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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A comprehensive, unbiased inventory of synuclein forms present in Lewy bodies from patients with dementia with Lewy bodies was carried out using two-dimensional immunoblot analysis, novel sandwich enzyme-linked immunosorbent assays with modification-specific synuclein antibodies, and mass spectroscopy.
Why it matters
In brain tissue from people with dementia with Lewy bodies, this lab study found that the main chemical change to alpha-synuclein inside Lewy bodies is a single phosphorylation at Ser-129, and it found the same pattern in familial Parkinson's disease (A53T) and multiple system atrophy. Small amounts of the phosphorylated and Asp-119-truncated forms also appeared in normal brains, which the authors read as a sign that these forms come from ordinary protein turnover, while ubiquitination was seen only inside Lewy bodies. It is a post-mortem tissue analysis of Lewy body diseases, not Alzheimer's, and it does not test any diagnosis or treatment.
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Apraxia of speech (AOS) is a motor speech disorder characterized by slow speaking rate, abnormal prosody and distorted sound substitutions, additions, repetitions and prolongations, sometimes accompanied by groping, and trial and error articulatory movements.
Why it matters
In 17 autopsy-examined people whose illness began with a degenerative speech or language disorder, all 11 who had apraxia of speech (a motor speech problem with slow, distorted speech) had tau-based pathology, while 5 of the 6 without it did not (P = 0.001); MRI linked apraxia of speech to the premotor and supplementary motor cortex and non-fluent aphasia to the anterior peri-sylvian region. None of the cases had Alzheimer's disease: the diagnoses were progressive supranuclear palsy, corticobasal degeneration, FTLD with ubiquitin-only changes and Pick's disease. This small case series helps separate apraxia of speech from aphasia and link it to underlying pathology, but it tests no treatment and the authors say the classifications still need refining.
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Why it matters
Reports that microglia derived from bone marrow play a critical role in restricting senile plaque formation in Alzheimer's disease.
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The new HipMask technique provides accurate and rapid assessment of the hippocampus on PET without the use of regions of interest.
Why it matters
This study developed a new automated method for measuring glucose metabolism in the hippocampus on PET scans and found reductions in both mild cognitive impairment and Alzheimer disease that standard voxel-based analysis had missed. It is a diagnostic imaging technique, not a treatment, so it may improve how patients are identified for trials but does not itself cure or prevent Alzheimer's.
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The clinical diagnosis of progressive supranuclear palsy (PSP) relies on the identification of characteristic signs and symptoms.
Why it matters
This study of pathologically confirmed progressive supranuclear palsy identified two clinical phenotypes with different disease duration and age at death. It concerns progressive supranuclear palsy, not Alzheimer's disease, and reports no treatment, cure, or prevention.
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Subjects included 96 males and 118 females with a mean age at death of 86 years (SD, 7).
Why it matters
In 214 deceased participants, carrying the APOE ε4 allele raised the odds of having a cerebral infarction found at autopsy by about 2.3-fold. This links a gene to vascular brain damage but does not test any treatment or prevention.
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Elimination of apoptotic neurons without inflammation is crucial for brain tissue homeostasis, but the molecular mechanism has not been firmly established.
Why it matters
This study shows that TREM2 is expressed in microglia and that TREM2 stimulation increases phagocytosis of apoptotic neurons without inflammation. It is laboratory work on a mechanism and does not test an Alzheimer's treatment or cure.
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55/100
Parkin is an E3 ubiquitin ligase involved in the ubiquitination of proteins that are important in the survival of dopamine neurons in Parkinson's disease (PD).
Why it matters
Parkin was found to be S-nitrosylated in vitro, in a mouse model of Parkinson's disease, and in brains of patients with Parkinson's disease and diffuse Lewy body disease. S-nitrosylation inhibited parkin's ubiquitin E3 ligase activity and its protective function, which the authors suggest could contribute to degeneration by impairing ubiquitination of parkin substrates.
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There was no control group, but worsening of akinesia, speech, postural stability, freezing of gait, and cognitive function between the first and the fifth year is consistent with the natural history of Parkinson's disease.
