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 3D GRASE pCASL offers better repeatability than 2D EPI pCASL, thereby may provide a reliable imaging marker for the evaluation of disease progression and treatment effects in MCI and early AD subjects.
Why it matters
This small imaging study compared two arterial spin labeling MRI methods in elderly people, including those with mild cognitive impairment and one with Alzheimer's disease. It found one method had better repeatability, which may make it a more reliable imaging marker, but it did not test treatment or prevention.
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Phagocytosis controls CNS homeostasis by facilitating the removal of unwanted cellular debris.
Why it matters
In cells and mouse brains, this study found that the brain's immune cells (microglia) need the protein beclin 1 to clear debris efficiently. When beclin 1 was impaired, this went along with lower levels of the cell's "retromer" recycling machinery and poorer recycling of the debris-sensing receptors CD36 and Trem2. The authors report that this pathway is impaired in Alzheimer's disease, but this is early laboratory work and does not show that targeting beclin 1 prevents or treats Alzheimer's in people.
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Disorders characterized by α-synuclein (α-syn) accumulation, Lewy body formation and parkinsonism (and in some cases dementia) are collectively known as Lewy body diseases.
Why it matters
This review summarizes current knowledge and hypotheses about the different structural and aggregation states of alpha-synuclein and their possible role in Lewy body diseases, noting that the mechanism of toxicity remains unknown. It is a discussion of alpha-synuclein biology, not a treatment, cure or prevention for Alzheimer's disease.
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54/100
MLGPs provide an alternative analytical approach to predict an individual's genetic risk for episodic memory performance, a surrogate indicator of LOAD.
Why it matters
Combinations of gene variants, especially involving PICALM and CLU, were linked to poorer episodic memory in families with late-onset Alzheimer disease. This is a genetic association study of memory performance, not a test of treatment or prevention.
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These results suggest that GSTO locus variants may lower brain GSTO2 levels and consequently confer AD risk in older age.
Why it matters
This association study found that one GSTO2 variant was linked to slightly increased Alzheimer disease risk in people diagnosed after age 80, and a GSTO1 variant to decreased risk in familial Parkinson disease. The authors note inconsistent follow-up designs make interpretation difficult, and no treatment, cure, or prevention is tested.
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Rapid eye movement sleep behavior disorder (RBD) is common in Parkinson disease (PD), but its relationship to the varied neurotransmitter deficits of PD and prognostic significance remain incompletely understood.
Why it matters
In people with Parkinson disease without dementia, symptoms of REM sleep behavior disorder were linked to loss of the brain chemical acetylcholine. This does not show a treatment or cure, but it may help explain why some of these patients are more likely to develop thinking problems.
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In Alzheimer disease (AD), amyloid β peptide (Aβ) accumulates in plaques in the brain.
Why it matters
In a mouse model of Alzheimer's disease, a RAGE-specific inhibitor called FPS-ZM1 blocked amyloid-beta binding to RAGE, was nontoxic to mice and crossed the blood-brain barrier, reducing amyloid-beta-mediated brain disorder. This is animal and in-vitro work only and reports no treatment, cure or prevention for people.
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Our study showed an association between neurofibrillary pathology and frontal PVWMH and DWMH (rather than parietal), as a surrogate of small vessel disease, particularly in very old community-dwelling individuals.
Why it matters
In 132 autopsied subjects over 85, frontal periventricular and deep white matter hyperintensities were more extensive in the Alzheimer disease group and were associated with higher Braak staging and neuritic plaque load. This is a postmortem association study linking vascular imaging signs to Alzheimer pathology, not a treatment or prevention finding.
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Among adults with DS, decreasing levels of plasma Aβ42, a decline in the Aβ42/Aβ40 ratio, or increasing levels of Aβ40 may be sensitive indicators of conversion to AD, possibly reflecting compartmentalization of Aβ peptides in the brain.
Why it matters
In 225 adults with Down syndrome without dementia at baseline, 61 (27.1%) developed Alzheimer's disease, and a decrease in plasma Abeta42 levels or in the Abeta42/Abeta40 ratio, or an increase in Abeta40 levels, were related to conversion to Alzheimer's disease. The authors conclude these changes may be sensitive indicators of conversion.
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Doubly dissociated areas of hypoperfusion in FTLD and AD are consistent with areas of significant histopathologic burden in these groups.
