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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This article presents a wavelet coherence investigation of electroencephalograph (EEG) readings acquired from patients with Alzheimer disease (AD) and healthy controls.
Why it matters
Wavelet coherence analysis of EEG signals showed statistically significant differences between Alzheimer's disease patients and controls, with decreased coherence in temporocentral regions in the delta band and in parietal and central regions in the theta and alpha bands. This method can differentiate between healthy controls and Alzheimer's disease patients by studying cortical connectivity.
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Lithium salts have a well-established role in the treatment of major affective disorders.
Why it matters
This review discusses evidence that lithium may have neuroprotective effects, and notes one placebo-controlled trial in amnestic mild cognitive impairment where long-term lithium may have slowed progression of cognitive and functional deficits. The authors suggest lithium may have disease-modifying effects, but this is presented as a possibility rather than established.
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Aging and early-stage Alzheimer disease (AD) have been shown to be associated with increased RT intraindividual variability (IIV, as reflected by the coefficient of variation) and an exaggeration of the slow tail of the reaction time (RT) distribution in attentional control tasks, based on ex-Gaussian analyses.
Why it matters
In cognitively normal and early-stage Alzheimer's disease individuals, larger cerebral and regional white matter volumes were associated with less reaction time intraindividual variability and less slowing in the tail of the reaction time distribution. These results support a role of white matter integrity in reaction time variability and distributional skewing, consistent with breakdowns in executive control processes.
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The biggest risk factor for Alzheimer's disease is the process of ageing, but the mechanisms that lead to the manifestation of the disease remain to be elucidated.
Why it matters
This review explores how the metal ions iron, copper and zinc may interact with amyloid-beta peptides in Alzheimer's disease. It discusses possible mechanisms but reports no treatment or cure.
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Alzheimer's disease (AD) is a highly disabling progressive neurodegenerative disorder characterized by a steadily growing number of patients, by the absence of a cure for the disease and by great difficulties in diagnosing in the preclinical phase.
Why it matters
This review of antioxidant trials in MCI and Alzheimer's disease found conflicting results and no substantial clinical benefit, though the data were hard to compare. It does not support the routine use of antioxidants and calls for more research, including on vascular damage.
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42/100
Imaging of brain β-amyloid plaques with (18)F-labeled tracers for PET will likely be available in clinical practice to assist the diagnosis of Alzheimer disease (AD).
Why it matters
Imaging of brain β-amyloid plaques with 18F-labeled tracers for PET will likely become available in clinical practice to assist in diagnosing Alzheimer's disease. Physicians reading these scans will need to understand the complex relationship between amyloid and cognitive decline and how to recognize tracer binding patterns.
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Clinical criteria for the diagnosis of Alzheimer's disease include insidious onset and progressive impairment of memory and other cognitive functions.
Why it matters
This report presents clinical criteria for the diagnosis of Alzheimer's disease, including insidious onset and progressive impairment of memory and other cognitive functions. It is a diagnostic criteria paper and does not directly address treating, curing, or preventing Alzheimer's disease.
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There is not a specific test to diagnose Alzheimer's disease (AD).
Why it matters
This study used a machine learning method on EEG recordings to distinguish people with Alzheimer's disease from normal individuals, reaching about 80% accuracy on epochs and 87% accuracy per patient. It is a diagnostic aid, not a treatment, cure or prevention.
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42/100
Enolase enzymes are abundantly expressed, cytosolic carbon-oxygen lyases known for their role in glucose metabolism.
Why it matters
This paper discusses how the enzyme enolase is oxidatively modified and up-regulated in amnestic mild cognitive impairment and Alzheimer's disease, and that it has regulatory functions beyond glucose metabolism. It states it is unclear whether the hypometabolic environment is a consequence of or contributes to Alzheimer's disease pathology, so no treatment or prevention is established.
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The field of aging and dementia research is advancing rapidly toward the stage of earlier identification of clinical symptoms.
