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.
-
Immune cells of myeloid lineage are encountered in the Alzheimer's disease (AD) brain, where they cluster around amyloid-β plaques.
Why it matters
In two mouse models of amyloid buildup, replacing the brain's resident immune cells with peripheral monocytes did not change amyloid deposition. This indicates that this type of immune cell replacement does not reduce amyloid plaques, at least in these animal models.
-
Amyloid precursor protein (APP) metabolites (amyloid-β (Aβ) peptides) and Tau are the main components of senile plaques and neurofibrillary tangles, the two histopathological hallmarks of Alzheimer disease.
Why it matters
This review discusses how APP metabolites and Tau reach the nucleus and may control protein expression at the transcriptional level. It describes possible nuclear roles and reports no treatment, cure or prevention for Alzheimer's disease.
-
Cerebral small vessel disease is common in elderly persons.
Why it matters
This population-based study investigated whether cerebral small vessel disease is related to disturbed sleep and 24-hour activity rhythms. It does not show that treating small vessel disease or sleep problems prevents or treats Alzheimer's disease.
-
Apolipoprotein E (APOE) is a lipid-transport protein abundantly expressed in most neurons in the central nervous system.
Why it matters
This review describes how apolipoprotein E binds amyloid-beta and regulates its aggregation and clearance, and how different APOE isoforms influence brain lipid transport, glucose metabolism, neuronal signaling, neuroinflammation, and mitochondrial function. It suggests that targeting APOE may be a potential approach for diagnosis, risk assessment, prevention, and treatment, but no treatment is tested here.
-
Factors unrelated to aging may drive an increase in deposition during early Alzheimer's disease pathogenesis.
Why it matters
In 68 nondemented adults with Down syndrome, PET imaging showed age-related amyloid-beta deposition, but the correlation with age stopped being significant once elevated cortical retention appeared. This is an imaging study that suggests factors unrelated to aging may drive deposition in early Alzheimer's disease, and it tests no treatment.
-
Global obesity is a pandemic status, estimated to affect over 2 billion people, that has resulted in an enormous strain on healthcare systems worldwide.
Why it matters
In mice, a high-fat diet starting at weaning produced memory deficits independent of beta-amyloid, along with effects on brain insulin regulation and mitochondria. This is animal research, so it cannot yet show what these findings mean for treating or preventing Alzheimer's disease in people.
-
The logopenic variant of primary progressive aphasia (lvPPA) has been associated with Alzheimer disease, although this relationship is still subject to debate.
Why it matters
Among 16 patients with logopenic primary progressive aphasia, 11 were amyloid-positive, and the amyloid-negative patients showed a different pattern of brain metabolism. This supports using amyloid PET to identify which of these patients have Alzheimer's-related pathology, but it does not test any treatment, cure or prevention.
-
Mutations of the glucocerebrosidase (GBA) gene are the most important risk factor yet discovered for Parkinson disease (PD).
Why it matters
This review reports that GBA mutations in homozygous or heterozygous form are associated with an approximately 20-fold increase in Parkinson disease risk, and that GBA-associated Parkinson disease is clinically indistinguishable from idiopathic Parkinson disease except for slightly earlier onset and more frequent cognitive impairment. It describes mechanisms including reduced enzyme activity and mutant protein trapped in the endoplasmic reticulum leading to impaired lysosomal function.
-
The dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) gene is located within the Down Syndrome (DS) critical region on chromosome 21 and is implicated in the generation of Tau and amyloid pathologies that are associated with the early onset Alzheimer's Disease (AD) observed in DS.
Why it matters
A new compound, EHT 5372, blocks the DYRK1A enzyme and reduces tau phosphorylation and amyloid beta production in laboratory cell and biochemical assays. These are in vitro results only, and the authors say the compound and its class need testing in living animals before any therapy for Alzheimer's disease can be considered.
-
In the healthy adult brain synapses are continuously remodelled through a process of elimination and formation known as structural plasticity.
