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 5,209 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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Clinical and neuropathological overlap between Alzheimer's (AD) and Parkinson's disease (PD) is now well recognized.
Why it matters
This work links glial activation and overexpression of the inflammatory molecule interleukin-1 to the brain changes seen in people with both Alzheimer's disease and Lewy body disease. It suggests shared inflammatory mechanisms between the two conditions, but it does not report a treatment that alters the course of either disease.
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Alzheimer's disease (AD) is characterized by cognitive decline and loss of neurons in specific brain regions.
Why it matters
This small pilot study measured BDNF levels in serum and cerebrospinal fluid in 30 patients at different stages of Alzheimer's disease compared with 10 non-demented controls. It only looked at a possible marker of the disease and did not test any treatment, cure or prevention.
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Previous studies show increased levels of lipid peroxidation and neurotoxic by-products of lipid peroxidation including 4-hydroxynonenal (HNE) and acrolein in vulnerable regions of the Alzheimer's disease (AD) brain.
Why it matters
Levels of the lipid peroxidation markers HNE and acrolein were significantly increased in several brain regions of people with mild cognitive impairment compared with age-matched controls. This suggests lipid peroxidation occurs early in the disease process, but it does not test any treatment, cure, or prevention.
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A valid quantitative imaging method for the measurement of amyloid deposition in humans could improve Alzheimer's disease (AD) diagnosis and antiamyloid therapy assessment.
Why it matters
Tested quantitative PET imaging with Pittsburgh Compound-B (PIB), an amyloid-binding tracer, in five people with Alzheimer's disease, five with mild cognitive impairment, and five controls. Retention was greater in Alzheimer's cortical areas than in controls, people with mild cognitive impairment looked either 'AD-like' or 'control-like', and the authors found the Logan analysis method stable and valid.
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Transgenic mice made by crossing animals expressing mutant amyloid precursor protein (APPswe) to mutant presenilin 1 (PS1dE9) allow for incremental increases in Abeta42 production and provide a model of Alzheimer-type amyloidosis.
Why it matters
This study found episodic-like memory deficits in APPswe/PS1dE9 mice and related them to amyloid deposition and neurotransmitter abnormalities. It is an animal study describing a model of Alzheimer-type amyloidosis, not a treatment, cure, or prevention.
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Biomarkers to assist in the diagnosis and medical management of Alzheimer disease (AD) are a pressing need.
Why it matters
Using a proteomic method, this study quantified relative protein changes in cerebrospinal fluid from Alzheimer's patients and age-matched controls and found differences of 20% or more in over half of the proteins measured. It is biomarker discovery work and reports no treatment, cure or prevention.
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The most visible and, until very recently, the only hypothesis regarding the involvement of microglial cells in Alzheimer's disease (AD) pathogenesis is centered around the notion that activated microglia are neurotoxin-producing immune effector cells actively involved in causing the neurodegeneration that is the cause for AD dementia.
Why it matters
This review critically examines the evidence for the idea that detrimental neuroinflammation drives Alzheimer's disease and points out weaknesses in that hypothesis. It also considers an alternative microglial dysfunction hypothesis, but does not establish a treatment or cure.
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Amyloid plaques appear early during Alzheimer's disease (AD), and their development is intimately linked to activated astrocytes and microglia.
Why it matters
This paper describes how activated astrocytes and microglia appear to contribute to the formation and evolution of amyloid plaques. It is a mechanistic, tissue-based discussion that highlights possible therapeutic targets, but no treatment was tested in patients.
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The introduction of acetylcholine esterase (AChE) inhibitors as a symptomatic treatment of Alzheimer's disease (AD) has made patients seek medical advice at an earlier stage of the disease.
Why it matters
This review found that cerebrospinal fluid biomarkers such as total tau, phospho-tau, and beta-amyloid can help tell Alzheimer's disease apart from several other conditions. It also noted that some other candidate biomarkers have shown interesting results but have been studied much less.