Why it matters
Patients with frontotemporal lobar degeneration and those with Alzheimer disease showed different patterns of blood flow on brain imaging, with each group having reduced flow in different regions. This imaging approach may help distinguish the two conditions, but it does not treat or prevent either.
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Neurodegenerative tauopathies characterized by hyperphosphorylated tau include frontotemporal dementia and Parkinsonism linked to chromosome 17 (FTDP-17) and Alzheimer's disease (AD).
Why it matters
This laboratory study found that a chemical modification called acetylation prevents the breakdown of phosphorylated tau, and that blocking the enzyme p300 reduced this toxic tau in experiments. Modulating tau acetylation is suggested as a possible new therapeutic strategy, but this has not been tested as a treatment in patients.
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These plasma ceramides may be early indicators of AD progression.
Why it matters
In this small clinic sample, two plasma ceramides were lower in mild cognitive impairment than in normal controls or Alzheimer's disease, and higher baseline levels of these ceramides in the MCI group predicted cognitive decline and hippocampal volume loss over one year. The study was cross-sectional for its main comparisons and involved only 25 controls, 17 MCI, and 21 early Alzheimer's patients, so it is preliminary and does not show that measuring ceramides prevents or treats the disease.
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The text describes cerebral small vessel disease as a group of pathological processes affecting the brain's small vessels, with age-related and hypertension-related forms and cerebral amyloid angiopathy being most common.
Why it matters
Covers cerebral small vessel disease, from how it develops and its clinical characteristics to the challenges of treating it.
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Obesity is associated with lower brain volumes in cognitively normal elderly subjects, but no study has yet investigated the effects of obesity on brain structure in patients with mild cognitive impairment (MCI) or Alzheimer's disease (AD).
Why it matters
This study examined whether higher body mass index is linked to brain volume deficits in people with mild cognitive impairment or Alzheimer's disease. It is observational, so it cannot show that weight loss treats or prevents Alzheimer's disease.
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Systemic infection and drugs with anticholinergic effects are well-recognised and prevalent risk factors for delirium in elderly people.
Why it matters
This review proposes that microglial activation mediates behavioural effects of systemic infection and that loss of cholinergic inhibition could make microglia neurotoxic, linking delirium to long-term cognitive impairment. It offers no treatment, cure or prevention for Alzheimer's disease.
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Mutations in the gene encoding TDP-43-the major protein component of neuronal aggregates characteristic of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) with ubiquitin-positive inclusion bodies-have been linked to familial forms of both disorders.
Why it matters
In rat brain neurons grown in a dish, a form of the protein TDP-43 carrying a mutation linked to inherited ALS was toxic, and the toxicity tracked with how much of it had moved out of the nucleus into the cytoplasm. Neurons died whether or not visible clumps formed, and the amount of TDP-43 in the nucleus did not affect survival, while the amount in the cytoplasm was "a strong and independent predictor of neuronal death". This is lab-dish work on ALS and frontotemporal lobar degeneration, not Alzheimer's, and it tests no treatment.
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TDP-43 (TAR-DNA binding protein) aggregates in neuronal inclusions in motoneuron disease (MND), as well as in frontotemporal lobar degeneration (FTLD) and FTLD associated with MND (FTLD-MND).
Why it matters
TARDBP mutations were found in two patients with motoneuron disease associated with frontotemporal lobar degeneration, suggesting TDP-43 may have a direct pathogenic role in these disorders. This involves only two patients and concerns frontotemporal lobar degeneration, not Alzheimer's disease, and reports no treatment, cure or prevention.
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Tauopathies are neurodegenerative diseases characterized by aggregation of the microtubule-associated protein Tau in neurons and glia.
Why it matters
In Alzheimer's and related diseases, tau pathology starts in small brain regions and later spreads, and this study tested whether clumped tau can carry its misfolded shape into cells "similar to prions." In cultured cells, tau clumps (aggregates), but not single tau molecules, were taken up and made the cell's own tau form fibrils; those new fibrils could seed more fibrils in a test tube and passed between neighbouring cells. This is laboratory cell work that suggests one way tau misfolding might spread; it did not study people or animals and does not test a treatment.
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Parkinson's disease (PD), dementia with Lewy bodies and multiple system atrophy, collectively referred to as synucleinopathies, are associated with a diverse group of genetic and environmental susceptibilities.
