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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To analyze the relationship between the deposition of amyloid beta peptides (Abeta) and neuronal loss in transgenic models of Alzheimer's disease (AD), we examined the frontal neocortex (Fc) and CA1 portion of hippocampus (CA1) in PSAPP mice doubly expressing AD-associated mutant presenilin 1 (PS1) and Swedish-type mutant beta amyloid precursor protein (APPsw) by morphometry of Abeta burden and neuronal counts.
Why it matters
This study found that transgenic mice with both mutant presenilin 1 and mutant APP developed amyloid-beta deposits early but showed no significant difference in neuronal counts compared with other mice. It is animal research and does not test any treatment, cure, or prevention in people.
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We have identified new activating receptors of the Ig superfamily expressed on human myeloid cells, called TREM (triggering receptor expressed on myeloid cells).
Why it matters
Identifies TREM-1, a receptor on human blood neutrophils and some monocytes whose engagement triggers the release of inflammatory signals and which works through the adapter DAP12. The authors suggest TREM-1 may have a predominant role in inflammatory responses. It is not about Alzheimer's disease.
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Cerebrospinal fluid (CSF) concentrations of tau protein were measured using an enzyme-linked immunosorbent assay which measures both normal and hyperphosphorylated tau.
Why it matters
This study measured tau levels in cerebrospinal fluid from 17 patients with Alzheimer's disease, 23 with frontotemporal dementia and healthy controls, and found tau was raised in both patient groups. It is a small measurement study of a possible marker, not a treatment or cure.
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Abundant tau-positive neurofibrillary lesions constitute a defining neuropathological characteristic of Alzheimer's disease.
Why it matters
This review states that tau-positive neurofibrillary lesions define Alzheimer's disease and are central to several other dementias, and that tau mutations in FTDP-17 established tau's relevance to neurodegeneration. It mentions laboratory assays for testing compounds that block tau filament formation, but reports no treatment or cure.
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Recently exonic and intronic mutations in the gene for microtubule-associated protein tau have been discovered in cases of familial frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17).
Why it matters
The tau mutations G272V, P301L, V337M, and R406W each markedly reduced tau's ability to promote microtubule assembly in this laboratory study. This partial loss of function is proposed as a possible primary effect of these missense mutations, but no treatment or prevention is tested.
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The analysis of 14-3-3 protein in cerebrospinal fluid (CSF) was shown to be highly sensitive and specific for the diagnosis of Creutzfeldt-Jakob disease (CJD).
Why it matters
Testing spinal fluid for the 14-3-3 protein was highly sensitive and specific for Creutzfeldt-Jakob disease, though false positives occurred in some other conditions including progressive dementia of unknown cause. This concerns diagnosing CJD, not treating, curing, or preventing Alzheimer's disease.
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49/100
To study the pathogenesis of central nervous system abnormalities in Down syndrome (DS), we have analyzed a new genetic model of DS, the partial trisomy 16 (Ts65Dn) mouse.
Why it matters
This study describes a mouse model of Down syndrome that shows age-related loss of certain brain cells and other changes resembling Alzheimer's disease pathology. These are findings in mice, so they cannot yet be directly applied to treating or preventing Alzheimer's in people.
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The majority of HIV-1-infected individuals manifest a plethora of central nervous system (CNS) diseases unrelated to opportunistic infections, including AIDS dementia complex, encephalitis, and various other disorders of the CNS.
Why it matters
This study examined brain tissue from 22 people who died with AIDS to identify which cells harbor HIV-1 in the central nervous system. It is a post-mortem descriptive study of HIV neuropathogenesis and provides no information about treating, curing or preventing Alzheimer's disease.
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Deposition of PrP amyloid in cerebral vessels in conjunction with neurofibrillary lesions is the neuropathologic hallmark of the dementia associated with a stop mutation at codon 145 of PRNP, the gene encoding the prion protein (PrP).
Why it matters
This paper describes the neuropathology of a prion protein cerebral amyloidosis caused by a stop codon 145 mutation in PRNP, including vascular amyloid and tau-positive neurofibrillary tangles. It reports no treatment, cure or prevention for Alzheimer's disease.
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Transgenic FVB/N mice overexpressing human (Hu) or mouse (Mo) Alzheimer amyloid precursor protein (APP695) die early and develop a CNS disorder that includes neophobia and impaired spatial alternation, with diminished glucose utilization and astrogliosis mainly in the cerebrum.
