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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Aberrant cholesterol metabolism has been implicated in Alzheimer disease (AD) and other neurological disorders.
Why it matters
This review describes how oxysterols activate LXR receptors, which regulate cholesterol homeostasis and can induce apoE production and reduce amyloid-beta production. It suggests that targeting cholesterol metabolism pathways may be a potential therapeutic approach, though this is a review of mechanisms rather than a clinical trial.
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Cerebrovascular dysfunction contributes to the cognitive decline and dementia in Alzheimer's disease (AD), and may precede cerebral amyloid angiopathy and brain accumulation of the Alzheimer's neurotoxin, amyloid beta-peptide (Abeta).
Why it matters
This paper reviews the neurovascular hypothesis, which proposes that faulty blood-brain barrier clearance of amyloid beta through LRP1 and RAGE transport may contribute to Alzheimer's disease. It is a review of a hypothesis, not a clinical study, so it does not establish that targeting the blood-brain barrier treats or prevents the disease.
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Identification of preclinical markers is required for early diagnosis of Alzheimer's disease (AD) and cognitive dysfunction in advancing age.
Why it matters
In non-demented relatives of Alzheimer disease patients, carrying the APOE ε4 allele was associated with abnormal EEG patterns during hyperventilation, which the authors suggest may appear decades before symptoms. This is a preliminary physiological finding and does not show that any treatment can delay dementia.
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Neurofibrillary tangle predominant dementia (NFTPD) is a subset of late onset dementia, clinically different from traditional "plaque and tangle" Alzheimer disease (AD): later onset, shorter duration, less severe cognitive impairment, and almost absence of ApoE epsilon4.
Why it matters
Neurofibrillary tangle predominant dementia differs from classical Alzheimer's disease by later onset, shorter duration, milder cognitive impairment, and almost no APOE ε4, with few or no amyloid plaques. However, its tau pathology involving both 3R and 4R tau was not significantly different from classical Alzheimer's disease.
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Alzheimer disease (AD) is the most prominent cause of dementia in the elderly.
Why it matters
Comparing gene expression in the hippocampus of people with mild to moderate dementia against non-demented controls who had high Alzheimer's pathology, this study found increased inflammatory gene changes early in the disease. It is an observational post-mortem study and does not test any treatment, cure or prevention.
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First-degree family history of sporadic Alzheimer disease (AD) and the apolipoprotein E epsilon4 (APOE4) are risk factors for developing AD.
Why it matters
In middle-aged adults, having a first-degree family history of Alzheimer's disease was an important predictor of hippocampal activation during memory encoding and appeared to modify the effect of APOE4. This suggests an unspecified factor in family history influences brain function before symptoms appear.
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No correlation with neuropsychiatric symptoms such as apathy and depression was found.
Why it matters
This study found that behavioral symptoms such as hallucinations, unusual motor behavior, and nighttime behaviors were the strongest predictors of caregiver burden. It suggests that managing these specific symptoms may help reduce the burden on caregivers.
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The decline in mental fitness associated with Alzheimer disease is accompanied by physical changes in the brain, including the development of characteristic plaques and neurofibrillary tangles, but the pathogenesis of those changes is not clear.
Why it matters
This review proposes that activated microglia start an inflammatory cascade, first mediated by interleukin 1, that leads to neuronal death and becomes self-sustaining. It is a proposed explanation of how Alzheimer's disease may progress, not a tested treatment or cure.
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Apolipoprotein (apo) E, a multifunctional protein with central roles in lipid metabolism and neurobiology, has three common isoforms (apoE2, apoE3, and apoE4) with different effects on lipid homeostasis and neurobiology.
Why it matters
This review explains that the apoE4 form of apolipoprotein E is associated with increased risk of Alzheimer's disease, unlike the more common apoE3 form. It states that the mechanisms behind apoE4's effects are still poorly understood, so no treatment is yet based on this.
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Alzheimer's disease (AD) is a late-onset dementia that is characterized by the loss of memory and an impairment of multiple cognitive functions.
Why it matters
This paper reviews evidence from cell and animal models that amyloid beta and other amyloid precursor protein derivatives enter mitochondria, generate free radicals, and cause oxidative damage in Alzheimer's disease. It is a review of laboratory findings, not a clinical trial, so it does not show that any treatment targeting these processes works in patients.
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This study examined the functionality of the medial temporal lobe (MTL) and posterior cingulate (PC) in mild cognitive impairment amnestic type (MCI), a syndrome that puts patients at greater risk for developing Alzheimer disease (AD).
Why it matters
In 14 people with amnestic mild cognitive impairment, functional MRI showed less activity in the posterior cingulate during recognition and in the right hippocampus during encoding compared with controls, despite similar task performance. This is a small imaging study of brain function and does not test any treatment, cure, or prevention.
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Showa University Karasuyama Hospital, Tokyo, Japan.
Why it matters
This study of 436 elderly subjects examined whether lower serum insulin-like growth factor-1 levels were a risk factor for Alzheimer's disease and vascular dementia, finding MMSE scores positively correlated with serum IGF-1. This describes an association between IGF-1 levels and cognition, but it does not show that altering IGF-1 treats or prevents dementia.
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45/100
Clinicians should be aware of the high rates of anxiety as well as depressive symptoms in family caregivers of people with AD, especially in female caregivers.
Why it matters
About a quarter of family caregivers scored at or above the level for anxiety and about a tenth for depression. Care-recipient daily living impairment, living with the care recipient, being female, a poorer relationship, and poor caregiver health predicted anxiety, while irritability, poor health, and a poorer relationship predicted depression.
