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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To evaluate whether magnetic resonance imaging (MRI) of white matter changes in Alzheimer's disease either under- or overestimates the findings on neuropathology.
Why it matters
In six Alzheimer brains, postmortem MRI underestimated the extent of white matter changes compared with pathology, though the missed lesions were minor. This is a comparison of imaging with tissue findings and does not address treatment or prevention.
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The potential of impairments in oxidative/energy metabolism to cause diseases of the brain had been proposed even before the major pathways of oxidative/energy metabolism were described.
Why it matters
This review proposes that impairments in oxidative and energy metabolism, through a downward mitochondrial spiral, may be a proximate cause of Alzheimer dementia. It is a hypothesis and does not report a tested treatment or prevention.
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We suggest that the APP23 Tg mouse may develop an earlier blockage in A beta clearance than the Tg2576 mice, resulting in a more severe accumulation of A beta in the perivascular drainage pathways and in the brain.
Why it matters
In APP23 mice engineered to make human amyloid, soluble amyloid-beta in the brain was 4 times control levels at 2 months and 33 times at 20 months, while blood levels never differed from normal mice; insoluble deposits climbed sharply after 9 months, ApoE rose and sat inside plaques, and amyloid in blood vessel walls became far more severe than in another model, Tg2576. The authors suggest this points to an early blockage in clearing amyloid from the brain, though the study measured amyloid levels rather than clearance itself. All findings are in mice and no treatment was tested.
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Down syndrome (DS) is a genetic disease with developmental brain abnormalities resulting in early mental retardation and precocious, age-dependent Alzheimer-type neurodegeneration.
Why it matters
In post-mortem brain tissue, this study found no significant differences in amino acid levels, including GABA, in Down syndrome compared with controls, while Alzheimer's disease showed significant losses of GABA and of glutamate and aspartate in some regions. It is a tissue comparison that identifies no treatment or prevention.
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Exceptional advances have been made in understanding the genetics of how common polymorphisms of the apolipoprotein E gene influence the risk and age of onset of Alzheimer disease (AD).
Why it matters
This review describes how the APOE gene has three common forms, with each copy of APOE4 raising Alzheimer's risk and lowering the age of onset, while APOE2 appears protective. It notes that testing for APOE4 can help in early diagnosis, but how such small protein changes produce these effects remains unexplained, and much of the evidence for APOE's many possible roles comes from laboratory and animal studies.
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The Mini Mental State Examination (MMSE) is widely used to measure dementia severity in Alzheimer's disease patients.
Why it matters
Using registry data, this study modelled how MMSE scores change over time in Alzheimer's disease patients and examined the influence of sex, education and age at testing. It concerns describing disease progression on a test and does not address treating, curing or preventing Alzheimer's disease.
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Long-term cognitive decline in postmenopausal women is associated with aging and Alzheimer disease (AD).
Why it matters
This study found no association between estrogen receptor alpha gene polymorphisms or transcriptional activity and Alzheimer's disease. It reports a lack of association and does not show a treatment, cure, or prevention.
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The authors extended previous studies of the stage-specific prevalence of behavioral pathology to members of ethnic minority groups.
Why it matters
Behavioral disturbances occurred in 98% of this multi-ethnic sample and were most frequent among patients with moderate and severe dementia, with preliminary evidence of ethnic differences in behavioral profiles. This is about behavioral symptoms in Alzheimer's disease, not about treating, curing, or preventing it.
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40/100
To gain insights into the different forms of modified amyloid beta peptides (A beta) in the Alzheimer disease (AD) and Down syndrome (DS) brain, we used two-site ELISAs with antibodies specific for isomerized (i.e. A beta with L-isoaspartate at positions 1 and 7) and pyroglutamate-modified (i.e. A beta beginning with pyroglutamate at position 3) forms of A beta to quantitate the levels of these different A beta peptides in formic acid extracts of AD and DS frontal cortex.
Why it matters
In formic acid extracts of frontal cortex from Alzheimer's disease and Down syndrome brains, the major amyloid-beta species were AbetaN3(pyroGlu)-42 and Abeta x-42, while isomerized amyloid-beta was a minor species. The authors suggest these distinct forms could play important roles in amyloid-beta deposition in both conditions.
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Determining the relative contributions of environment and heredity to the cause of Parkinson's disease (PD) is more than an academic issue because its resolution dictates future research directions to an enormous degree.
Why it matters
This review of Parkinson's disease argues that a known genetic mutation explains only a small share of cases, that genetics matter more in younger-onset disease, and that aging is the only clear risk factor. It is about causes of Parkinson's disease, not about treating, curing, or preventing Alzheimer's disease.
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The main hypothesis was that subtle vitamin B12 deficiencies occur more commonly in senile dementia of Alzheimer type (SDAT) that in healthy elderly individuals, and may be revealed by elevated total serum homocysteine (tHcy).
Why it matters
This small case-controlled survey looked at whether elevated total serum homocysteine might reveal subtle vitamin B12 deficiencies in people with senile dementia of Alzheimer type. It only examined a possible nutritional marker and did not test any treatment, cure or prevention.
