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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Arterial spin labeling (ASL) magnetic resonance imaging uses arterial blood water as an endogenous tracer to measure cerebral blood flow (CBF).
Why it matters
This review discusses arterial spin labeling MRI as a way to measure cerebral blood flow in normal aging, mild cognitive impairment, Alzheimer's disease, and other dementias. It describes the technique as promising for early detection, monitoring progression, and differential diagnosis, but does not report any treatment, cure, or prevention.
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A growing body of literature has suggested that obstructive sleep apnea (OSA) and habitual short sleep duration are linked to poor cognitive function.
Why it matters
This study tested whether sleep apnea and short sleep duration are linked to changes in brain structure seen on MRI scans years later. It involved a relatively small number of participants, so the results are preliminary and do not show that treating sleep problems prevents dementia.
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Although the two pathological hallmarks of Alzheimer's disease (AD), senile plaques composed of amyloid-β (Aβ) peptides and neurofibrillary tangles (NFTs) consisting of hyperphosphorylated tau, have been studied extensively in postmortem AD and relevant animal and cellular models, the pathogenesis of AD remains unknown, particularly in the early stages of the disease where therapies presumably would be most effective.
Why it matters
This review describes how amyloid plaques and neurofibrillary tangles are present in varying degrees before and throughout dementia progression, and notes that cognitive decline correlates better with tangles than plaques, and even better with synaptic loss. It summarizes research into the early stages where therapies would presumably be most effective, but presents no treatment or cure.
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Late-onset dementia is a major health concern in the ageing population.
Why it matters
This review proposes that chronic cerebral hypoperfusion caused by ageing and cardiovascular conditions may initiate the neurodegenerative process in late-onset Alzheimer's disease. It is a review of a proposed mechanism and does not provide a treatment, cure, or prevention.
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Alzheimer's disease (AD) is the most common form of dementia affecting elderly people.
Why it matters
This review describes evidence that Alzheimer's disease may involve brain insulin resistance, and that restoring insulin signaling, such as by intranasal insulin, could have therapeutic potential. It is a review of current knowledge, not a trial, so it does not yet show that any insulin-based treatment works in patients.
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Neuroplasticity involves molecular and structural changes in central nervous system (CNS) throughout life.
Why it matters
This review discusses findings that the hippocampus is capable of neural plasticity during mild cognitive impairment and early Alzheimer's disease, with remodeling acting as a compensatory mechanism to maintain brain function. It describes a possible compensatory process but does not report any treatment, cure, or prevention.
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Cerebral amyloid angiopathy (CAA) involves cerebrovascular amyloid deposition and is classified into several types according to the amyloid protein involved.
Why it matters
This 2015 review explains that cerebral amyloid angiopathy (CAA), where amyloid builds up in the brain's blood vessels, is most commonly found in older people and in people with Alzheimer's disease, and is linked to bleeding in the brain, stroke-like damage, dementia and inflammatory brain disease. It says sensitive MRI scans can detect tiny cortical bleeds and surface iron deposits (cortical superficial siderosis), which it reports are closely associated with transient focal neurological episodes. Amyloid PET scans can detect CAA but, as the review notes, cannot tell amyloid in blood vessels apart from amyloid plaques in brain tissue.
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Missense mutations in alanine 673 of the amyloid precursor protein (APP), which corresponds to the second alanine of the amyloid β (Aβ) sequence, have dramatic impact on the risk for Alzheimer disease; A2V is causative, and A2T is protective.
Why it matters
In human APP-overexpressing primary neurons, the protective A2T mutation decreased amyloid-beta production while the causative A2V mutation increased it, and the mutations changed aggregation properties. This is laboratory work on disease mechanism and does not test a treatment or prevention.
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Individuals with Down's syndrome (DS) develop early Alzheimer's disease (AD) with β-amyloid (Aβ) plaque pathology.