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This EEG study investigates the role of the cholinergic system, cortico-cortical connections, and sub-cortical white matter on the relationship between individual EEG frequencies and their relative power bands.
Why it matters
This EEG study examined individual EEG frequencies and band power in mild Alzheimer's disease, vascular dementia, and normal elderly subjects. It is a physiological comparison study, not a treatment, cure, or prevention study.
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Alzheimer's disease (AD) includes etiologically heterogeneous disorders characterized by senile or presenile dementia, extracellular amyloid protein aggregations containing an insoluble amyloid precursor protein derivative, and intracytoplasmic tau protein aggregations.
Why it matters
This paper proposes a 'mitochondrial cascade hypothesis' for late-onset sporadic Alzheimer's disease, citing excess neuronal aneuploidy, programmed cell death and mitochondrial dysfunction, and noting that the amyloid cascade hypothesis does not specify what initiates the common sporadic form. It is a proposed hypothesis and reports no treatment, cure or prevention.
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We conducted a quantitative investigation of brain arterial atherosclerotic damage and its relationship to sporadic Alzheimer's disease (AD).
Why it matters
In this autopsy study, Alzheimer's disease cases had significantly more severe atherosclerosis of the circle of Willis arteries than age-matched controls, suggesting atherosclerosis-induced reduced brain blood flow contributes to the disease. The authors describe this as a risk factor association and report no treatment or cure.
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The diagnosis of Alzheimer's disease (AD), the most common form of dementia in the general population, usually relies upon the presence of typical clinical features and structural changes on brain magnetic resonance imaging.
Why it matters
Using a protein-chip method, the study found five spinal fluid polypeptides that differed significantly between Alzheimer's patients and healthy controls, and the combination classified six of nine Alzheimer's patients. This is an early biomarker study with a very small number of patients, and it does not test any treatment, cure, or prevention.
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Protein kinase B (PKB) is an important intermediate in the phosphatidylinositol-3 kinase signaling cascade that acts to phosphorylate glycogen synthase kinase-3 (GSK-3) at its serine 9 residue, thereby inactivating it.
Why it matters
In brain tissue from people at different stages of Alzheimer's tangle pathology, the amount of the active form of protein kinase B (p-Thr308) rose in step with tangle stage as measured by AT8 staining and Braak's criteria. It appeared especially in the neurons that are known to go on to form tangles. This is a laboratory tissue study that shows an association, not cause, and it does not test any treatment or prevention.
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Alzheimer's disease (AD) and prion disease are characterized neuropathologically by extracellular deposits of Abeta and PrP amyloid fibrils, respectively.
Why it matters
This work reports that amyloid deposits in Alzheimer's disease and prion disease are accompanied by inflammation-related proteins and activated microglia, suggesting a locally induced chronic inflammatory response. It describes an association in tissue and does not show that reducing this inflammation treats or prevents the disease.
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46/100
The prefrontal cortex (PFC) is a heterogeneous cortical structure that supports higher cognitive functions, including working memory and verbal abilities.
Why it matters
This volumetric MRI study examined whether any region within the prefrontal cortex is more vulnerable to deterioration with late aging or Alzheimer's disease. It is descriptive imaging research and does not test a treatment, cure, or prevention.
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Both patient groups performed equally poorly on tests of episodic and semantic memory with the exception of immediate and delayed story recall, which was worse in the AD group.
Why it matters
In this small study, people with dementia with Lewy bodies had more trouble with perception, attention and working memory than people with Alzheimer's disease, while both groups did similarly poorly on memory tests. This is about distinguishing the two dementias, not about treating or preventing either one.
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Alzheimer disease (AD)-like neuropathology increases progressively during aging in most primates, and, in some species, is concurrent with reproductive decline in females and cognitive impairments.
Why it matters
This paper hypothesizes that the uniquely human APOE ε3 allele evolved from the ε4 allele of primate ancestors in relation to increasing brain size and the emergence of grandmothering. It proposes that the schedule of Alzheimer's-like neurodegeneration had to slow so that parental caregivers would not become impaired.
