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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AV-1451 may have limited utility for in vivo selective and reliable detection of tau aggregates in these non-Alzheimer tauopathies.
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Many neurodegenerative proteinopathies share a common pathogenic mechanism: the abnormal accumulation of disease-related proteins.
Why it matters
In cell and Drosophila screens, this study found that tau levels are regulated by the kinase Nuak1, and reducing Nuak1 decreased tau and reversed phenotypes in a tauopathy mouse model. This is early animal and laboratory work and does not establish any treatment, cure, or prevention in people.
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Cerebrospinal fluid synaptotagmin-1 is a promising biomarker to monitor synaptic dysfunction and degeneration in Alzheimer's disease that may be useful for clinical diagnosis, to monitor effect on synaptic integrity by novel drug candidates, and to explore pathophysiology directly in patients with Alzheimer's disease.
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The world's population is steadily ageing and as a result, health conditions related to ageing, such as dementia, have become a major public health concern.
Why it matters
This work links airborne particulate matter to Alzheimer's and Parkinson's disease as an environmental factor, but it reports no treatment, cure or prevention. It only describes disease numbers and possible causes, so it does not change how these diseases are managed.
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Study objectives To evaluate the role of orexin-A with respect to cerebrospinal fluid (CSF) Alzheimer disease (AD) biomarkers, and explore its relationship to cognition and sleep characteristics in a group of cognitively normal elderly individuals.
Why it matters
In 63 cognitively normal elderly people, this study examined whether orexin-A relates to cerebrospinal fluid Alzheimer's biomarkers, cognition, and sleep characteristics. It is an observational study of a possible marker, not a test of treating, curing, or preventing Alzheimer's disease.
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We report kinetic modeling results of dynamic acquisition data from 0 to 100 min after injection with the tau PET tracer 18 F-AV-1451 in 19 subjects.
Why it matters
In 19 people ranging from young healthy adults to people with Alzheimer's, this study tracked a tau PET tracer for 100 minutes after injection. In the Alzheimer's group, the tracer cleared more slowly and unevenly from the brain's outer layer, and a shorter scan taken 80–100 minutes after injection "provided a reasonable substitute" for the full 100-minute scan in those regions. In the putamen, a deep brain area, the signal behaved the same way in every group, which may mean the tracer also binds to something other than tau there. The study is small and tests no treatment.
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The kynurenine pathway (KP) of tryptophan metabolism has emerged in recent years as a key regulator of the production of both neuroprotective (e.g. kynurenic and picolinic acid, and the essential cofactor NAD+) and neurotoxic metabolites (e.g. quinolinic acid, 3-hydroxykynurenine).
Why it matters
This review describes how dysregulated kynurenine pathway metabolism has been strongly associated with neurological diseases, and notes drug development efforts to use inhibitors that block certain enzymes in the pathway. It is a review of associations and proposed mechanisms, not a trial showing that any treatment works.
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Studies have assessed individual components of a western diet, but no study has assessed the long-term, cumulative effects of a western diet on aging and Alzheimer's disease (AD).
Why it matters
In mice, a long-term western-style diet increased activation of glial immune cells, and this was greater in a mouse model of Alzheimer's disease. These are animal findings and do not establish that diet changes prevent or treat Alzheimer's disease in people.
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In the past five years, a series of large-scale genetic studies have revealed novel risk factors for Alzheimer's disease (AD).
Why it matters
This review discusses how genetic studies have pointed to immune processes and microglial function in Alzheimer's, focusing on six genes including TREM2 and APOE. It summarizes existing literature and does not report a treatment or cure.
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Multiple sclerosis (MS) is a demyelinating disease of the central nervous system, leading to memory impairment in up to 65% of patients.
Why it matters
This study examined whether complement proteins C1q and C3 are involved in synapse loss in the hippocampus of people with multiple sclerosis, a disease different from Alzheimer's disease. It does not provide evidence about treating, curing, or preventing Alzheimer's disease.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is a DAP12-associated receptor expressed in microglia, macrophages, and other myeloid-derived cells.
Why it matters
The study shows that DAP12 stabilizes the C-terminal fragment of TREM2, a risk gene for Alzheimer's disease, and protects against an LPS-induced pro-inflammatory response. This is cell-based work on immune signaling and does not demonstrate a treatment, cure, or prevention for patients.
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Traumatic brain injury (TBI) represents a major cause of death and disability in developed countries.
Why it matters
This review discusses how astrocytes and microglia contribute to traumatic brain injury, which can trigger complications including dementia. It concerns traumatic brain injury rather than Alzheimer's disease and reports no treatment, cure or prevention for Alzheimer's.
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The findings provide further in vivo evidence that astrocytosis occurs early in AD, preceding Aβ plaque deposition.
Why it matters
In APPswe transgenic mice, astroglial tracer binding was higher at 6 months while amyloid tracer retention was higher only at 18-24 months, suggesting astrocytosis precedes amyloid plaque deposition. This is an animal imaging study and reports no treatment, cure or prevention.
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Microglial MVs are neurotoxic and myelinotoxic in the presence of Aβ1-42 .
Why it matters
Higher levels of myeloid microvesicles were found in the cerebrospinal fluid of Alzheimer's disease patients and mild cognitive impairment patients who converted within three years, and these levels were associated with tau but not with Aβ1-42. The microvesicles correlated with white matter tract damage in mild cognitive impairment and with hippocampal atrophy in Alzheimer's disease.
