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 4,766 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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44/100
Neuropsychiatric symptoms (NPS) are prevalent, emerge early, and are associated with poorer outcomes in Lewy body dementia (LBD).
Why it matters
In this small study of 57 participants, no significant correlations were found between neuropsychiatric symptom severity and network connectivity in MCI with Lewy bodies. In Parkinson's disease MCI, affective symptoms, anxiety and psychosis were linked to patterns of brain network connectivity, but this does not establish a treatment or cure.
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Mutations in the TARDBP gene encoding TDP-43 protein are linked to loss of function in neurons and familial frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS).
Why it matters
In mice, nuclear loss of TDP-43 in brain endothelial cells disrupted the blood-brain barrier and caused hallmarks of frontotemporal dementia including fibrin deposition, gliosis, phospho-Tau accumulation, and impaired memory and social interaction. These data show a mechanism by which TDP-43 mutation may contribute to ALS-FTD, based on animal models.
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We found that pharmacological activation of TREM2 suppressed laser-induced choroidal neovessel formation.
Why it matters
In this study, pharmacological activation of TREM2 suppressed laser-induced choroidal neovessel formation in the eye by reducing TNF and promoting phagocytosis in mononuclear phagocytes. These findings concern pathological angiogenesis in the eye rather than Alzheimer's disease itself, and no Alzheimer's treatment or prevention was tested.
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TDP-43 mislocalization and aggregation are key pathological features of amyotrophic lateral sclerosis (ALS)- and frontotemporal dementia (FTD).
Why it matters
A new knock-in mouse model expressing mislocalized TDP-43 showed DNA repair impairment, inflammation, cellular senescence and motor deficits. The authors suggest it opens avenues for developing DNA repair-targeted approaches, but this is animal research and no treatment has been tested in patients.
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The underlying mechanisms of mild behavioral impairment (MBI), a marker for cognitive impairment and dementia, have remained unclear especially in a multiethnic Asian population.
Why it matters
This study examined whether three blood biomarkers could predict the later appearance of mild behavioral impairment in older Asian adults without dementia. It is about prediction and biomarkers, not about treating, curing or preventing Alzheimer's disease.
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We identified that the APOE4 genotype affected ΔHV in females.
Why it matters
In this 2-year study of 73 people with amnestic mild cognitive impairment, a significant interaction was found between APOE4 genotype and sex on hippocampal atrophy, with female APOE4 carriers showing 2.3 times higher atrophy. It does not test a treatment or cure, but it suggests sex-specific effects may matter when using hippocampal volume in trials or for predicting progression.
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Here, we found that the level of histone deacetylase 7 (HDAC7) was remarkably increased in the astrocytes of AD patients and P301S tau transgenic (PS19) mice.
Why it matters
In this study, inhibiting HDAC7 in mice improved clearance of tau and cognitive function, and the findings suggest downregulating HDAC7-TFEB signaling may help arrest Alzheimer's and other tauopathies. The work is in mice and human tissue and does not yet demonstrate a treatment for people.
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These findings support the interpretation that acute rises in CSF NfL concentration are likely to be related to passive release or CSF clearance failure.
Why it matters
This study supports the interpretation that acute rises in cerebrospinal fluid neurofilament light are likely related to passive release or clearance failure. It is about a biomarker's behavior and does not test a treatment for Alzheimer's disease.
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Despite the central role attributed to neuroinflammation in the etiology and pathobiology of Alzheimer's disease (AD), the direct link between levels of inflammatory mediators in blood and cerebrospinal fluid (CSF) compartments, as well as their potential implications for AD diagnosis and progression, remains inconclusive.
Why it matters
This study aimed to identify inflammatory mediators in blood and spinal fluid that correlate between the body and the central nervous system and to assess their potential significance for Alzheimer's diagnosis and progression. It is an observational study and does not test any treatment or cure.
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Gene therapy to treat hereditary disorders conventionally delivers the normal allele to compensate for loss-of-function mutations.
