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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Dementia is one of the major causes of disability in later life, and ischemic heart disease is a leading cause of morbidity and mortality.
Why it matters
This review discusses how apolipoprotein E plays a role in lipoprotein metabolism in the brain and periphery and is implicated in both dementia and ischemic heart disease. It notes that whether plasma apoE levels are associated with increased risk of dementia independent of APOE genotype has only recently been established, but no treatment is tested.
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Alzheimer's disease (AD) is a neurodegenerative disease characterized by formation of amyloid-β (Aβ) plaques, activated microglia, and neuronal cell death leading to progressive dementia.
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Neurodegenerative diseases are distinguished by characteristic protein aggregates initiated by disease-specific 'seed' proteins; however, roles of other co-aggregated proteins remain largely unexplored.
Why it matters
This study purified hippocampal protein aggregates from Alzheimer's and control brains and analyzed their components by proteomics. It is basic laboratory research on protein aggregation and does not test any treatment, cure, or prevention.
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Positron emission tomography (PET) imaging of brain amyloid beta is now clinically available in several countries including the United States and the United Kingdom, but not Canada.
Why it matters
These Canadian consensus guidelines update advice on when amyloid PET imaging is appropriate in dementia care and aim to encourage a regulatory submission in Canada. They concern the use of a diagnostic scan and do not treat, cure or prevent Alzheimer's disease.
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Selecting a set of relevant markers to predict conversion from mild cognitive impairment (MCI) to Alzheimer's disease (AD) has become a challenging task given the wealth of regional pathologic information that can be extracted from multimodal imaging data.
Why it matters
This study used imaging markers and statistical methods to predict conversion from mild cognitive impairment to Alzheimer's disease dementia in a small sample. It does not show that any treatment prevents conversion, and the work is about improving prediction rather than curing or preventing dementia.
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Increasing evidence suggests that free radical-mediated oxidation of biological substrates is a key feature of Alzheimer's disease (AD) pathogenesis.
Why it matters
This review says biomarkers of lipid peroxidation are elevated in the brain and body fluids in Alzheimer's disease and are also found in mild cognitive impairment and preclinical Alzheimer's disease. It suggests lipid peroxidation may be a target for future therapeutics and could help with early detection, but no treatment is tested here.
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Decline in olfactory activity was correlated with the AD structural degeneration in the POC.
Why it matters
Atrophy in the primary olfactory cortex and hippocampus was found in both Alzheimer's disease and mild cognitive impairment and correlated with behavioral measures. Olfactory activation declined more steeply in mild cognitive impairment than tissue volume did, suggesting it may be a potential early biomarker, though this was a small study.
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FLIO set-up uses a scanning laser ophthalmoscope (HRA2, Heidelberg Engineering, Germany), which was modified by the use of an excitation pulse laser BLD440 (Becker&Hickl, Berlin, Germany) and detection of fluorescence lifetime by time-correlated single photon counting (TCSPC; Becker&Hickl) in two spectral channels (channel 1: 490-560 nm, channel 2: 560-700 nm).
Why it matters
This pilot study used fluorescence lifetime imaging ophthalmoscopy to look for retinal changes in patients with Alzheimer's disease. It is a small observational imaging study and does not test any treatment, cure, or prevention.
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Alzheimer's disease is the most common form of dementia, characterized by two pathological hallmarks: amyloid-β plaques and neurofibrillary tangles.
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We tested association of nine late-onset Alzheimer's disease (LOAD) risk variants from genome-wide association studies (GWAS) with memory and progression to mild cognitive impairment (MCI) or LOAD (MCI/LOAD) in older Caucasians, cognitively normal at baseline and longitudinally evaluated at Mayo Clinic Rochester and Jacksonville (n>2000).
Why it matters
Of nine late-onset Alzheimer risk variants tested in over 2000 older adults, only APOE-e4 was strongly linked to worse memory and progression to mild cognitive impairment or Alzheimer disease. The collective effect of the other variants appeared limited, and no treatment was tested.
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Alzheimer's disease (AD) is the most common cause of dementia worldwide.
Why it matters
Immunotherapy targeting amyloid beta has worked in many animal models but shown much less benefit in limited human data, with encephalitis in a minority of actively immunized patients and vasogenic edema or amyloid-related imaging abnormalities in some passive immunization trials. Tau-targeted therapy has been tested only in mouse models, and no approach targeting both pathologies concurrently had been attempted until very recently.
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Targeting amyloid-β peptide (Aβ) within the brain is a strategy actively sought for therapy of Alzheimer's disease (AD).
Why it matters
In laboratory and animal experiments, liposomes carrying a modified ApoE-derived peptide bound amyloid-beta, inhibited its aggregation, triggered disaggregation of preformed aggregates, and crossed the blood-brain barrier. These results suggest potential for therapy but are preliminary and have not been tested in humans.
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It is well known that a specific set of genetic and non-genetic risk factors contributes to the onset of Alzheimer disease (AD).
Why it matters
This review argues that vascular and metabolic risk factors such as diabetes and mid-life hypertension contribute to cognitive dysfunction in Alzheimer's disease through short-term and long-term effects. It suggests that managing these non-genetic risk factors might support treatment in Alzheimer's patients, but it is a review and does not present new trial results.
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41/100
Due to rapidly aging populations, the number of people worldwide experiencing dementia is increasing, and the projections are grim.
