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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Dietary influences on Alzheimer disease (AD) are gaining recognition.
Why it matters
In two Alzheimer transgenic mouse models, caloric restriction substantially reduced amyloid plaque accumulation and decreased astrocytic activation. This is animal evidence only, and the authors suggest dietary interventions in adult life might slow disease progression, which is not yet shown in people.
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Alzheimer's disease is characterized both by a lower mean level of functional connectivity as well as by diminished fluctuations in the level of synchronization.
Why it matters
This small EEG study found that people with Alzheimer disease had lower average synchronization in some frequency bands and diminished fluctuations of synchronization compared with people with subjective memory complaints. It describes a possible marker of brain network dysfunction, not a treatment, cure, or prevention.
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Although possession of the APOE epsilon4 allele is a risk factor for AD in old age, it does not modify the progression of the disease during the preclinical period.
Why it matters
This population-based study found that although APOE ε4 is a risk factor for Alzheimer disease in old age, it did not modify the rate of cognitive decline during the preclinical period. It is an observational study and does not test any treatment, cure, or prevention.
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Myeloperoxidase, a heme protein expressed by professional phagocytic cells, generates an array of oxidants which are proposed to contribute to tissue damage during inflammation.
Why it matters
This study found that myeloperoxidase, an oxidant-generating enzyme, is present in human brain and increased in Alzheimer's tissue, including in neurons and plaques. It describes a disease-associated change but tests no treatment or prevention.
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Increasing evidence points to synaptic plasticity impairment as one of the first events in Alzheimer's disease (AD).
Why it matters
This study describes the progressive age-related development of Alzheimer-like pathology in APP/PS1 mice, noting conflicting results on synaptic dysfunction in different transgenic models. It is an animal study characterizing a model, not a treatment, cure, or prevention.
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48/100
CSF Abeta42 was significantly lower and CSF total tau and CSF Ptau-181 significantly higher in EAD patients than FTLD patients and control subjects.
Why it matters
This study measured cerebrospinal fluid amyloid beta(1-42), total tau, and tau phosphorylated at threonine-181 to see how well they distinguish early-onset Alzheimer disease from frontotemporal lobar degeneration. It is a diagnostic accuracy study and does not test any treatment, cure, or prevention.
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Alzheimer disease (AD), a progressive neurodegenerative disorder, is the most common cause of dementia in the elderly.
Why it matters
This review discusses how clinical, neuropsychological and imaging assessments, including MRI and CT, can support early and accurate diagnosis of Alzheimer's disease, with coronal MRI useful for documenting atrophy of the hippocampus and entorhinal cortex. It is about diagnosis and does not provide a treatment, cure or prevention.
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Alzheimer's disease (AD) and vascular dementia (VaD) are the two most common forms of dementia.
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When comprehensive assessment procedures are employed, AD can be diagnosed with reasonably high accuracy in very mildly impaired individuals.
Why it matters
This study followed patients with very mild impairment who were diagnosed with Alzheimer's disease, verifying the diagnosis by autopsy or later evaluation. The diagnosis was confirmed in 89% of cases, and neuropsychological measures of delayed recall, verbal fluency and global cognitive status helped distinguish them from normal controls.
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Since the value of scientific evidence generally revolves around probability and chance, it is concluded that the data presented here pose a powerful argument in support of the proposal that AD should be classified as a vascular disorder.
Why it matters
This review argues that sporadic Alzheimer's disease should be classified as a vascular rather than a neurodegenerative disorder, based on evidence such as vascular risk factors reducing cerebral perfusion and cerebral hypoperfusion preceding cognitive decline and neurodegeneration. It concludes that the data pose a powerful argument for this reclassification, but reports no treatment, cure or prevention.
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There has been great interest in the prospects of using single-nucleotide polymorphisms (SNPs) in the search for complex disease genes, and several initiatives devoted to the identification and mapping of SNPs throughout the human genome are currently underway.