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There is equal efficacy and safety between Hup in capsule and tablet for treating patients with AD, and Hup can reduce the pathological changes of the oxygen free radicals in the plasma and erythrocytes of patients with AD.
Why it matters
This small trial compared huperzine-A capsules with tablets in 60 patients with Alzheimer's disease and found equal efficacy and safety between the two forms. It does not show that huperzine-A cures or prevents Alzheimer's disease.
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All mutations known to cause familial Alzheimer's disease (AD) act by increasing the levels of soluble beta-amyloid peptide (A beta), especially the longer form, A beta42.
Why it matters
In this study, cerebrospinal fluid Aβ42 was strongly elevated in early and mid stages of sporadic Alzheimer's disease and then declined with disease progression, and it was also higher in people with cognitive impairment and in a depression reference group than in healthy controls. This describes how a biomarker changes over the disease course and does not test any treatment, cure, or prevention.
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Alzheimer's disease results from severe cytoskeletal alterations in only a few neuronal types within the human central nervous system.
Why it matters
This review describes how neurofibrillary tangles and neuropil threads spread in a predictable sequence through the brain in Alzheimer's disease. It is a descriptive pathology paper and does not report any treatment, cure or prevention.
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Lesions in such chronic neurodegenerative disorders as Alzheimer disease (AD), Parkinson disease, the parkinsonism dementia complex of Guam, and amyotrophic lateral sclerosis have associated with them a variety of proteins known to be involved in inflammatory processes.
Why it matters
This review describes inflammatory proteins in Alzheimer's disease lesions and suggests inflammatory reactions contribute to neuronal loss. It is based on postmortem tissue and cultured cells, and does not establish a treatment or cure.
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In this study increased carer burden was related independently to increased levels of patient behaviour disturbance and decreased levels of informal social support.
Why it matters
In 50 Alzheimer patients and their carers, patient behavior disturbance and lower informal social support independently predicted greater carer burden, while patient cognitive and functional status did not. It concerns caregiver burden and offers no treatment, cure or prevention for Alzheimer's disease.
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Recent studies indicate that impairments in two cognitive domains characterize the cognitive abnormalities that appear earliest in the course of Alzheimer disease (AD).
Why it matters
This paper describes preliminary evidence that memory and executive function tests, along with APOE-4 status and brain imaging, may help identify which people with early cognitive changes will progress to Alzheimer's disease. It concerns prognostic markers and does not offer a treatment or cure.
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46/100
Little information exists on the performance of black versus white patients with Alzheimer's disease on neuropsychological tests for dementia.
Why it matters
This study found that Black and white patients with Alzheimer's disease performed differently on some neuropsychological tests, with Black patients scoring lower on visual naming, constructional praxis, and the Mini-Mental State Examination. It suggests cultural or experiential differences may affect test performance 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.
- Is there evidence for cognitive intervention in Alzheimer disease? A systematic review of efficacy, feasibility, and cost-effectiveness
- Diagnostic performance and prediction of clinical progression of plasma phospho-tau181 in the Alzheimer’s Disease Neuroimaging Initiative
- Structural MRI–based Computer-aided Diagnosis Models for Alzheimer Disease: Insights into Misclassifications and Diagnostic Limitations
- β-Amyloid-Dependent and -Independent Genetic Pathways Regulating CSF Tau Biomarkers in Alzheimer Disease
- The cortical origin and initial spread of medial temporal tauopathy in Alzheimer's disease assessed with positron emission tomography
- ABCA7 frameshift deletion associated with Alzheimer disease in African Americans
- Plasma biomarkers for prediction of Alzheimer's disease neuropathologic change
- Identifying incipient dementia individuals using machine learning and amyloid imaging
- Research criteria for the diagnosis of Alzheimer's disease: revising the NINCDS-ADRDA criteria
- T1 mapping in Alzheimer’s disease: a quantitative MRI study with amyloid-PET correlation