Why it matters
In mice with humanized APOE4, a gene therapy delivering the APOE2-Christchurch variant reduced amyloid and tau pathology more effectively than unmodified APOE2. These are animal results only and do not yet show whether this approach would work or be safe in people.
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Here, we observed significant compromise in macroautophagy/autophagy in the brains of mlkl knockout (KO) mice, as evidenced by the downregulation of BECN1/Beclin1 and ULK1 (unc-51 like autophagy activating kinase 1).
Why it matters
In mice, loss of Mlkl disrupted autophagy in the brain and worsened Alzheimer-like pathology in an Alzheimer mouse model. This is animal research and does not show any treatment, cure, or prevention for people.
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Pulsatile secretion of gonadotropin-releasing hormone (GnRH) is essential for activating and maintaining the function of the hypothalamic-pituitary-gonadal axis, which controls the onset of puberty and fertility.
Why it matters
This review discusses evidence that pulsatile GnRH therapy improved smell and cognition in preclinical Down syndrome and Alzheimer's disease models. The findings are from animal models, and the review also notes potential risks of long-term continuous GnRH administration, so this is not yet established as a treatment for people.
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The repair of white matter injury is of significant importance for functional recovery after ischemic stroke, and the up-regulation of triggering receptors expressed on myeloid cells 2 (TREM2) after ischemic stroke is neuroprotective and implicated in remyelination.
Why it matters
In rats with ischemic stroke, moderate physical exercise promoted remyelination and functional recovery, and silencing Trem2 affected this process. This is an animal study of stroke, not Alzheimer's disease, so it does not show how to treat, cure or prevent Alzheimer's.
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Unfortunately, many current Trem2 R47H mouse models are associated with cryptic mRNA splicing of the mutant allele that produces a confounding reduction in protein product.
Why it matters
This study created a new Trem2 R47H mouse model without the cryptic splicing that confounds older models, and found age- and disease-dependent tissue damage and synaptic loss in response to plaques. This is animal research only and reports no treatment, cure or prevention for people.
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Triggering receptor expressed on myeloid cells-2 (TREM2), a cell surface receptor mainly expressed on microglia, has been shown to play a critical role in Alzheimer's disease (AD) pathogenesis and progression.
Why it matters
In mice and cells, upregulating TREM2 inhibited tau hyperphosphorylation and neuronal apoptosis through the PI3K/Akt/GSK-3β pathway. This is animal and in-vitro work, so it is early and does not yet show a treatment for people.
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Microglia, the resident phagocytes of the retina, are believed to influence the development of retinopathy, but their exact contributions to vascular integrity and neuronal loss are unknown.
Why it matters
In diabetic mice, depleting and repopulating microglia reduced vascular and neuronal damage in the retina. This is an animal study of diabetic eye disease, not Alzheimer's disease, so it does not show a treatment or prevention for Alzheimer's disease.
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Tumor-associated macrophages (TAMs) represent a key component of the tumor microenvironment and are generally associated with immunosuppression and poor prognosis.
Why it matters
This review discusses TREM2 as a marker of pro-tumorigenic macrophages in cancer, where blocking TREM2 improved tumor control in models. It is about cancer, not Alzheimer's disease, and does not show a treatment or cure for Alzheimer's.
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Microglial polarization plays an essential role in the progression and regression of neurodegenerative disorders.
Why it matters
This study investigated whether cyanidin-3-O-glucoside regulates M1/M2 microglial polarization and Aβ42 phagocytosis through TREM2 in an Alzheimer's disease model, using cells and animals. It is early laboratory and animal research and does not establish any treatment, cure, or prevention for Alzheimer's disease in people.
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However, it remains unknown whether white matter (WM) decline due to AD is associated with specific Tau phosphorylation site(s).
Why it matters
In autosomal dominant Alzheimer's disease mutation carriers and non-carriers, cerebrospinal fluid tau phosphorylation at Thr205 was associated with loss of white matter integrity. It is a biomarker association study, so it does not show a treatment, cure or prevention.