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Recent literature has pointed to the existence of inflammasome-mediated inflammatory pathways in central nervous system (CNS) disorders and associated changes in behavior.
Why it matters
This review describes inflammasome-mediated inflammatory pathways in the central nervous system and suggests that NLRP inflammasomes may play a role in the causes of Alzheimer's disease. It states that therapies targeting NLRP inflammasomes could be used to reduce neuroinflammation and treat associated psychiatric illnesses, although this is not yet established.
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These data reinforce the link between gut dysbiosis and neurologic dysfunction and suggest that dietary and/or pharmacologic manipulation of gut microbiota could attenuate the neurologic complications of obesity.
Why it matters
In mice, gut bacteria taken from donors on a high-fat diet caused changes in behavior and thinking even without the mice becoming obese. This is early animal research and does not show that the same happens in people or that it can be treated.
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Elevated levels of amyloid-β peptide (Aβ) in the human brain are linked to the pathogenesis of Alzheimer disease.
Why it matters
In Alzheimer model mice, injected exosomes trapped amyloid-β and carried it into microglia, and continuous injection decreased amyloid-β pathologies. This is animal work, so it does not show that the same approach treats or prevents Alzheimer's disease in people.
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Calbindin-D28k (CB), one of the major calcium-binding and buffering proteins, has a critical role in preventing a neuronal death as well as maintaining calcium homeostasis.
Why it matters
Mice with familial Alzheimer's disease mutations were crossed with calbindin-D28k knockout mice to study the role of calbindin-D28k in disease-related dysfunction. This is an animal study and does not show any treatment, cure, or prevention for Alzheimer's disease in humans.
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Differentiation of logopenic (lvPPA) and nonfluent/agrammatic (nfvPPA) variants of Primary Progressive Aphasia is important yet remains challenging since it hinges on expert based evaluation of speech and language production.
Why it matters
This study found that a measure of relative vowel duration helped distinguish nonfluent from logopenic primary progressive aphasia, matching expert judgment in most cases. It is a diagnostic study of speech and does not test any treatment, cure, or prevention for Alzheimer's disease.
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47/100
Age-associated dementia and Alzheimer's disease (AD) are currently epidemic.
Why it matters
In mice, a diet supplemented with glycotoxins led to metabolic syndrome, increased brain amyloid-beta42, and cognitive deficits, and older humans showed correlations between circulating glycotoxins and impaired cognition and insulin sensitivity. The authors identify dietary glycotoxins as a modifiable cause in their models, but this does not establish that reducing them prevents dementia in people.
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Brain changes reminiscent of Alzheimer disease (AD) have been previously reported in a substantial portion of elderly cognitive healthy (HC) subjects.
Why it matters
In 54 cognitively healthy elderly people followed for 3 to 4 years, lower FDG-PET values in medial temporal and parietal regions and worse executive function predicted conversion to mild cognitive impairment or Alzheimer's dementia, while gray matter volume did not. This concerns predicting progression and does not show that any treatment, cure or prevention works.
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Recent studies have highlighted a group of 4-repeat (4R) tauopathies that are characterised neuropathologically by widespread, globular glial inclusions (GGIs).
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The claimed beneficial effects of the Mediterranean diet include prevention of several age-related dysfunctions including neurodegenerative diseases and Alzheimer-like pathology.
Why it matters
In double transgenic TgCRND8 mice, eight weeks of dietary supplementation with oleuropein aglycone, the main polyphenol in extra virgin olive oil, protected against beta-amyloid plaque pathology. This is a mouse study of a dietary compound and does not show that it prevents or treats Alzheimer's disease in people.
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Down syndrome (DS) is the result of triplication of chromosome 21 (trisomy 21) and is the prevailing cause of mental retardation.
Why it matters
This review describes how extra copies of chromosome 21 genes, including APP and S100B, plus inflammatory changes driven by interleukin-1, may drive Alzheimer-like pathology in people with Down syndrome. It proposes that early immune and inflammatory events could accelerate Alzheimer pathogenesis, but it reports no treatment or prevention trial.
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Early to mid-adolescence is an important developmental period for subcortical brain maturation, but longitudinal studies of these neurodevelopmental changes are lacking.
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.
- Neurodegenerative disease mutations in TREM2 reveal a functional surface and distinct loss-of-function mechanisms
- The Trem2 R47H Alzheimer's risk variant impairs splicing and reduces Trem2 mRNA and protein in mice but not in humans
- Higher circulating α-carotene was associated with better cognitive function: an evaluation among the MIND trial participants
- Recurrent seizures may cause hippocampal damage in temporal lobe epilepsy
- Neuroinflammation demonstrated by 11 C‐ER176 PET with amyloid and tau pathology
- Microglial senescence contributes to female-biased neuroinflammation in the aging mouse hippocampus: implications for Alzheimer's disease
- Atherosclerotic calcification relates to cognitive function and to brain changes on magnetic resonance imaging
- HMOX1-LDHB interaction promotes ferroptosis by inducing mitochondrial dysfunction in foamy macrophages during advanced atherosclerosis
- Tubulin immunopositive structures resembling intracellular neurofibrillary tangles
- A harmonized classification system for FTLD-TDP pathology