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This report summarizes the consensus recommendations of a panel of neuropathologists from the United States and Europe to improve the postmortem diagnostic criteria for Alzheimer's disease.
Why it matters
Summarizes consensus recommendations from a panel of neuropathologists in the United States and Europe for improving the criteria used to diagnose Alzheimer's disease after death, reassessing the original NIA criteria published in 1985. It is a criteria paper and does not itself treat Alzheimer's.
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The presence of perihippocampal damage involving the amygdala proper, its surrounding cortex, and the subiculum further increased the severity of memory impairment attributable to hippocampal damage in Alzheimer's disease.
Why it matters
Patients with Alzheimer's disease had poor verbal and non-verbal memory test performance and significant volume reduction in medial temporal lobe structures. Volumes of the amygdaloid complex and subiculum correlated with memory performance, while hippocampal atrophy did not predict severity of memory impairment.
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The status of semantic priming in Alzheimer's disease (AD) was examined using the speech elicited N400 component of the event-related brain potential (ERP).
Why it matters
This study found that in Alzheimer's disease the brain's N400 response to speech was abnormal, suggesting a failure of semantic priming and possibly impaired semantic knowledge. It is a small physiological study and reports no treatment or prevention.
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Recent advances indicate soluble amyloid beta (A beta) protein is produced constitutively during normal metabolism of the amyloid precursor protein (APP).
Why it matters
Increased amounts of soluble amyloid-beta were found in isolated vascular tissues from people with Alzheimer's disease compared to controls. This is an observational study and does not show any treatment, cure, or prevention for Alzheimer's disease.
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Fas antigen (CD95) is a cell surface protein that mediates apoptosis.
Why it matters
In postmortem brain tissue, Fas antigen was found in senile plaques and in a subset of reactive astrocytes in Alzheimer-type dementia. This is a tissue study from 1995 and does not test any treatment, cure or prevention.
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Meningeal blood vessels were studied in Alzheimer disease (AD) and control brain specimens obtained from autopsies within 16 hours after death.
Why it matters
This autopsy study found non-fibrillar beta-amyloid protein associated with smooth muscle cells of vessel walls in Alzheimer's disease. It describes vessel pathology but does not test or establish any treatment, cure or prevention.
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We designed this questionnaire-based study to determine the risk of auto crashes among Alzheimer's disease (AD) patients who continued to drive after the onset of AD, compared with normal age-matched control subjects and other drivers' statistical records.
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Upon acute activation, microglia, the immuneffector cells of the brain parenchyma, express the amyloid precursor protein (APP) that is otherwise prominent in pathological structures related to Alzheimer's disease.
Why it matters
Activated microglia were found to rapidly synthesize amyloid precursor protein de novo, and microglia activation had mostly been viewed as secondary to amyloid deposits. This is a mechanistic study in cells and animal tissue and does not offer a treatment or prevention.
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There is demand on community pathologists to perform autopsies to confirm the clinical diagnosis of Alzheimer's disease, the most common cause of dementia in our increasingly aging society.
Why it matters
This article provides pathologists with a practical protocol for autopsy examination to confirm the clinical diagnosis of Alzheimer's disease, adapted from guidelines used by Alzheimer's disease research centers. It states there is no absolute diagnostic gold standard and that histopathologic diagnosis remains imperfect, so it concerns diagnosis after death rather than treatment, cure or prevention.
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We examined the abilities of 15 patients with dementia of the Alzheimer type (DAT), 22 patients with Parkinson's Disease (PD), and 141 healthy subjects (ranging in age from 30 to 79 years) to detect and correct their own speech errors.
Why it matters
Patients with Alzheimer's disease and Parkinson's disease corrected far fewer of their own speech errors than healthy subjects, pointing to a communication problem not previously recognized. No treatment, cure, or prevention is reported.
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We reanalyzed and compared current prevalence estimates of Alzheimer's disease in Europe.
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The extent and location of neuronal losses necessary or sufficient to produce dementia in patients with Alzheimer's Disease (AD) is unknown.
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Nuclear magnetic resonance (NMR) imaging was employed to study 10 patients with Alzheimer's disease (AD) and seven healthy elderly control subjects.
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One hundred fifty autopsy brains from patients with clinically diagnosed Alzheimer's disease (AD) were examined pathologically.
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.
- Neue Alzheimer-Therapien: Vortrag zu ARIA für eine sichere MRT-Diagnostik
- Tracing inflammasomes in Alzheimer's: insights from bibliometric analysis
- The relative importance of imaging markers for the prediction of Alzheimer's disease dementia in mild cognitive impairment - Beyond classical regression
- Cell-weighted polygenic risk scores are associated with β-amyloid and tau biomarkers in Alzheimer’s disease
- Association Between Elevated Brain Amyloid and Subsequent Cognitive Decline Among Cognitively Normal Persons
- Multimodal Precision Prevention - A New Direction in Alzheimer's Disease
- What is the amygdala?
- A 24-week randomized, controlled trial of memantine in patients with moderate-to-severe Alzheimer disease
- A novel pathway for amyloid precursor protein processing
- Developing the ATX(N) classification for use across the Alzheimer disease continuum