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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Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are progressive adult-onset neurodegenerative diseases with overlapping pathological and genetic origins.
Why it matters
This study compared behaviour, cognition and sensory function in two knock-in mouse models of frontotemporal dementia and amyotrophic lateral sclerosis, finding age-related short-term memory deficits in one model and weight, fat mass, locomotion and marble burying changes in the other. These are animal model characterisation findings intended to inform future research design and do not test any treatment, cure or prevention for Alzheimer's disease.
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Recent advances in our understanding of non-cell-autonomous mechanisms in neurodegenerative diseases (NDDs) have highlighted microglial dysfunction as a core driver of disease progression.
Why it matters
This review discusses microglial dysfunction as a driver of several neurodegenerative diseases and lists therapeutic targets and biomarkers being studied. It notes that many biomarkers remain limited to preclinical studies and face challenges before clinical use, so no treatment is established here.
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NfL holds potential as a blood-based biomarker for symptomatic genetic FTD carriers, with moderate accuracy to distinguish PPD from mild forms including C9orf72 .
Why it matters
Blood levels of neurofilament light chain were higher in people with genetic frontotemporal dementia than in those with primary psychiatric disorders, and a cutoff value could distinguish the two groups with reasonable accuracy. This may improve diagnosis, but it does not address treating, curing, or preventing Alzheimer's disease.
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Intrinsic capacity (IC) is a recent key concept proposed by the World Health Organization (WHO) based on aspects of functional ability (both physical and mental) rather than the presence or absence of diseases, with a potential to predict several health outcomes.
Why it matters
This observational analysis of the MAPT study explored links between intrinsic capacity, plasma p-tau181 and cognitive function over 5 years in community-dwelling older adults. It examines associations over time and does not test any treatment, cure or prevention.
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A total of 43 trials of 327,264 participants with 42,016 major adverse cardiovascular events where included.
Why it matters
This meta-regression is about cholesterol lowering and cardiovascular events, not Alzheimer's disease, and reports no findings on dementia. It found that lowering remnant cholesterol was associated with part of the cardiovascular risk reduction seen in statin, ezetimibe, and PCSK9 inhibitor trials.
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The Mediterranean diet (MD) is widely recognized for its health benefits, particularly in modulating gut microbiota composition and reducing the risk of metabolic, cardiovascular, and neurodegenerative diseases.
Why it matters
This review reports that the Mediterranean diet is associated with improved markers of cognitive function and may support neuroprotective mechanisms, based on clinical and preclinical studies. It calls for further long-term clinical trials, so it does not establish that this diet prevents or treats Alzheimer's disease.
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Soluble N-ethylmaleimide-sensitive factor attachment proteins receptors (SNARE) proteins, such as VAMP-2 and SNAP-25, are implicated in α-synuclein pathophysiology and CSF levels of these proteins are associated with pathophysiological biomarkers and cognitive decline in Alzheimer’s disease (AD).
Why it matters
Levels of the proteins VAMP-2 and SNAP-25 in spinal fluid were lower in pure Lewy body dementia but higher in Lewy body dementia with Alzheimer's changes, and they tracked with other biomarkers and cognitive test results. These proteins may help tell these conditions apart, but this is biomarker research, not a treatment.
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The benefits of regular physical activity (PA) on disease prevention and treatment outcomes have been recognized for centuries.
Why it matters
This review is about exercise, the gut microbiome and gastrointestinal diseases and contains no information on Alzheimer's disease. It reports no findings relevant to treating, curing or preventing dementia.
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They remain a significant focus of scientific and clinical interest due to their increasing medical and social importance.
Why it matters
This review reports that use of polyphenols, alkaloids, and terpenoids is related to improvements in cognition, memory, and several behavioral symptoms. It is a review of existing evidence and does not establish these compounds as proven treatments for Alzheimer's disease.
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Synaptic degeneration has been linked to cognitive decline.
Why it matters
This study found that cerebrospinal fluid SNAP-25 was higher in Alzheimer's disease and in non-neurodegenerative diseases such as vascular dementia than in controls, but did not differ between Alzheimer's and non-Alzheimer's neurodegenerative diseases. It suggests SNAP-25 may be a potential biomarker, not a treatment, cure or prevention.
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MAFLD was associated with an increased risk of WMH over 4.1 years in middle‐aged adults.
Why it matters
Over a median 4-year follow-up, metabolic dysfunction-associated fatty liver disease was linked to a higher risk of white matter hyperintensities and to greater decline in executive function, but not to brain volume changes. This is an observational cohort finding and does not show that treating fatty liver disease prevents cognitive decline.
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Metabolic syndrome is a cluster of risk factors, including abdominal obesity, insulin resistance, hypertension, dyslipidemia (intended as an increase in triglyceride levels and a reduction in HDL cholesterol levels), and elevated fasting glucose, that increase the risk of cardiovascular disease and type 2 diabetes.
Why it matters
This review concerns the Mediterranean diet and components of metabolic syndrome, such as abdominal obesity, insulin resistance, hypertension, dyslipidemia and elevated fasting glucose. It reports improvements in blood pressure, lipid levels, insulin sensitivity and blood glucose, but says nothing about Alzheimer's disease.
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The PD-MCI nonreversion group had greater p-tau:amyloid beta and t-tau:amyloid beta ratios relative to the PD-MCI reversion group.
Why it matters
This longitudinal study found that people with Parkinson's disease and mild cognitive impairment who reverted to normal cognition had more favorable cerebrospinal fluid markers of Alzheimer's disease pathology than those who did not revert. It describes a prognostic difference and does not test any treatment, cure, or prevention.