Why it matters
This study followed patients with advanced Parkinson's disease who received bilateral stimulation of the subthalamic nucleus and found improved motor function off medication and less dyskinesia over five years. It concerns Parkinson's disease, not Alzheimer's disease, and there was no control group.
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Excessive daytime sleepiness was present overall in 327 (51%) of the 638 patients and in 213 (51%) of the 420 drivers.
Why it matters
This survey found excessive daytime sleepiness in 51% of Parkinson's disease patients and identified sleepiness scale scores as risk factors for falling asleep at the wheel. It concerns sleepiness and driving safety in Parkinson's disease and does not address treating, curing, or preventing Alzheimer's disease.
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Parkinson disease is a common neurodegenerative disorder characterized by the loss of dopaminergic neurons and the presence of intracytoplasmic-ubiquitinated inclusions (Lewy bodies).
Why it matters
Parkin was shown to ubiquitinate synphilin-1, and co-expressing alpha-synuclein, synphilin-1 and parkin produced Lewy-body-like inclusions, while parkin mutations disrupted this. This is cell-based Parkinson's disease research with no treatment tested.
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Previous work has established that compound mutations and homozygous loss of function of the parkin gene cause early-onset, autosomal recessive parkinsonism.
Why it matters
In two families with early-onset parkinsonism, compound heterozygous parkin mutations were found, and autopsy of one proband showed Lewy body pathology typical of idiopathic Parkinson's disease. The findings suggest compound heterozygous parkin mutations and loss of parkin protein may lead to early-onset parkinsonism with Lewy body pathology, but no treatment or cure is reported.
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beta-Amyloid plaques and neurofibrillary tangles (NFTs) are the defining neuropathological hallmarks of Alzheimer's disease, but their pathophysiological relation is unclear.
Why it matters
Injecting amyloid-beta Aβ42 fibrils into the brains of mice carrying a mutant tau gene (P301L) caused fivefold increases in neurofibrillary tangles in the amygdala. The authors say the data support the hypothesis that Aβ42 fibrils can accelerate tangle formation in vivo.
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55/100
Abnormal accumulation of the amyloid-beta peptide (Abeta) in the brain appears crucial to pathogenesis in all forms of Alzheimer disease (AD), but the underlying mechanisms in the sporadic forms of AD remain unknown.
Why it matters
In aged transgenic mice, increasing astroglial TGF-beta1 production reduced amyloid plaques and amyloid load in the brain. This is animal research, so it is too early to know whether this approach would help people with Alzheimer's disease.
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CST3 is a susceptibility gene for late-onset AD, especially in patients aged 75 years and older.
Why it matters
In a case-control study of 517 Alzheimer's patients and 390 controls, homozygosity for haplotype B of the cystatin C gene was significantly associated with late-onset Alzheimer's disease, with an odds ratio of 3.8. This suggests a genetic association, but no treatment or prevention is tested.
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One hallmark of Alzheimer disease is the accumulation of amyloid beta-peptide in the brain and its deposition as plaques.
Why it matters
Earlier work had shown that immunizing PDAPP mice with human amyloid-beta "reduces plaque burden and its associated pathologies". This 2000 study reports that giving antibodies against amyloid-beta from outside the brain "was sufficient to reduce amyloid burden", and its title says the antibodies entered the central nervous system. Our record gives no effect sizes, memory or safety data, and these were genetically engineered mice, so it does not show that the approach works or is safe in people.
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The epsilon4 allele of the apolipoprotein E (APOE) gene confers an increased risk for the development of AD.
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Amyloid plaques are a neuropathological hallmark of Alzheimer's disease (AD), but their relationship to neurodegeneration and dementia remains controversial.
Why it matters
In mice engineered to make human amyloid protein precursor, high levels of Aβ1-42 were linked to fewer presynaptic nerve terminals even in mice that formed no plaques. The authors conclude that amyloid-beta is synaptotoxic even in the absence of plaques.
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The relationship between NFD and Alzheimer-type dementia, and the criteria for a biochemical diagnosis of AD, are documented, and an association between AD and the extent of NFD in defined brain areas is shown.