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Cerebral small vessel disease (SVD) causes lacunar stroke and vascular cognitive impairment in older people.
Why it matters
In brain tissue from 52 people, a vasculocentric pattern of axonal pNfH was more common in older people with small vessel disease than in those with severe Alzheimer's disease. This is a tissue study of a lesion pattern and does not test any treatment, cure or prevention.
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New research shows that disease-associated microglia in neurodegenerative brains present features of elevated phagocytosis, lysosomal functions, and lipid metabolism, which benefit brain repair.
Why it matters
This mouse study reports that elevated microglial oxidative phosphorylation and phagocytosis stimulated post-stroke brain remodelling and cognitive recovery. It concerns stroke recovery in mice and does not report any treatment, cure, or prevention for Alzheimer's disease.
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Non-neuronal responses in neurodegenerative disease have received increasing attention as important contributors to disease pathogenesis and progression.
Why it matters
In three mouse models with tau only, amyloid only, or both, this study used single-cell RNA sequencing to compare how 13 brain cell types respond. It reports two distinct gene-activity states in oligodendrocytes, the brain's myelin-making cells, that appear differently depending on the type of pathology. The title describes the oligodendrocyte, astrocyte and T cell responses as TREM2-independent, a finding from deleting Trem2 in the combined-pathology mice. This is mouse gene-expression work: it does not test a treatment, and it does not show that these responses occur in people or affect symptoms.
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Secretases are a group of proteases that are major drug targets considered for the prevention and treatment of Alzheimer's disease (AD).
Why it matters
This review describes how secretases process both the amyloid precursor protein and TREM2, thereby controlling microglial functions, and notes that secretases are considered drug targets for Alzheimer's disease. It summarizes laboratory and genetic findings rather than reporting a proven treatment or cure.
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Glial fibrillary acidic protein (GFAP) is a well-established astrocytic biomarker for the diagnosis, monitoring and outcome prediction of traumatic brain injury (TBI).
Why it matters
In brain tissue from 52 people who died after traumatic brain injury and 17 controls, apparent GFAP staining inside neurons was most likely a staining artefact because negative controls also showed it. This finding concerns traumatic brain injury, not Alzheimer's disease treatment, and suggests caution in interpreting neuronal GFAP signals.
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44/100
The importance of mitogen-activated protein kinase (MAPK) pathway signaling in regulating microglia-mediated neuroinflammation in Alzheimer's disease (AD) remains unclear.
Why it matters
In a mouse model of Alzheimer's pathology and in postmortem human brain tissue, phosphorylated ERK was the most strongly increased signaling protein within microglia. This identifies a signaling pathway that may regulate microglial immune responses, but it is early research and not a tested treatment.
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.
- Distinct differences in prion-like seeding and aggregation between Tau protein variants provide mechanistic insights into tauopathies
- Multi-faced neuroprotective effects of Ginsenoside Rg1 in an Alzheimer mouse model
- Associations between [18F]AV1451 tau PET and CSF measures of tau pathology in a clinical sample
- Mexico City normal weight children exposed to high concentrations of ambient PM2.5 show high blood leptin and endothelin-1, vitamin D deficiency, and food reward hormone dysregulation versus low pollution controls. Relevance for obesity and Alzheimer disease
- Five-year follow-up of bilateral stimulation of the subthalamic nucleus in advanced Parkinson's disease
- Arc mediates intercellular tau transmission via extracellular vesicles
- The TspanC8 subgroup of tetraspanins interacts with A disintegrin and metalloprotease 10 (ADAM10) and regulates its maturation and cell surface expression
- Rebalancing Immune Interactions within the Brain-Spleen Axis Mitigates Neuroinflammation in an Aging Mouse Model of Alzheimer’s Disease
- RAN proteins and RNA foci from antisense transcripts in C9ORF72 ALS and frontotemporal dementia
- Uric acid and allantoin levels in Down syndrome: antioxidant and oxidative stress mechanisms?