Why it matters
This study genotyped 60 single-nucleotide polymorphisms in a 1.5-Mb region around APOE and found association with Alzheimer disease for 7 of 13 SNPs, including the APOE-4 polymorphism. It is a methods-focused genetic study showing that associations can be detected near a complex disease gene, not a treatment or prevention.
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Advanced glycation end products (AGEs) have been implicated in the chronic complications of diabetes mellitus and have been reported to play an important role in the pathogenesis of Alzheimer's disease.
Why it matters
Staining of post-mortem brain tissue found advanced glycation end products (AGEs), protein changes also linked to diabetes complications, together with apolipoprotein E in most amyloid plaques and blood-vessel amyloid in Alzheimer's disease, and mainly inside nerve-cell tangles; about 5% of plaques were AGE-positive but amyloid-beta-negative. Similar patterns appeared in progressive supranuclear palsy, Pick's disease and Guamanian ALS/Parkinsonism-dementia complex. The authors suggest AGEs may contribute to nerve-cell dysfunction and death across these diseases, but this tissue study shows where AGEs are, not that they cause disease, and it tested no treatment.
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Mutations in the presenilin 1 (PS1) and presenilin 2 (PS2) genes increase the production of the highly amyloidogenic 42-residue form of amyloid beta-protein (Abeta42) in a variety of cell lines and transgenic mice.
Why it matters
This cell study found that APP coimmunoprecipitates with presenilin 1 and presenilin 2 proteins in mammalian cells, suggesting an interaction relevant to amyloid-beta 42 production. It is laboratory research and does not test any treatment, cure, or prevention in people.
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beta-amyloid protein (A beta) formation was reconstituted in permeabilized neuroblastoma cells expressing human Alzheimer beta-amyloid precursor protein (beta APP) harboring the Swedish double mutation associated with familial early-onset Alzheimer disease.
Why it matters
In permeabilized neuroblastoma cells, amyloid-beta was generated in the trans-Golgi network even when formation of post-TGN vesicles was inhibited. This is laboratory research and does not test a treatment or cure for Alzheimer's disease.
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Alzheimer disease (AD), the most common cause of dementia in the elderly, exists in both familial and sporadic forms.
Why it matters
This review describes how mutations in the APP, PS1, and PS2 genes can cause familial Alzheimer's disease by raising levels of the Aβ42/43 fragment, and how the APOE ε4 allele increases risk in a dose-dependent manner. It does not report a treatment or cure, but identifies genetic targets and notes that APOE genotyping may be useful as an adjunct to diagnosis and for identifying patient groups for therapeutic intervention.
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Cerebral deposition of the amyloid beta protein (A beta) is an early and invariant feature of Alzheimer disease (AD).
Why it matters
This work indicates that the 42- and 40-amino acid forms of amyloid beta are made by different protease activities, with the 42 form deposited earliest and making up most plaques. It identifies a possible target for interfering with amyloid production but reports no treatment or cure.
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We assessed remote memory in 33 patients with dementia of Alzheimer's type (DAT) with Mini-Mental State Examination (MMSE) scores between 17 and 30, and 30 matched controls using a Famous Faces Test and Famous Names Test designed to assess face recognition, identification and naming, and name recognition and identification, respectively, together with a range of anterograde episodic and semantic memory tests.
Why it matters
This study tested remote memory for famous faces and names in 33 patients with Alzheimer's disease and 30 matched controls. It is about understanding memory loss in the disease, not about treating, curing or preventing it.
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This study evaluated neuronal changes related to Alzheimer's disease using specific immunocytochemical methods (AT8) before the actual formation of neurofibrillary tangles and neuropil threads.
Why it matters
Describes staging of Alzheimer's disease-related neurofibrillary changes in the brain.
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Data available on the relationship between salivary function and specific drug therapy are sparse.
Why it matters
This is a single-patient (N=1) study measuring saliva flow in one person with Alzheimer's disease taking different medications. It found inconsistent effects for thiothixene, no effect for oxazepam, and generally negative effects for diphenhydramine, and says nothing about treating or preventing Alzheimer's itself.
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Senile plaques are polymorphous beta-amyloid protein deposits found in the brain in Alzheimer disease and normal aging.