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Depression is a frequent condition in Alzheimer's disease (AD).
Why it matters
This study compared four scales for detecting depression in people with Alzheimer's disease. It is about measuring depression, not about treating, curing or preventing Alzheimer's disease.
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Controversy persists regarding whether Alzheimer's disease (AD) is a distinct entity or instead exists on a continuum with nondemented aging.
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Alzheimer disease (AD) involves glial inflammation associated with amyloid plaques.
Why it matters
This review presents evidence that microglia act mainly by phagocytosing amyloid plaques rather than forming them, and discusses why they associate with certain plaque types. It is a mechanistic review and does not report any treatment, cure or prevention for Alzheimer's disease.
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Nosologically, Alzheimer disease is not a single disorder in spite of a common clinical phenotype.
Why it matters
This review states that about 5% or less of Alzheimer's disease cases are due to mutations in three genes, while 95% or more are sporadic with old age as the main risk factor, and it discusses disturbances in neuronal insulin signal transduction. It offers an explanation of disease types but does not report a treatment, cure, or prevention.
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The association of neurofibrillary tangles with delayed verbal recall may reflect associated hippocampal atrophy.
Why it matters
This study using Nun Study autopsy data found that hippocampal volume was strongly associated with delayed verbal recall performance about a year before death, and it remained significant even when neuropathologic measures were considered together. It helps explain how brain structure relates to memory, but it does not test a treatment, cure, or prevention.
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Sporadic, late-onset Alzheimer disease (AD) constitutes the most frequent cause of dementia in the elderly population.
Why it matters
This study examined how two kinds of blood vessel damage, cerebral amyloid angiopathy and arteriosclerosis/lipohyalinosis, relate to cognitive decline in people with Alzheimer's disease. It does not test any treatment or show how to cure or prevent Alzheimer's disease.
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The antemortem diagnosis of Alzheimer disease (AD) requires time-consuming and costly procedures.
Why it matters
This study looked at whether combining two cerebrospinal fluid markers, phosphorylated tau protein and beta-amyloid peptide42, could improve diagnosis of Alzheimer disease compared with using single markers alone. It is a diagnostic study, so it does not test any treatment, cure, or prevention.
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We examined the associations of postmortem neocortical immunoreactivities for microglia, astrocytes, Abeta and Tau with cognitive changes in clinically characterized subjects with pathological diagnoses (CERAD classification) of definite AD (9), possible AD (15) and age-matched controls (11).
Why it matters
This study examined postmortem brain tissue from people with definite Alzheimer's disease, possible Alzheimer's disease and controls, finding that amyloid deposits appear early but cannot account for cognitive decline, while microglia and astrocyte immunoreactivity increased in different groups. It is a tissue study describing associations and does not test any treatment, cure or prevention.
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45/100
Over the past several years, experiments with synthetic amyloid-beta peptide (Abeta) and animal models have strongly suggested that pathogenesis of Alzheimer's disease (AD) involves soluble assemblies of Abeta peptides (Trends Neurosci. 24 (2001) 219).
Why it matters
This paper proposes that soluble amyloid-beta assemblies called ADDLs, rather than insoluble fibrillar deposits, may drive Alzheimer's pathology and could serve as targets for vaccines and drugs. The evidence comes from synthetic peptide experiments and animal models, so it is early laboratory work and not yet a proven treatment.
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AD changes are frequently present in brains of demented PD patients.
Why it matters
This study assessed the impact of coexisting Alzheimer pathology on the natural history of Parkinson's disease. It examines how pathology affects disease course and does not test a treatment, cure, or prevention.
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45/100
Doubly transgenic mice expressing both a mutated amyloid precursor protein and a mutated presenilin-1 protein accumulate A(beta) deposits as they age.
Why it matters
In doubly transgenic mice, amyloid deposits formed with age, starting as fibrillar compact plaques and later spreading as nonfibrillar deposits. This describes disease-like changes in an animal model and does not show any treatment or prevention.
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Postmortem demonstration of increased expression of biologically active S100B in Alzheimer's disease (AD) and its relation to progression of neuropathological changes across the cortical regions suggests involvement of this astrocytic cytokine in the pathophysiology of AD.
Why it matters
This study measured S100B levels in cerebrospinal fluid from 68 Alzheimer's patients and 25 healthy older people to test whether the protein relates to symptom progression. It is biomarker research, not evidence about treating, curing or preventing the disease.
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.
- Mechanisms behind the neuroprotective actions of cholinesterase inhibitors in Alzheimer disease
- Studies in aging of the brain: IV. Familial Alzheimer disease: Relation to transmissible dementia, aneuploidy, and microtubular defects
- Geographic disparities in mortality from Alzheimer's disease and related dementias
- Cholinergic plasticity in hippocampus of individuals with mild cognitive impairment: correlation with Alzheimer's neuropathology
- Apolipoprotein E epsilon 4 and the pattern of regional brain atrophy in Alzheimer's disease
- The neuropsychological profile of Alzheimer disease
- Alzheimer risk associated with a copy number variation in the complement receptor 1 increasing C3b/C4b binding sites
- Predicting clinical decline and conversion to Alzheimer's disease or dementia using novel Elecsys Aβ(1-42), pTau and tTau CSF immunoassays
- Neuropsychological test performance in African-American and white patients with Alzheimer's disease
- Acetylcholinesterase and its inhibition in Alzheimer disease