The latest medical research on Geriatric Medicine

The research magnet gathers the latest research from around the web, based on your specialty area. Below you will find a sample of some of the most recent articles from reputable medical journals about geriatric medicine gathered by our medical AI research bot.

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Which MCI Patients Should be Included in Prodromal Alzheimer Disease Clinical Trials?

Alzheimer Disease and Associated Disorders

Prodromal Alzheimer disease (AD) clinical trials enroll patients with mild cognitive impairment (MCI) meeting biomarker criteria, but specific enrollment criteria vary among trials.

We used data from AD Neuroimaging Initiative (ADNI) MCI participants to assess AD biomarker eligibility, variation in trial outcome measures, and statistical power.

Most (65%) participants meet eligibility criteria based on low cerebrospinal fluid amyloid beta (Aβ). Relative to trials enrolling exclusively based on low cerebrospinal fluid Aβ, trials including participants with a high ratio of phosphorylated tau to Aβ would include an additional 15% of participants. Fewer (34% to 62%) participants met criteria for Aβ and tau. Differences in clinical and demographic characteristics of modeled trial samples were minimal. Those with low Aβ and high tau showed the greatest change over time on outcome measures.

Eligibility rates for prodromal trials vary depending on the specific biomarker criteria, though differences in demographics and the variation associated with outcome measures are minimal. Broadening inclusion criteria beyond amyloid alone may facilitate recruitment but include patients showing slower progression over time. Biomarker criteria selection should be informed by the goal of enrolling individuals most likely to utilize and benefit from the intervention under investigation in a particular setting.

Cognitive Complaints in Nondemented Parkinson's Disease Patients and Their Close Contacts do not Predict Worse Cognitive Outcome.

Alzheimer Disease and Associated Disorders

The main purpose of this study was to investigate 4 methods of eliciting subjective cognitive complaints (SCCs) in Parkinson's disease (PD) patients without dementia and determine the relationship between their SCC and cognitive performance.

SCCs were elicited through a modified Neurobehavioral Inventory administered to patients and close contacts, a general complaint question, and Movement Disorders Society Unified Parkinson's Disease Rating Scale item question 1.1 administered to patients. Clinical evaluation, formal neuropsychological testing and Disability Assessment for Dementia were conducted in Ontario state. Agreement between SCCs eliciting methods was calculated. Associations between SCC, cognitive testing, and mild cognitive impairment (MCI) were assessed.

Of 139 participating nondemented PD patients, 42% had PD-MCI at baseline. Agreement between SCC eliciting methods was low. Neither patient-reported nor close contact-reported SCCs were associated with impaired baseline cognitive testing or PD-MCI nor were they associated with cognitive decline over time. In PD patients with normal baseline cognition, 26% of patients with 1-year follow-up and 20% of patients with 2-year follow-up met MCI criteria.

Agreement between SCC eliciting methods is poor and no SCC method was associated with cognitive testing or decline over time. With no clear superior method for eliciting SCCs, clinicians should consider performing regular screening.

Women and Men Presenting to a Rural and Remote Memory Clinic in Saskatchewan, Canada Show Similar Cognitive Findings for Dementia.

Alzheimer Disease and Associated Disorders

The course of dementia may differ between men and women. Men, for example, are more likely to exhibit aggression. It is unclear if sex differences are present at initial presentation. The present study examines sex differences among patients at initial referral to a memory clinic.

Three hundred seventy-five (159 males, 216 females) patients referred to the University of Saskatchewan's Rural and Remote Memory Clinic participated. Data were collected from patients and caregivers at initial assessment. Cognitive, functional, and demographic information were compared between males and females.

Males and females presented to the clinic at similar ages. Females were more likely to have a son or daughter caregiver and to live alone. Males were more likely to be currently working. No statistically significant differences were found for cognitive or functional assessment scores.

Within this rural and remote sample, there was equivalence between male and female level of cognitive decline, function and neuropsychiatric symptoms at initial referral. Both sexes were of similar ages at the time of initial presentation. These findings may provide reassurance to patients and their family members as it does not appear that patients of one sex were referred later than the other.