Why it matters
Amyloid precursor protein-immunoreactive neurites were found in senile plaques, and only a subset of these neurites showed markers of neurofibrillary pathology. This is tissue-based research and does not test a treatment or cure for Alzheimer's disease.
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The turnover and processing of the Alzheimer beta/A4 amyloid precursor protein (beta APP) has been studied in PC12 cells after treatment with agents that regulate protein phosphorylation.
Why it matters
In PC12 cells, a protein kinase C activator (phorbol 12,13-dibutyrate) and a phosphatase inhibitor (okadaic acid) both lowered levels of mature amyloid precursor protein and raised 15- and 19-kDa fragments that "appeared to be COOH-terminal fragments." The kinase inhibitor H-7 "apparently decreased" this processing, which suggests that cell signalling through phosphorylation helps control how the protein is cut. This was a cell-culture experiment with no patients, so it does not show any treatment, cure or prevention for Alzheimer's in people.
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An inhibitor of coagulation factor XIa was purified from serum-free conditioned medium of HepG2 liver cells.
Why it matters
A clotting-factor inhibitor purified from cultured liver cells, and also released by stimulated platelets, turned out to be a shortened form of the Alzheimer's amyloid precursor protein. It contains a protease-inhibitor (Kunitz-type) region and at least part of amyloid beta, and in lab tests heparin made it block factor XIa about 15 times more strongly. This links the protein behind Alzheimer's amyloid to blood clotting. It is lab protein chemistry, not a study of patients, and says nothing about treating or preventing Alzheimer's.
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Speech and language alterations were assessed in 51 patients with Parkinson's disease (PD) and 10 patients with dementia of the Alzheimer type (DAT).
Why it matters
This comparison of 51 Parkinson's disease patients and 10 Alzheimer's disease patients found that Alzheimer's disease produced greater language disturbances while Parkinson's disease produced more motor speech abnormalities. It describes differences in speech and language alterations and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Pivotal trials demonstrated statistically significant but modest average slowing of decline: Clarity AD showed a 0.45-point between-group difference in CDR-SB worsening at 18 months, and TRAILBLAZER-ALZ 2 showed a 3.25-point iADRS difference in the low/medium-tau population at 76 weeks.
Why it matters
This review reports that lecanemab and donanemab substantially reduce amyloid and modestly slow average clinical decline in selected patients, but neither restores lost function. It notes that ARIA-E occurred in 12.6% of lecanemab-treated and 24.0% of donanemab-treated participants, with higher risk in APOE ε4 carriers, and that treatment requires biomarker-guided selection and monitoring.
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47/100
There is a need for early, objective markers of Alzheimer's disease (AD)-related synapse dysfunction in adults with Down syndrome (DS).
Why it matters
In this cross-sectional study of 131 people, serum beta-synuclein was elevated in adults with Down syndrome and is described as an early blood-based marker of synaptic dysfunction. It is a biomarker finding only and does not test any treatment, cure, or prevention.
From across this topic
10 of the 5,172 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.
- Alzheimer's Disease Neuroimaging Initiative (ADNI): clinical characterization
- EEG spectral analysis as a putative early prognostic biomarker in nondemented, amyloid positive subjects
- ER stress and UPR in Alzheimer's disease: mechanisms, pathogenesis, treatments
- Neuropsychiatric symptoms and quality of life in patients with very mild and mild Alzheimer's disease
- Tau conformational changes correspond to impairments of episodic memory in mild cognitive impairment and Alzheimer's disease
- Lecanemab, aducanumab, and donanemab bind the same human Alzheimer disease Aβ aggregates at different epitopes
- CSF multianalyte profile distinguishes Alzheimer and Parkinson diseases
- Novel tau biomarkers phosphorylated at T181, T217 or T231 rise in the initial stages of the preclinical Alzheimer's continuum when only subtle changes in Aβ pathology are detected
- Screening of Alzheimer's disease by facial complexion using artificial intelligence
- Genetic variability in response to amyloid beta deposition influences Alzheimer's disease risk