Why it matters
In yeast, roundworms and other lab models, this study found that the Parkinson's-linked gene PARK9 (ATP13A2) interacts with alpha-synuclein: adding PARK9 "rescued" alpha-synuclein-driven loss of dopamine neurons, and reducing it in worms "enhances alpha-syn misfolding." In yeast, PARK9 also helped protect cells from manganese toxicity, which the authors present as a link between Parkinson's genes and an environmental risk factor. These are early model-system results about Parkinson's and related synucleinopathies, not human evidence and not a treatment, cure or prevention for Alzheimer's disease.
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The targeted brain dysfunction that accompanies aging can have a devastating effect on cognitive and intellectual abilities.
Why it matters
This review discusses white matter hyperintensities seen on MRI, which are common in older adults and have been linked to cognitive decline, with some evidence they may reflect vascular deposition of beta-amyloid. It is a discussion of imaging findings, not a test of any treatment, so it does not show how to cure or prevent Alzheimer's disease.
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These results suggest that phosphorylated TDP-43 is a major component of the inclusions, and that abnormal phosphorylation of TDP-43 is a critical step in the pathogenesis of FTLD-U and ALS.
Why it matters
This laboratory study of post-mortem brain tissue from people with frontotemporal lobar degeneration (FTLD-U) and ALS made antibodies that recognise only the phosphorylated (chemically tagged) form of the protein TDP-43; they stained more of the disease inclusions than ubiquitin antibodies and, unlike commercial TDP-43 antibodies, did not stain normal cell nuclei. The tags sat in the protein's tail end, were added by the enzymes casein kinase-1 and -2, and increased TDP-43 clumping in the authors' experiments, leading them to suggest that abnormal phosphorylation is "a critical step" in FTLD-U and ALS. It does not study Alzheimer's disease or living patients, gives no case numbers, and tests no treatment.
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We previously demonstrated that degeneration of the distal axons of the cardiac sympathetic nerve precedes loss of their mother neurons in the paravertebral sympathetic ganglia, suggesting distal dominant degeneration of the cardiac sympathetic nerve in PD.
Why it matters
This tissue study found that alpha-synuclein aggregates appear in the distal axons of the cardiac sympathetic nerve before loss of their parent neurons in Parkinson's disease. It describes disease progression, not a treatment, cure or prevention for Alzheimer's disease.
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The association between moderate-severe chronic kidney disease and white matter hyperintensity volume highlights the growing importance of kidney disease as a possible determinant of cerebrovascular disease and/or as a marker of microangiopathy.
Why it matters
This study found that chronic kidney disease is associated with greater white matter hyperintensity volume, which has itself been linked to increased risk of stroke, cognitive decline and dementia. It does not test any treatment or show that treating kidney disease prevents dementia.
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Serine protease inhibitors (serpins), the acute phase reactants and regulators of the proteolytic processing of proteins, have been recognized as potential contributors to the pathogenesis of Alzheimer disease (AD).
Why it matters
This study measured plasma and cerebrospinal fluid levels of serpins along with standard biomarkers in patients with Alzheimer disease, dementia with Lewy bodies, and controls. It is a biomarker comparison study and does not test any treatment, cure, or prevention.
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The SPM analysis showed that patients with MCI had significantly higher [(11)C]PIB uptake vs control subjects in the frontal, parietal, and lateral temporal cortices as well as in the posterior cingulate showing the most prominent differences.
Why it matters
In this small PET study, patients with amnestic mild cognitive impairment had higher amyloid tracer uptake than controls in several brain regions. It supports early amyloid buildup in mild cognitive impairment but does not test any treatment or show that this predicts benefit from any therapy.
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.
- Apoptosis protein markers in comorbid type 2 diabetes mellitus and depression; relationships with cognitive performance, incident dementia, and white matter hyperintensities
- Inflammasomes link vascular disease with neuroinflammation and brain disorders
- The brain in Down syndrome
- Treatment of autonomic dysfunction in Parkinson disease and other synucleinopathies
- FUS pathology defines the majority of tau- and TDP-43-negative frontotemporal lobar degeneration
- Plasma p-tau212 as a biomarker of sporadic and Down syndrome Alzheimer's disease
- Triad of TDP43 control in neurodegeneration: autoregulation, localization and aggregation
- Quantitative Assessment of the Effect of Chronic Kidney Disease on Plasma P-Tau217 Concentrations
- TREM2-independent microgliosis promotes tau-mediated neurodegeneration in the presence of ApoE4
- Cutaneous Phosphorylated Alpha‐Synuclein in Lewy Body Dementia