Endogenous Alu RNAs form double-stranded RNAs recognized by double-stranded RNA sensors and activate IRF and NF-kB transcriptional paths and innate immunity. Deamination of adenosines to inosines by the ADAR family of enzymes, a process termed A-to-I editing, disrupts double-stranded RNA structure and prevents innate immune activation. Innate immune activation is observed in Alzheimer's disease, the most common form of dementia. We have previously reported loss of A-to-I editing in hippocampus vasculature, but no change in cortex or cortex vasculature, associated with Alzheimer's disease.

Understanding the sequential progression of cognitive decline in autosomal dominant Alzheimer's disease (ADAD) in the Latino population is crucial for enhancing early identification for targeted interventions. Given the tablet-based administration and increasing frequency of use in epidemiological research, validating this progression within the NIH Toolbox cognitive battery (NIHTB-CB) is important.

Mild cognitive impairment (MCI) represents a stage between cognitively normal and Alzheimer's disease. Despite much published research on MCI, there continues to be a knowledge gap of volumetric brain changes in MCI versus cognitively normal (CN) in racially diverse, community-based samples.

SPI1, a transcription factor implicated in myeloid cell development, has emerged as a genetic risk factor for Alzheimer's disease (AD). Recent in vivo studies reveal that knockdown in mice exacerbates AD pathology by increasing amyloid-β aggregation and gliosis while overexpression ameliorates these features. Transcriptomic analyses suggest that regulates microglial immune response, complement activation, and phagocytosis. SPI1 regulation of these processes may explain how SPI1 affects AD risk. Further studies, including human validation, are needed to explore the dynamic influence of SPI1 across AD stages, its applicability to clinical settings, and its potential as a therapeutic target.

Sodium-glucose cotransporter 2 (SGLT2) inhibitors is a novel category of medications for diabetes, exhibiting neuroprotective potential. However, evidence regarding whether the use of SGLT2 inhibitors effectively reduces the risk of Alzheimer's disease (AD) remains unclear.

Survival after an Alzheimer's disease (AD) diagnosis is vital for patients, their families, caregivers, and healthcare providers. Hawaii, known for its diverse ethnic population, exhibits significant racial health disparities.

Our previous studies have established that the broad-spectrum anti-epileptic drug lamotrigine (LTG) confers protection against cognitive impairments, synapse and nerve cell damage, as well as characteristic neuropathologies in APP/PS1 mice, a mouse model of Alzheimer's disease (AD). However, the precise molecular mechanisms responsible for this protective effect induced by LTG remain largely elusive.

This study evaluated the diagnostic performance of plasma biomarkers for Alzheimer's disease (AD) using an automated platform. In a cohort of 74 consecutive patients, plasma p-Tau181 levels were significantly higher in AD compared to non-AD groups and showed correlation with cerebrospinal fluid biomarkers. Plasma p-Tau181 demonstrated high diagnostic accuracy for AD, with an area under the curve of 0.854. The findings suggest that plasma biomarkers, particularly p-Tau181, could improve the accessibility and efficiency of AD diagnostics in clinical settings, offering a less invasive and cost-effective alternative to traditional methods.

The VA Million Veteran Program (MVP) is a nationwide initiative that seeks to examine how genes influence health and behaviors in military veterans. An article by Merritt et al. analyzing data from the MVP, developing and testing algorithms to query dementia and Alzheimer's disease (AD) diagnoses from the VA's electronic health record system and examining genetic factors, provides an extraordinarily important contribution to the dementia and AD fields. The analyses presented in the article show how large databases can be used to further understand dementia and AD, pointing the way for many more important advances for this field.