Why it matters
This study mapped the step-by-step spread of neurofibrillary degeneration through the brain in aging and Alzheimer's disease, finding it could be asymptomatic up to a certain stage. It describes the disease process but does not test or report any treatment, cure, or prevention.
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The aims of this study were to examine the relationships of hippocampal T2 (HCT2) relaxation time and magnetic resonance (MR)-based hippocampal volume (HCV) to neuronal (ND) and glial cell densities (GD) of hippocampal neuronal cell layers, and to obtain a better clinicopathological definition of hippocampal sclerosis (HS) and end folium sclerosis (EFS).
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In addition, the hematocrit correlated significantly with severity, independent of the longer duration of symptoms in nonanemic patients.
Why it matters
This paper reports that the hematocrit correlated significantly with severity of neurologic aspects of cobalamin deficiency, independent of the longer duration of symptoms in nonanemic patients. No information on treating, curing, or preventing Alzheimer's disease is provided in the available text.
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55/100
Among 141 consecutive patients with neuro-psychiatric abnormalities due to cobalamin deficiency, we found that 40 (28 percent) had no anemia or macrocytosis.
Why it matters
This study found that neuropsychiatric symptoms from cobalamin deficiency can occur without anemia or enlarged red blood cells, and that measuring methylmalonic acid and total homocysteine helps diagnose these patients. Almost all patients improved with cobalamin therapy, but this concerns cobalamin deficiency, not Alzheimer's disease.
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Infection with human immunodeficiency virus type 1 (HIV-1) is frequently complicated in its late stages by the AIDS dementia complex, a neurological syndrome characterized by abnormalities in cognition, motor performance, and behavior.
Why it matters
This paper describes the AIDS dementia complex, a neurological syndrome caused largely by direct HIV-1 infection of the brain, with productive infection confined mainly to macrophages, microglia and related multinucleated cells. It concerns HIV-associated dementia, not Alzheimer's disease, and reports no Alzheimer's treatment, cure or prevention.
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A monoclonal antibody to the microtubule-associated protein tau (tau) labeled some neurofibrillary tangles and plaque neurites, the two major locations of paired-helical filaments (PHF), in Alzheimer disease brain.
Why it matters
Using an antibody to the protein tau, researchers studied neurofibrillary tangles and plaque neurites in Alzheimer brain tissue. The findings suggest that tau in the Alzheimer brain is an abnormally phosphorylated component of the paired helical filaments found in these lesions.
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This cross-sectional study evaluates the performance of the US Food and Drug Administration–cleared phosphorylated tau 217 (p-tau217) to β-amyloid 42 ratio cut points used to detect amyloid pathology associated with Alzheimer disease.
Why it matters
This cross-sectional study evaluates how the FDA-cleared p-tau217 to β-amyloid 42 ratio cut points perform at detecting amyloid pathology. It is a diagnostic performance assessment and reports nothing about treatment, cure or prevention.
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.
- Convergence of neuroinflammation across major neurotropic viral exposomes in AD and ADRD
- Exploring the relationship between epilepsy and neurodegenerative diseases
- Apolipoprotein E4 and Insulin Resistance Interact to Impair Cognition and Alter the Epigenome and Metabolome
- A Novel TREM2 Small Molecule Agonist MTX46943 Re‐Programs Human Microglia and Reduces Amyloid Pathology In Vivo
- α-Synuclein and tau concentrations in cerebrospinal fluid of patients presenting with parkinsonism: a cohort study
- Insulin resistance as a key link for the increased risk of cognitive impairment in the metabolic syndrome
- Specific human astrocyte subtype revealed by affinity purified GFAP antibody; unpurified serum cross-reacts with neurofilament-L in Alzheimer
- TDP-43 promotes microRNA biogenesis as a component of the Drosha and Dicer complexes
- The tau biomarker cascade is condensed in Down syndrome compared with sporadic Alzheimer's disease
- Generation of Alzheimer disease-associated amyloid β42/43 peptide by γ-secretase can be inhibited directly by modulation of membrane thickness