Why it matters
This study evaluated whether cerebrospinal fluid biomarkers for amyloidosis, axonal degeneration, microglial activation, and sleep regulation were altered in young and old patients with Down's syndrome. It is an observational study of markers in Down's syndrome, not a treatment, cure, or prevention for Alzheimer's disease.
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Perturbed Endoplasmic Reticulum (ER) calcium (Ca2+) homeostasis emerges as a central player in Alzheimer disease (AD).
Why it matters
This review describes altered expression and function of ryanodine receptors in Alzheimer's-affected brains, in cells with familial mutations, and in transgenic mouse models, linking them to amyloid production, neuronal death, synaptic function and memory. It is a summary of findings across models and reports no treatment, cure or prevention.
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Intervention and treatment in Alzheimer's disease dementia (AD-dementia) can be cost effective but the majority of patients are not diagnosed in a timely manner.
Why it matters
This UK health-economic modelling study asked how much the timing of treatment changes its cost-effectiveness in Alzheimer's disease. Using published data on cognitive decline in the years before diagnosis, it modelled hypothetical symptomatic and disease-modifying treatments, assuming early and standard treatment work equally well but that early treatment could start up to eight years before standard diagnosis. It is a model, not a trial. No real drug or patient was tested, so it does not show that earlier diagnosis or treatment prevents, slows or cures the disease.
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Alzheimer's disease (AD) is a complex and heterogeneous neurodegenerative disorder, classified as either early onset (under 65 years of age), or late onset (over 65 years of age).
Why it matters
This review describes genes involved in early-onset Alzheimer's (APP, PSEN1, PSEN2) and risk factors for late-onset disease including APOE E4 and genes from genome-wide association studies. It summarizes genetic knowledge and does not report a treatment or cure.
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The limited effectiveness of current therapies against Alzheimer's disease (AD) highlights the need for intensifying research efforts devoted to developing new agents for preventing or retarding the disease process.
Why it matters
Targeting the endogenous cannabinoid system has emerged as a potential therapeutic approach to treat Alzheimer's disease. Several findings indicate that activation of both CB1 and CB2 receptors by natural or synthetic agonists may be relevant, but this is presented as a potential approach rather than an established treatment.
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The salience network (SN) serves to identify salient stimuli and to switch between the central executive network (CEN) and the default-mode network (DMN), both of which are impaired in Alzheimer's disease (AD)/amnestic mild cognitive impairment (aMCI).
Why it matters
This study found structural and functional changes in the salience network in normal aging and in people with amnestic MCI and Alzheimer's disease. It describes brain changes associated with the disease but does not test any treatment or prevention.
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The prevention of Alzheimer's disease (AD) has become a real challenge due to its rising prevalence and the lack of an effective cure.
Why it matters
This review found that observational studies point to a protective role for certain nutrients such as omega-3 fatty acids, antioxidants and B vitamins, and for dietary patterns such as the Mediterranean diet. However, randomized controlled trials do not show a consistent effect, so no dietary factor can be recommended as protective against Alzheimer's disease.
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The structural brain network of patients showed reduced local efficiency compared to controls.
Why it matters
Patients with early Alzheimer's disease showed reduced local efficiency in their structural brain networks compared to controls, and worse memory and executive function related to these network changes. This adds information about how brain connectivity relates to cognitive symptoms, but it does not test any treatment or prevention.
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There is a great deal of evidence suggesting an important role for systemic inflammation in the pathogenesis of Alzheimer's disease.
Why it matters
This review states that systemic inflammation is generally considered a contributor to Alzheimer's disease rather than a cause, though emerging evidence suggests its role may predate amyloid deposition. It notes that therapies aimed at reducing inflammation in people with mild cognitive impairment and Alzheimer's disease have been disappointing, and it does not report any treatment or cure.
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The specific CB2 cannabinoid receptor agonist JWH-133 induced cognitive improvement in double AβPP/PS1 transgenic mice, a genetic model of Alzheimer's disease.