Dance or rhythmic movement-based training has demonstrated significant efficacy in addressing a range of motor and cognitive deficits associated with neurodegenerative diseases like Parkinson's and Alzheimer's diseases. Leveraging both human and non-human animal behavioral and neurobiological evidence, I hypothesize a possible untapped role of dance training in mitigating impairments in the motor control of speech, a complex sensorimotor behavior affected in these conditions. Here, this hypothesis is supported by an in-depth examination of motor speech deficits in Parkinson's and Alzheimer's diseases, at a behavioral, physiological, and neural level. Additionally, literature on the impact of dance training on behaviors and brain pathways possibly relevant to speech motor control in populations with neurodegenerative diseases is thoroughly reviewed. Synthesizing these findings, I propose repurposing dance as a novel treatment for motor speech deficits and outline specific experiments to test this hypothesis. By comprehensively investigating the full spectrum of the effects of a motor-based training, i.e., dance, on often overlooked motor-based behaviors, such as speech, we may uncover novel therapeutic avenues of a practice that has already shown promising implications.

Little is known about the utilization of outpatient support services by people with mild cognitive impairment (MCI).

Alzheimer's disease (AD) is an irreversible age-related neurodegenerative condition characterized by the deposition of amyloid-β (Aβ) peptides and neurofibrillary tangles. Di Huang Yi Zhi (DHYZ) formula, a traditional Chinese herbal compound comprising several prescriptions, demonstrates properties that improve cognitive abilities in clinical. Nonetheless, its molecular mechanisms on treating AD through improving neuron cells mitochondria function have not been deeply investigated.

The prevalence of Alzheimer's disease or dementia in the elderly population has been increasing both nationally and globally. Males and females are impacted differently when it comes to cognitive health, and this can be influenced by various risk factors.

Cognivue is an FDA-cleared computerized cognitive test to screen for cognitive impairment included in the Bio-Hermes Study to test blood-based and digital biomarkers' ability to screen for mild cognitive impairment (MCI) and Alzheimer's disease (AD). A subset of cognitively normal individuals have amyloid deposition (Preclinical AD) but no current assessment can identify these individuals in the absence of expensive biomarkers.

Although the association between dementia such as Alzheimer's disease and traumatic brain injury (TBI) is well established, there are significant knowledge gaps with respect to the perspective of dementia and epilepsy without TBI. We aimed to investigate the relationship between dementia and epilepsy in a population-based study of patients without history of TBI. This study included a random sample of 30,715 patients with no history of TBI, including 6143 with epilepsy as the study cohort and 24,572 without epilepsy as the comparison cohort. Stratified Cox proportional hazard regression was used to calculate the adjusted hazard ratio (HR), with 95% confidence interval, for the risk of developing dementia in the two cohorts. Patients with epilepsy but no history of TBI had increased risk of dementia (adjusted HR = 1.84). For patients aged 55-64 years, the adjusted HR for dementia was 4.5-fold higher among females in the study cohort than among males. Additionally, this study revealed that risk of dementia among above 75-year population lowest than other age subgroups (adjusted HR = 1.45). The study demonstrated an association between dementia and epilepsy in the patients who had no history of TBI. The effect was pronounced in patients aged 55-64 years, especially in the female population, suggesting that epilepsy needs to be more intensively prevented and controlled in this age group.

The introduction of therapeutics for Alzheimer's disease has led to increased interest in precisely quantifying amyloid-β (Aβ) burden for diagnosis, treatment monitoring, and further clinical research. Recent positron emission tomography (PET) hardware innovations including digital detectors have led to superior resolution and sensitivity, improving quantitative accuracy. However, the effect of PET scanner on Centiloid remains relatively unexplored and is assumed to be minimized by harmonizing PET resolutions.

Subjective cognitive decline (SCD) is the early predementia syndrome. that occurs even before the development of objective cognitive decline. SCD plus refers to an additional set of criteria that increases the likelihood of developing mild cognitive impairment and further progressing to Alzheimer's disease (AD). Studying the progression of SCD-plus participants will help in understanding the importance of diagnosing this condition at an early stage and delaying its onset.

Declining physical functionality is an indicator of cognitive impairment, distinguishing normal cognition (NC) from dementia. Whether this extends to pre-dementia stages is unclear.

Some studies have suggested that glaucoma may be associated with neurodegeneration and a higher risk of dementia.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder that predominantly affects elderly individuals across the globe. While genetic, environmental, and lifestyle factors are known to influence the onset of AD, the underlying mechanisms remain unclear.