anoxia-ischemia.
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40/100
It is generally accepted that human Alzheimer's disease (AD) neuropathology markers are completely absent in rodent brains.
Why it matters
Aged wild-type Octodon degu rodents were found to develop amyloid-beta deposits, tau accumulations, astrocytic response and other features resembling Alzheimer pathology, unlike most rodents. This describes a possible animal model for study and does not show any way to treat, cure or prevent the disease in humans.
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Synaptic dysfunction and failure are processes that occur early in Alzheimer disease (AD) and are important targets for protective treatments to slow AD progression and preserve cognitive and functional abilities.
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Synaptic damage and loss are factors that affect the degree of dementia experienced in Alzheimer disease (AD) patients.
Why it matters
In two transgenic mouse lines expressing mutant amyloid precursor protein, imaging of hippocampal neurons showed swollen dystrophic neurites and loss of dendritic spines compared with normal mice. This is an animal study describing structural changes and does not test a treatment for people.
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Neuroimaging studies in healthy subjects have yielded controversial results about the neural substrates of autobiographical memory.
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Abnormal cleavage of amyloid precursor protein (APP) in the central nervous system has been linked to the development of Alzheimer's disease.
Why it matters
This study found increased expression and processing of the Alzheimer amyloid precursor protein in pancreatic cancer cells, where it may influence cellular proliferation. It is about cancer biology, not Alzheimer's disease treatment, so it does not show how to treat, cure or prevent Alzheimer's disease.
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Borderline personality disorder (BPD) is a common disorder associated with emotional dysregulation and other symptoms that have been hypothesized to be related to dysfunction of limbic brain areas including hippocampus and amygdala.
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The amyloid plaque, a neuropathological hallmark of Alzheimer's disease, is produced by the deposition of beta-amyloid (Abeta) peptide, which is cleaved from Amyloid Precursor Protein (APP) by the enzyme beta-secretase.
Why it matters
This study found decreased alpha-secretase activity and increased beta-secretase activity in the temporal cortex of people with sporadic Alzheimer's disease. It describes a change associated with the disease but does not show that altering these enzymes treats or prevents it.
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Oxidative damage is present within the brains of patients with Alzheimer's disease (AD), and is observed within every class of biomolecule, including nucleic acids, proteins, lipids and carbohydrates.
Why it matters
This review notes that vitamin E and Ginkgo biloba extract have shown only modest benefit in Alzheimer's clinical trials, and a trial of vitamin E in mild cognitive impairment was ongoing. Combinations of antioxidants might have greater potential, but this is not established and no cure is claimed.
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.
- Clinical Utility of Amyloid Imaging in a Complex Case of Corticobasal Syndrome Presenting with Psychiatric Symptoms
- Accelerated MRI-predicted brain ageing and its associations with cardiometabolic and brain disorders
- Explaining the Variability of Alzheimer Disease Fluid Biomarker Concentrations in Memory Clinic Patients Without Dementia
- Effectiveness of Personalized Hippocampal Network-Targeted Stimulation in Alzheimer Disease: A Randomized Clinical Trial
- Temporal lobe atrophy on MRI in Parkinson disease with dementia: a comparison with Alzheimer disease and dementia with Lewy bodies
- APOE ε4, white matter hyperintensities, and cognition in Alzheimer and Lewy body dementia
- Association of low plasma Abeta42/Abeta40 ratios with increased imminent risk for mild cognitive impairment and Alzheimer disease
- The Role of Amyloid- and Tau PET in the New Era of Alzheimer Disease Therapies
- Stability of the preclinical episodic memory deficit in Alzheimer's disease
- Rates of Amyloid Imaging Positivity in Patients With Primary Progressive Aphasia