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Our results pertaining to menopause-related characteristics, such as age at menopause or menopause hormonal therapy, did not replicate the literature reporting an association with WMH volumes.
Why it matters
In this cross-sectional UK Biobank sample, higher white matter hyperintensity volumes were found in premenopausal women compared to postmenopausal women in some analyses, and menopause-related characteristics such as age at menopause or hormone therapy did not show the previously reported associations with WMH volume. These findings question the idea that the menopausal transition directly drives this dementia-related risk factor, but the study cannot show cause and effect.
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Advanced atherosclerosis is the pathological basis for acute cardiovascular events, with significant residual risk of recurrent clinical events despite contemporary treatment.
Why it matters
This study found that iron accumulation promoted ferroptosis of foamy macrophages in advanced atherosclerosis, particularly in TREM2-low cells. It is about atherosclerosis and not Alzheimer's disease, so it has no implications for treating, curing or preventing Alzheimer's.
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Atherosclerosis is a chronic disease of the vascular wall driven by lipid accumulation and inflammation in the intimal layer of arteries, and its main complications, myocardial infarction and stroke, are the leading cause of mortality worldwide [1], [2].
Why it matters
This study found that TREM2 deficiency increased and TREM2 agonism decreased necrotic core formation in early atherosclerosis in mice. It concerns vascular disease, not Alzheimer's disease, and offers no treatment for dementia.
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Osteoarthritis (OA) is the most prominent chronic arthritic disease, affecting over 3 billion people globally.
Why it matters
This study is about osteoarthritis, not Alzheimer's disease, and examines how TREM2 affects macrophage polarization in that condition. It provides no information on treating, curing or preventing Alzheimer's disease.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is a transmembrane receptor protein predominantly expressed in microglia within the central nervous system (CNS).
Why it matters
This study is about TREM2 and brain injury after ischemic stroke, not Alzheimer's disease. It provides no information on treating, curing or preventing Alzheimer's disease.
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Microglia are resident macrophages of the central nervous system that have key functions in its development, homeostasis and response to damage and infection.
Why it matters
This review describes microglia as having crucial roles in neurological homeostasis and regeneration, including regulation of the maintenance and regeneration of myelin. It notes that myelin is damaged with normal ageing and in neurodegenerative diseases such as Alzheimer's, but does not report a treatment or cure.
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Demyelination is a hallmark of multiple sclerosis, leukoencephalopathies, cerebral vasculopathies, and several neurodegenerative diseases.
Why it matters
This mouse study used single-nucleus RNA sequencing to map gene expression changes during demyelination and remyelination, identifying specific cell types. It is about demyelination models and does not report any treatment, cure, or prevention for Alzheimer's disease.
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49/100
Structured Abstract Introduction People with Down syndrome (DS) often develop Alzheimer disease (AD).
Why it matters
In two large Down syndrome cohorts, blood levels of NT1-tau and Aβ42 were related to age and cognitive function. These are candidate blood markers that may help track cognitive impairment, but the study does not test any treatment, cure or prevention.
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Nonalcoholic fatty liver disease (NAFLD) is the most common liver pathology worldwide.
Why it matters
In this study of nonalcoholic fatty liver disease, TREM2-positive macrophages prevented a pro-inflammatory response in vitro and Trem2 expression regulated the ability of macrophages to phagocytose apoptotic cells. This is a liver disease study, so it does not provide evidence about treating, curing or preventing Alzheimer's disease.
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Immune checkpoint inhibitors targeting programmed cell death protein 1, programmed death-ligand 1, and cytotoxic T-lymphocyte-associated protein 4 provide deep and durable treatment responses which have revolutionized oncology.
Why it matters
This review is about targeting tumor-resident myeloid cells for cancer immunotherapy. It contains no information relevant to treating, curing or preventing Alzheimer's disease.
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Osteoarthritis (OA) is the most common joint disease, affecting over 300 million people world-wide.
Why it matters
This study used single-cell RNA sequencing to describe immune cell changes in post-traumatic osteoarthritis in joints. It is not about Alzheimer's disease and reports no treatment, cure, or prevention for it.
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49/100
The advent of high-throughput single-cell transcriptomic analysis of microglia has revealed different phenotypes that are inherently associated with disease conditions.
Why it matters
This review summarizes evidence that galectin-3 is upregulated in activated microglial phenotypes such as disease-associated microglia and interacts with receptors including TLR4 and TREM2. It discusses possible roles in neuroprotection or neurotoxicity but reports no treatment or cure.
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.
- Prion protein-mediated toxicity of amyloid-β oligomers requires lipid rafts and the transmembrane LRP1
- Seeding of normal Tau by pathological Tau conformers drives pathogenesis of Alzheimer-like tangles
- Neuropathology provides clues to the pathophysiology of Gaucher disease
- Deficits in cholinergic neurotransmission and their clinical correlates in Parkinson's disease
- Tau missorting and spastin-induced microtubule disruption in neurodegeneration: Alzheimer Disease and Hereditary Spastic Paraplegia
- Association of Apolipoprotein E ε4 With Medial Temporal Tau Independent of Amyloid-β
- Direct and indirect role of non-coding RNAs in company with amyloid and tau protein in promoting neuroinflammation in post-ischemic brain neurodegeneration
- BDNF Val66Met Genotype, DNA Methylation, mRNA, and Protein Levels as Potential Blood-Based Biomarkers for Dementia and Cognitive Decline
- Spermidine intake is associated with cortical thickness and hippocampal volume in older adults
- n-3 Fatty acid erythrocyte membrane content, APOE varepsilon4, and cognitive variation: an observational follow-up study in late adulthood