-
The TREM2 variant is associated with: (i) AD (odds ratio: 4.76; P = .014); (ii) increased density of amyloid plaques and neurofibrillary tangles in multiple brain regions; (iii) increased TREM2 (P = .041) and TYROBP (P = .006) gene expression; (iv) decreased TREM2 protein levels (P = .016); and (v) upregulation of proinflammatory cytokines (regulated on activation, norma
Why it matters
The TREM2 R47H variant was associated with higher odds of Alzheimer's dementia, more amyloid plaques and neurofibrillary tangles, and signs of increased inflammation in brain tissue. This links the variant to more severe disease features, but it is an association study and does not test any treatment.
-
Triggering receptor expressed by myeloid cells 2 (TREM2), a member of the immunoglobulin superfamily, has anti-inflammatory phagocytic function in myeloid cells.
Why it matters
This study measured TREM2 protein in post-mortem temporal cortex samples from people with Alzheimer's disease and from people without it, and reports that changes in TREM2 protein correlate with Alzheimer's brain pathology. The stored summary does not say which way TREM2 changed or how many brains were studied. The link between a TREM2 gene variant and Alzheimer's risk comes from earlier studies, not this one. It is a correlation in tissue from people who had died, so it cannot show cause and does not test any treatment.
-
Accumulation of oxidative damage is a common feature of neurodegeneration that, together with mitochondrial dysfunction, point to the fact that reactive oxygen species are major contributors to loss of neuronal homoeostasis and cell death.
Why it matters
This review describes how redox proteomics has identified oxidatively modified proteins in both Down's syndrome and Alzheimer's disease, pointing to shared impaired pathways. It offers no treatment or cure, only a way to better understand the overlapping mechanisms that lead from normal aging to Alzheimer's disease.
-
Similar to Alzheimer's disease (AD), dementia with Lewy bodies (DLB) is characterized by a profound degeneration of cortically-projecting cholinergic neurons of the basal forebrain (BF) and associated depletion of cortical cholinergic activity.
Why it matters
This imaging study compared atrophy of the cholinergic basal forebrain in dementia with Lewy bodies and Alzheimer's disease dementia against healthy controls. It is about describing brain changes in these dementias, not about treating, curing or preventing Alzheimer's disease.
-
High level of homocysteine (Hcy) is a recognized risk factor for developing Alzheimer disease (AD).
Why it matters
In 3xTg mice, diet-induced high homocysteine worsened amyloid pathology, tau pathology and cognitive deficit. This is animal work on a risk factor and does not show that lowering homocysteine treats or prevents Alzheimer's disease in people.
-
Disrupted cholesterol homeostasis has been reported in Alzheimer disease and is thought to contribute to disease progression by promoting amyloid β (Aβ) accumulation.
Why it matters
This study shows that endoplasmic reticulum stress triggered by amyloid beta promotes cholesterol synthesis and mitochondrial cholesterol influx, resulting in mitochondrial glutathione depletion in older age amyloid precursor protein mice. It is mechanistic work in a mouse model and does not show that targeting this process treats, cures or prevents Alzheimer's disease in people.
-
Down syndrome (DS) is the most frequent genetic cause of intellectual disability characterized by the presence of three copies of chromosome 21 (Chr21).
Why it matters
In frontal cortex tissue, this study found hyperactivation of the PI3K/Akt/mTOR axis in people with Down syndrome, with and without Alzheimer pathology, along with decreased autophagy and inhibition of IRS1 and GSK3β. It suggests a mechanism that may operate early in the development of Alzheimer disease in Down syndrome but tests no treatment.
-
Alzheimer's disease (AD) is the most common type of dementia.
Why it matters
This study in Alzheimer's disease transgenic mice found that fisetin modulated p25 and inflammatory pathways and maintained cognitive function. Because it was done in mice, it is early and does not establish a treatment, cure, or prevention for people.