Why it matters
Transgenic mice overexpressing amyloid precursor protein developed a neurological disorder and died early, without forming extracellular amyloid. This suggests that some harmful effects of APP overexpression may occur independently of amyloid plaques, but it is animal research and no treatment was tested.
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We studied the clinical features, pathology, and molecular genetics of a family (Mo) with an autosomal dominant disinhibition, frontal lobe dementia, parkinsonism, and amyotrophy.
Why it matters
In one family with an inherited dementia linked to chromosome 17, illness began at an average age of 45. In twelve affected members it started with personality and behaviour changes such as disinhibition, withdrawal, alcoholism or overeating. Every member examined later developed Parkinson-like stiffness and slowness, and death came a mean of 13 years after onset. Brain tissue showed frontotemporal damage but no amyloid plaques, tangles or Lewy bodies, so this is a distinct disorder the authors named DDPAC, not Alzheimer's disease, and the study describes it rather than testing any treatment.
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We examine the evidence for free radical involvement and oxidative stress in the pathological process underlying Parkinson's disease, from postmortem brain tissue.
Why it matters
This study examined brain tissue from Parkinson's disease patients and found evidence of oxidative stress in the substantia nigra, but it did not find significant changes in many protective antioxidant mechanisms. It does not test any treatment or prevention for Alzheimer's disease, so it has no direct implications for treating, curing, or preventing the disease.
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Reactive microglia or macrophages expressing the histocompatibility glycoprotein HLA-DR were detected in many neurological diseases including Alzheimer's, Parkinson's, Pick's and Huntington's diseases, parkinsonism-dementia of Guam, amyotrophic lateral sclerosis, Shy-Drager syndrome, multiple sclerosis and AIDS encephalopathy.
Why it matters
This study detected reactive microglia or macrophages expressing HLA-DR in many neurological diseases including Alzheimer's, with a distinctive pattern in each disease. It reports no treatment, cure or prevention result.
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HLA-DR is a class II cell surface glycoprotein of the human histocompatibility complex usually expressed on the surface of cells that are simultaneously presenting foreign antigen to T-lymphocytes.
Why it matters
In postmortem brains of people with senile dementia of the Alzheimer type, reactive microglia positive for HLA-DR were concentrated around senile plaques, and their numbers correlated with plaques and lower cortical ChAT. This is an old descriptive pathology finding about inflammation, not a treatment or cure.
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The brains of 232 patients with a case-note diagnosis of schizophrenia or affective disorder who died in one mental hospital over a period of 22 years were weighed, and were assessed in a coronal section at the level of the interventricular foramina.
Why it matters
This postmortem study compared brain structure in patients with schizophrenia and affective disorder. It concerns schizophrenia and does not test any treatment, cure or prevention for Alzheimer's disease.
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Synaptic dysfunction is increasingly recognized as an early and biologically relevant component of α-synucleinopathies.
Why it matters
This systematic review pulled together seventeen reports using SV2A PET, a scan that measures the density of nerve-cell connections (synapses), in Parkinson's disease, Parkinson's disease dementia/dementia with Lewy bodies and multiple system atrophy. Parkinson's disease most often showed reduced binding in the substantia nigra, while Parkinson's disease dementia and dementia with Lewy bodies showed broader, more cortical changes linked to cognitive performance. The authors see it as a promising research tool, but say small cohorts and inconsistent methods mean it is not ready for clinical use.
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Older age was associated with greater odds of abnormal p-Tau217 (odds ratio [OR] 1.08 per year, 95% CI 1.07–1.09), as was APOE ε4 carrier status (OR 3.32, 95% CI 2.65–4.17).
Why it matters
In a diverse cohort, older age and APOE ε4 carrier status were associated with higher odds of abnormal plasma p-Tau217, while Black participants had lower odds than non-Hispanic White participants after adjustment. Abnormal p-Tau217 was associated with higher odds of clinical cognitive impairment, highlighting the need to consider race and ethnicity in biomarker interpretation.
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In amyloid PET–positive MCI, Ginkgo biloba use was associated with sustained clinical stability, reduced plasma Aβ oligomerization tendency, and attenuation of amyloid PET progression over 18 months.
Why it matters
In this small retrospective study of 35 amyloid PET-positive mild cognitive impairment patients, those taking Ginkgo biloba extract remained clinically stable over 18 months, while 57.1% of those not taking it showed cognitive decline, and none of the Ginkgo group converted to Alzheimer's disease dementia versus 28.6% of the non-Ginkgo group. This is a retrospective analysis, not a randomized trial, so it cannot prove that Ginkgo biloba treats or prevents Alzheimer's disease.