Why it matters
This book argues that efforts to detect Alzheimer's disease early through biomarkers have limitations and that a public health approach to prevention should complement the search for a cure. It does not report a new treatment or trial result, but it raises questions about how prevention and early detection efforts are framed.
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Alzheimer's disease (AD) is the leading cause for dementia in the world.
Why it matters
This review describes the innate immune system in Alzheimer's disease, including amyloid-beta and tau aggregates and risk factors such as ApoE4. It is a review and reports no treatment, cure or prevention.
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41/100
We previously described an intragenic functional copy number variation (CNV) in complement receptor 1 (CR1) that is associated with Alzheimer disease (AD) risk.
Why it matters
The study assessed whether the rare CR1 variant p.Ser1610Thr explains Alzheimer's risk and related traits in a Flanders-Belgian group. It is a genetic association study, so it does not provide a treatment, cure or prevention for Alzheimer's disease.
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β-Amyloid (Aβ) plaque deposition and neurodegeneration within temporoparietal and hippocampal regions may indicate increased risk of Alzheimer's disease (AD).
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This article gives an updated account of the clinical application of cerebrospinal fluid (CSF) biomarkers for Alzheimer disease (AD).
Why it matters
This article reviews how cerebrospinal fluid biomarkers total tau, phospho-tau, and Aβ42 can be used with other investigations to make a predementia diagnosis of Alzheimer's disease. It is about diagnosis and understanding the sequence of disease processes, not about treating, curing, or preventing Alzheimer's disease.
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The past decade has shed new light on the etiology of Alzheimer's disease (AD), which is the consequence of interactions between numerous lesions.
Why it matters
This review discusses metabolic syndrome, which includes visceral obesity, dyslipidemia, hyperglycemia and hypertension, as a possible modifiable risk factor for mild cognitive impairment and Alzheimer's disease, possibly linked through low-grade chronic inflammation from adipose tissue. However, the exact mechanisms connecting metabolic syndrome to Alzheimer's disease remain uncertain, and no treatment or prevention is established.
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41/100
Deficits in glutamate neurotransmission and mitochondrial functions were detected in the frontal cortex (FC) and hippopcampus (HIPP) of aged 3×Tg-Alzheimer's disease (AD) mice, compared with their wild type littermates (non-Tg).
Why it matters
In a mouse model of Alzheimer's disease, this study found deficits in glutamate neurotransmission and mitochondrial function in the frontal cortex and hippocampus. It is an animal study and does not test any treatment, cure or prevention in people.
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The amyloid-beta (Aβ) peptide is the derivative of amyloid precursor protein (APP) generated through sequential proteolytic processing by β- and γ-secretases.
Why it matters
This review discusses roles of amyloid precursor protein in neurogenesis and how impaired neurogenesis has been associated with Alzheimer's disease pathogenesis. It is a summary of laboratory findings and does not establish a treatment, cure, or prevention.
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Poorer cognitive function and an increased risk of vascular dementia (VaD) were found to be associated with a lower consumption of milk or dairy products.
Why it matters
This review reports that higher adherence to a Mediterranean-type diet was linked to slower cognitive decline and reduced risk of Alzheimer's disease in prospective studies. These are observational findings and do not prove that diet prevents or treats Alzheimer's disease.
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This study suggests that both tHcy and holoTC may be involved in the development of AD.
Why it matters
In this Finnish cohort, higher homocysteine and lower holotranscobalamin at baseline were linked to higher risk of developing Alzheimer disease over 7 years. The study suggests these markers may be involved in disease development but does not show that changing them prevents it.
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Alzheimer disease (AD) is an age-related neurodegenerative disorder, characterized histopathologically by the presence of senile plaques (SP), neurofibrillary tangles and synapse loss in selected brain regions.
Why it matters
This laboratory work found oxidatively modified proteins linked to mitochondria in the brains of people with Alzheimer's disease and mild cognitive impairment. It suggests oxidative stress and mitochondrial damage may be involved in the disease process, but it does not test any treatment or show that targeting this process helps patients.
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The AD subjects showed positive correlations between CSF-T-tau and CSF-P-tau versus CSF-Mn (r(s) = 0.22, p = 0.004; r(s) = 0.18, p = 0.021).
Why it matters
In 264 patients with Alzheimer disease and 54 healthy referents, cerebrospinal fluid metal concentrations were correlated with amyloid-beta, total tau and phosphorylated tau levels. The study reports associations only and does not show that any metal affects the disease or that changing metal levels would help.
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.
- Directed conversion of Alzheimer's disease patient skin fibroblasts into functional neurons
- Clinical Evolution of Neuropsychiatric Symptoms in Alzheimer's Disease and Dementia With Lewy Bodies in a Post‐Mortem Cohort
- Effect of Levetiracetam on Cognition in Patients With Alzheimer Disease With and Without Epileptiform Activity: A Randomized Clinical Trial
- [News on blood biomarker-based early diagnosis of the preliminary stages of Alzheimer's dementia]
- Attention Networks Connectivity After Cognitive Rehabilitation in Alzheimer’s Disease
- Sleep and longitudinal cognitive performance in preclinical and early symptomatic Alzheimer's disease
- Ryanodine receptors: physiological function and deregulation in Alzheimer disease
- Three-dimensional gray matter atrophy mapping in mild cognitive impairment and mild Alzheimer disease
- Metabolomic Signatures and Machine Learning Models for Distinguishing Alzheimer's Disease and Dementia with Lewy Bodies
- Disparity of Prescribed Psychotropics in Alzheimer’s Disease with Neuropsychiatric Symptoms