-
We have recently shown acetylation of tau at lysine residue 280 (AC-K280) to be a disease-specific modification in Alzheimer disease (AD), corticobasal degeneration, and progressive supranuclear palsy, likely representing a major regulatory tau modification.
Why it matters
This brain tissue study found acetylated tau at lysine 280 in several diseases including familial Alzheimer's disease, suggesting it is a shared tau change. It describes pathology only and does not test any treatment, cure, or prevention.
-
In 3T MRI visually inspected by experts, quantification of hippocampal volume and signal can increase the detection of hippocampal sclerosis in 28% of patients with mesial temporal lobe epilepsy.
-
Review of clinical and biological features of primary progressive aphasia (PPA).
Why it matters
This lecture review describes primary progressive aphasia as arising when the language-dominant hemisphere becomes the principal target of neurodegeneration, with subtypes linked to different underlying pathologies. It notes that Alzheimer disease appears to have biological variants with distinct patterns of lesion distribution and perhaps molecular background.
-
Gangliosides are the main glycolipids of neuronal plasma membranes.
Why it matters
This paper is about gangliosides and inherited ganglioside storage diseases such as GM1- and GM2-gangliosidoses, not Alzheimer's disease. It reports no treatment, cure or prevention for Alzheimer's disease.
-
45/100
For 20 years the amyloid cascade hypothesis of Alzheimer disease (AD) has placed the amyloid-β peptide (Aβ), formed from the amyloid precursor protein (APP), centre stage in the process of neurodegeneration.
Why it matters
This review points out that no new therapeutic agents have reached the clinic through the amyloid cascade hypothesis, and that APP metabolites including beta-amyloid have distinct physiological functions, with the intracellular domain regulating several genes. It is a discussion of the complexity of APP biology rather than a report of a working treatment.
-
Over the past decade, public awareness of the long-term pathological consequences of traumatic brain injury (TBI) has increased.
Why it matters
This review discusses the pathogenesis and biomarkers of acute and chronic traumatic encephalopathies, including chronic traumatic encephalopathy marked by features such as dementia. It is a review of a condition linked to repetitive traumatic brain injury and does not test a treatment, cure, or prevention for Alzheimer's disease.
-
Accumulation of amyloid-β (Aβ), believed to be a key trigger of Alzheimer disease (AD), could result from impaired clearance mechanisms.
Why it matters
The cysteine protease cathepsin B was shown to degrade amyloid-beta in mice expressing human amyloid precursor protein, and reducing cystatin C expression lowered amyloid-beta levels by enhancing this degradation. This is mouse research, and the authors note that most Alzheimer patients do not carry the mutations studied, so it does not establish a treatment for people.
From across this topic
10 of the 4,748 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.
- Herpes Viruses in the Baltimore Longitudinal Study of Aging: Associations With Brain Volumes, Cognitive Performance, and Plasma Biomarkers
- Baseline and longitudinal increases in diastolic blood pressure are associated with greater white matter hyperintensity volume: the northern Manhattan study
- The spectrum of neurodevelopmental, neuromuscular and neurodegenerative disorders due to defective autophagy
- Neuronal and glial coexpression of argininosuccinate synthetase and inducible nitric oxide synthase in Alzheimer disease
- RETRACTED: Revolutionizing medical imaging: A cutting-edge AI framework with vision transformers and perceiver IO for multi-disease diagnosis
- Plasma glial fibrillary acidic protein is raised in progranulin-associated frontotemporal dementia
- Glia and their cytokines in progression of neurodegeneration
- Using positron emission tomography and Carbon 11-labeled Pittsburgh Compound B to image Brain Fibrillar β-amyloid in adults with down syndrome: safety, acceptability, and feasibility
- Liver–metabolic stress, apolipoprotein E ε4, and cognition and amyloid burden: findings from the dementia platform Korea trial-ready registry
- Visualization of Aβ42(43) and Aβ40 in senile plaques with end-specific Aβ monoclonals: Evidence that an initially deposited species is Aβ42(43)