Why it matters
This study in AβPP/PS1 transgenic mice found that the CB2 cannabinoid receptor agonist JWH-133 improved cognition, with a more pronounced effect when given at the pre-symptomatic stage. Because it was done in mice, it is early and does not establish a treatment, cure, or prevention for people.
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APOE alleles ε2, ε3, and ε4 account for essentially all the inherited risk of AD associated with this region.
Why it matters
This large genetic analysis found that APOE alleles ε2, ε3, and ε4 account for essentially all the inherited risk of Alzheimer disease associated with this chromosome region. Other variants tested, including a poly-T track in TOMM40, were not independent risk or age-at-onset loci.
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46/100
Cigarette smoking has been proposed as a major risk factor for aging-related pathological changes and Alzheimer's disease (AD).
Why it matters
Male rats exposed to 4% cigarette smoke for one hour daily for eight weeks showed increased oxidative stress in the hippocampus and pre-Alzheimer-like neuropathology. This is animal research on smoking as a risk factor and does not provide a treatment, cure or prevention.
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Since the description by Alois Alzheimer, more than 50 years have passed during which senile dementia and pre-senile dementia have been considered Alzheimer disease (AD) on the basis of their common neuropathological and clinical manifestations.
Why it matters
This paper proposes that Alzheimer's is an age-related neurodegenerative process that affects most people by age 65 but leads to dementia in only a small percentage at that age. It is a conceptual proposal about disease definitions and does not test any treatment, cure, or prevention.
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Growing evidence supports the concept that AD is fundamentally a metabolic disease that results in progressive impairment in the brain's capacity to utilize glucose and respond to insulin and insulin-like growth factor (IGF) stimulation.
Why it matters
This paper proposes that Alzheimer's disease involves brain insulin resistance and deficiency, and that this may drive amyloid accumulation in a feedback loop. It suggests this could explain why anti-amyloid monotherapy trials have been disappointing, but it does not report a treatment or cure.
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46/100
The neurotoxic potential of the Aβ peptide results from its biochemical properties that favor aggregation into insoluble oligomers and protofibrils.
Why it matters
This paper describes how the Aβ peptide's tendency to clump into insoluble oligomers and protofibrils may drive nerve damage, and it outlines three phases of Alzheimer's disease from a pre-symptomatic stage through to dementia. It is a descriptive overview rather than a trial of any treatment, so it does not show that any therapy can prevent or cure the disease.
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We describe 56 novel autosomal dominant early-onset Alzheimer disease (ADEOAD) families with PSEN1, PSEN2, and AβPP mutations or duplications, raising the total of families with mutations on known genes to 111 (74 PSEN1, 8 PSEN2, 16 AβPP, and 13 AβPP duplications) in the French series.
Why it matters
This study describes families with autosomal dominant early-onset Alzheimer's disease and their genetic mutations and cerebrospinal fluid biomarker profiles. It is a descriptive genetic study and does not report any treatment, cure, or prevention for Alzheimer's disease.
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Alzheimer's disease (AD) is a fast growing world-wide epidemic.
Why it matters
This review states that there is a complete lack of disease-modifying or preventive therapy that may delay onset or substantially affect the pathophysiology of Alzheimer's disease. It describes the challenges and burden of the disease but reports no 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.
- In vivo tau PET imaging in dementia: Pathophysiology, radiotracer quantification, and a systematic review of clinical findings
- The Alzheimer's disease neuroimaging initiative (ADNI): MRI methods
- Neuroimaging markers of dementia across race/ethnicity and sex/gender using an intersectional approach within the HABS‐HD cohort
- Anxiety of Alzheimer's disease: prevalence, and comorbidity
- Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease
- Acupuncture for patients with mild to moderate Alzheimer's disease: a randomized controlled trial
- Mutant genes in familial Alzheimer's disease and transgenic models
- Myelin dysfunction drives amyloid-β deposition in models of Alzheimer's disease
- Astrocytes: implications for neuroinflammatory pathogenesis of Alzheimer's disease
- Use of medical foods and nutritional approaches in the treatment of Alzheimer's disease