Why it matters
This review discusses MCI as an intermediate state between normal aging and Alzheimer's disease and notes that it may already be too late for the earliest identification. It focuses on earlier diagnosis and trial design, not on treating or curing the disease.
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Cholesterol and docosahexenoic acid (DHA) may affect degenerative processes in Alzheimer's Disease (AD) by influencing Abeta metabolism indirectly via the vasculature.
Why it matters
In a mouse model of Alzheimer-like pathology, a DHA-enriched diet improved spatial memory and reduced amyloid deposits, while a Western-style diet reduced cerebral blood volume. These are animal findings and do not establish that such diets affect Alzheimer disease in people.
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Astrocyte pathology occurs in association with Alzheimer's disease (AD) and in brain ageing, but is poorly characterised.
Why it matters
This study found that Alzheimer-type pathology only partly explains differences in astrocyte markers, so other factors likely contribute to these cell changes. It does not test any treatment, so it offers no direct path to treating, curing or preventing Alzheimer's disease.
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Alzheimer's disease is the most common form of dementia in the elderly.
Why it matters
This review argues that Alzheimer disease is likely caused by a combination of diet, lifestyle, vascular, genetic, and amyloid-related factors rather than one sole mechanism. It suggests that diet and lifestyle changes might reduce risk, but this is a hypothesis and not proof that any specific intervention prevents the disease.
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Alzheimer disease is a common age-related neurodegenerative disease characterized pathologically by senile plaques, neurofibrillary tangles, synaptic disruption, and progressive neuronal deficits.
Why it matters
This review summarizes findings of oxidatively modified proteins in the brains of people with Alzheimer's disease and mild cognitive impairment. It discusses possible mechanisms in disease progression but reports no treatment or prevention results.
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Alzheimer disease (AD) includes inflammatory processes in the senile plaques and surrounding glia, with increased expression of acute phase proteins such as C-reactive protein (CRP) and IL-6.
Why it matters
This position paper notes that blood levels of CRP and IL-6 are associated with higher risk of Alzheimer's disease and cognitive decline during aging, linking systemic inflammation to the disease. It also discusses the hypothesis that the APOE4 allele may have been maintained in human populations because it once conferred advantages in fighting infections.
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42/100
Proteolytic processing and phosphorylation of amyloid precursor protein (APP), and hyperphosphorylation of tau protein, have been shown to be increased in Alzheimer's disease (AD) brains, leading to increased production of beta-amyloid (Abeta) peptides and neurofibrillary tangles, respectively.
Why it matters
This review discusses the protein Pin1, which is co-localized with phosphorylated tau in Alzheimer's disease brain and shows an inverse relationship to tau expression. It notes that Pin1 protects neurons under in vitro conditions and is oxidatively modified with reduced activity in the hippocampus in mild cognitive impairment and Alzheimer's disease.
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The transition from normal aging to mild cognitive impairment to Alzheimer disease (AD) is often indistinct.
Why it matters
This study examined the regional distribution of Alzheimer's disease pathology in brain donors who were cognitively intact, mildly impaired, or demented. It is a pathological study of 41 brain donors that describes where pathology appears but does not test any treatment, cure, or prevention.
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All cells rely on efficient protein synthesis in order to maintain cellular homeostasis.
Why it matters
In brain tissue from people with mild cognitive impairment and Alzheimer's, this study found less ribosomal RNA and more RNA oxidation inside the ribosome, suggesting these changes may contribute to reduced protein synthesis. The work is based on tissue samples and does not test any treatment or show cause and effect.
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We investigated whether previously reported differences between Alzheimer's disease and dementia with Lewy bodies (DLB) in resting occipital activity lead to activation differences within functionally specialized visual cortical areas and deactivation differences in the default network.
Why it matters
Using fMRI tasks, this small study found differences in brain activity between Alzheimer disease and dementia with Lewy bodies, but many differences could be explained by behavioural performance. It concerns using cognitive fMRI to detect differences between dementias, not treating, curing or preventing Alzheimer's disease.