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48/100
Individuals with Down syndrome (DS) have an increased risk of developing Alzheimer disease (AD), with nearly all individuals exhibiting AD neuropathology, including amyloid beta (Aβ) plaques and neurofibrillary tangles (NFT), by age 40 years.
Why it matters
In postmortem brain samples, burdens of three phosphorylated tau epitopes were similar between Down syndrome with Alzheimer's disease and late-onset Alzheimer's disease, and higher than in young Down syndrome and neurotypical controls. This is a cross-sectional autopsy study and reports no treatment or prevention.
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Alzheimer's disease (AD) and cancer are among the most devastating diseases worldwide.
Why it matters
In mice, peripheral cancer inhibited amyloid pathology and rescued cognition via secretion of cystatin-c, which binds amyloid oligomers and activates TREM2 in microglia to degrade existing plaques, and these effects were abolished by TREM2 or cystatin-c mutations. This is animal and mechanistic work proposing a distinct therapeutic avenue, not evidence that cancer or cystatin-c treats Alzheimer's disease in people.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is a key immunomodulatory receptor broadly expressed on myeloid cells such as macrophages and microglia.
Why it matters
This review describes how TREM2 signaling, including PI3K/Akt, MAPK, NF-κB, and STAT3 pathways, contributes to reducing neuroinflammation and slowing disease progression in Alzheimer's disease by promoting Aβ clearance and inhibiting tau hyperphosphorylation. It is a review of mechanisms, not a clinical trial, so it does not show that targeting TREM2 treats or cures Alzheimer's disease in people.
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TAR DNA-binding protein 43 (TDP-43) dysfunction is a hallmark of several neurodegenerative diseases, including frontotemporal dementia, amyotrophic lateral sclerosis, and Alzheimer's disease.
Why it matters
In post-mortem frontal cortex from people with frontotemporal lobar degeneration with TDP-43 pathology, this study found lengthening of the 3' untranslated region of VPS35 and ELK1, associated with markers of TDP-43 pathology and reduced VPS35 and VPS29 protein expression. This describes a molecular mechanism and does not test any treatment, cure or prevention.
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Lecanemab reduced amyloid PET in symptomatic participants with DIAD at Week 24.
Why it matters
In this early report, six months of open-label lecanemab cleared amyloid in the brains of 62 people with dominantly inherited Alzheimer's disease, matching what is seen in sporadic Alzheimer's disease. These are preliminary results from only the symptomatic group; the asymptomatic group has not yet been evaluated, so no conclusions about preventing or slowing disease can be drawn.
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Our findings demonstrate the capability of a fingerstick collection to accurately quantify p ‐tau217 levels longitudinally and genotype ApoE.
Why it matters
In 58 participants, p-tau217 measured from fingerstick samples correlated with plasma samples and discriminated CSF Aβ status with moderate accuracy over 12 months. This small study suggests fingerstick collection could support AD patient management, but it needs confirmation in larger groups.
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Eighty-three Black (mean 72±10.8-years-old, 63% female, 33% cognitively impaired) and 27 Latino participants (mean 65.8-years-old, 56% female, 11% cognitively impaired) completed neuroimaging.
Why it matters
This study found that tau PET patterns were similar across Black, Latino, and non-Hispanic white participants after adjusting for a marker of small vessel disease. It supports the use of tau PET in diverse groups and does not test any 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.
- Postoperative delirium is associated with increased plasma neurofilament light
- Cerebral glucose metabolism in patients with AD and different APOE genotypes
- Economic hardship and biological weathering: The epigenetics of aging in a U.S. sample of black women
- Local externalization of phosphatidylserine mediates developmental synaptic pruning by microglia
- Reversing EphB2 depletion rescues cognitive functions in Alzheimer model
- Molecular basis for the loss-of-function effects of the Alzheimer's disease-associated R47H variant of the immune receptor TREM2
- Poor glymphatic function is associated with mild cognitive impairment and its progression to Alzheimer's disease: A DTI-ALPS study
- Fluid biomarkers in atypical Parkinsonism: current state and future perspectives
- Chronic TREM2 activation exacerbates Aβ-associated tau seeding and spreading
- Evaluation of Copathology and Clinical Trajectories in Individuals With Tau-Clinical Mismatch