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Alzheimer's disease (AD) and normal pressure hydrocephalus (NPH) are common forms of dementia in the elderly.
Why it matters
This study measured BDNF concentrations in serum and cerebrospinal fluid in 27 Alzheimer's disease patients, 9 patients with normal pressure hydrocephalus and 28 age-matched healthy controls, finding a significant decrease of BDNF. It only examines a possible marker of the disease and does not test any treatment, cure or prevention.
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Familial Danish dementia is an early onset autosomal dominant neurodegenerative disorder linked to a genetic defect in the BRI2 gene and clinically characterized by dementia and ataxia.
Why it matters
In familial Danish dementia brain tissue, two amyloid proteins, ADan and beta-amyloid, were found together without compact plaques, and a specific interaction between them was shown in vitro. This is a biochemical study of a rare disorder and does not test treatment for Alzheimer's disease.
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Mild cognitive impairment is considered to be a transitional stage between normal aging and dementia.
Why it matters
In 16 patients with mild cognitive impairment, higher cerebrospinal fluid phosphorylated tau was associated with a pattern of reduced brain glucose metabolism typical of Alzheimer disease on PET imaging. This is a small study of diagnostic markers, not a test of any treatment or cure.
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Until recently, the only established function of acetylcholinesterase (AChE) was the termination of cholinergic neurotransmission.
Why it matters
This review states that acetylcholinesterase inhibitors were a rational approach for treating symptoms caused by cholinergic imbalances in Alzheimer's disease. It also notes that acetylcholinesterase and the cholinergic system may have broader effects in the disease, including pathways that promote nonamyloidogenic amyloid precursor protein processing and decrease tau phosphorylation.
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The construct of psychosis of dementia was validated, and the severity of both psychosis and aggressiveness was reduced with risperidone treatment in a robust and dose-related way, with a continuing response over the 12-week trial period.
Why it matters
In this subgroup analysis, risperidone at 1 mg or 2 mg per day reduced psychosis and aggressiveness symptoms compared with placebo in patients with psychosis of dementia. This concerns treating behavioral symptoms of Alzheimer's disease, not curing or preventing it.
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Several recent studies indicate that activity of cholinergic enzymes in the cortex of people with mild cognitive impairment (MCI) and early Alzheimer's disease (AD) are preserved.
Why it matters
In brain tissue from the Religious Order Study, people with mild cognitive impairment had *higher*, not lower, activity of the hippocampal enzyme that makes acetylcholine (ChAT), but only at the intermediate "limbic" (Braak III/IV) stage of Alzheimer's pathology. The rise was gone in mild Alzheimer's and ChAT was markedly depleted in severe cases. The authors hypothesise that the rise is a compensatory response to lost entorhinal input, and that memory loss in MCI "more likely relates to disrupted entorhinal-hippocampal connectivity" than to a cholinergic deficit. No treatment was tested.
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.
- Better stress coping associated with lower tau in amyloid-positive cognitively unimpaired older adults
- Predicting clinical scores from magnetic resonance scans in Alzheimer's disease
- Genome-wide meta-analysis identifies new loci and functional pathways influencing Alzheimer’s disease risk
- A Novel Ensemble-Based Machine Learning Algorithm to Predict the Conversion From Mild Cognitive Impairment to Alzheimer's Disease Using Socio-Demographic Characteristics, Clinical Information, and Neuropsychological Measures
- Biomarkers for Alzheimer's disease and mild cognitive impairment: Recent advances in task-based EEG
- Resting bold fMRI differentiates dementia with Lewy bodies vs Alzheimer disease
- Correlations between kynurenines in plasma and CSF, and their relation to markers of Alzheimer's disease pathology
- Alismatis Rhizoma prevents AβO-induced neuronal cell death and synaptic loss in Alzheimer’s disease models
- The Microbiota-Gut-Brain Axis and Alzheimer's Disease: Neuroinflammation Is to Blame?
- Endo-lysosomal and autophagic dysfunction: a driving factor in Alzheimer's disease?