Awareness in Dementia: Development and Evaluation of a Short Version of the Assessment Scale of Psychosocial Impact of the Diagnosis of Dementia (ASPIDD-s) in Brazil.

Alzheimer Disease and Associated Disorders

Awareness of disease is defined as the recognition of changes caused by the deficits related to the disease process. We aimed to examine the psycho...

Phenocopy syndrome of behavioral variant frontotemporal dementia: a systematic review.

Journal Alzheimers Research Therapy

The phenocopy syndrome of behavioral variant of frontotemporal dementia (phFTD) refers to patients presenting with neuropsychiatric symptoms mimicking the behavioral variant frontotemporal dementia (bvFTD), but lacking frontotemporal atrophy/hypometabolism on neuroimaging and not evolving to dementia during the follow-up. It is important to recognize phFTD for clinical and research purposes.

The aim of this study was to perform a systematic review of the available literature on phFTD taking into account its clinical, cognitive, imaging, genetic, and pathological features.

We searched for the following terms in two electronic databases (PubMed and Scopus): "frontotemporal dementia and slowly progressive," "frontotemporal dementia and phenocopy," "frontotemporal dementia and non-progressive," "frontotemporal dementia and benign progression," and "frontotemporal dementia and benign." We did not include review articles. Papers had to be written in English, French, Portuguese, or Spanish. Overall, 235 studies were retrieved in the initial search. A total of 31 studies composed the final selection, comprising 292 patients. Patients with phFTD are predominantly male and have no major cognitive deficits, with globally preserved executive functions and episodic memory. Some cases (n = 7) of slowly progressive FTD have been associated with C9orf72 genetic expansion. There are only four reports of phFTD neuropathological data, with two patients with no neurodegenerative findings and two with frontotemporal lobar degeneration with ubiquitin-positive inclusions.

The neurobiological underpinnings of phFTD remain unknown. It is controversial whether phFTD belongs to the FTD spectrum. Studies with biomarkers and pathological data are needed to solve the phFTD conundrum.

Systemic and CNS inflammation crosstalk: implications for Alzheimer's Disease.

Current Alzheimer Research

After years of failed therapeutic attempts targeting beta-amyloid (Aβ) in AD, there is now increasing evidence suggesting that inflammation holds a...

Characterization of Serum Exosomes from a Transgenic Mouse Model of Alzheimer's Disease.

Current Alzheimer Research

Alzheimer's disease (AD) is the most common type of dementia characterized by amyloid plaques containing amyloid beta (Aβ) peptides and neurofibrillary tangles containing tau protein. In addition to neuronal loss, cerebral amyloid angiopathy (CAA) commonly occurs in AD. CAA is characterized by Aβ deposition in brain microvessels. Recent studies have suggested that exosomes (cell-derived vesicles containing a diverse cargo) may be involved in the pathogenesis of AD.

Isolate and characterize brain-derived exosomes from a transgenic mouse model of AD that presents CAA.

Exosomes were isolated from serum obtained from 13-month-old wild type and AD transgenic female mice using an exosome precipitation solution. Characterization of exosomal proteins was performed by western blots and dot blots.

Serum exosomes were increased in transgenic mice compared to wild types as determined by increased levels of the exosome markers flotillin and alix. High levels of neuronal markers were found in exosomes, without difference between the 2 groups. Markers for endothelial-derived exosomes were decreased in the transgenic model, while astrocytic-derived exosomes were increased. Exosome characterization showed increased levels of oligomeric Aβ and oligomeric and monomeric forms tau on the transgenic animals. Levels of amyloid precursor protein were also increased. In addition, pathological and phosphorylated forms of tau were detected, but no difference was observed between groups.

These data suggest that monomeric and oligomeric forms Aβ and tau are secreted into serum via brain exosomes, most likely derived from astrocytes in the transgenic mouse model of AD with CAA. Studies on the implication of this event in the propagation of AD are underway.

In silico evaluation of acetylation mimics in the 27 lysine residues of human tau protein.

Current Alzheimer Research

Various neurodegenerative diseases, including Alzheimer's disease (AD), are related to abnormal hyper-phosphorylated microtubule-associated protein tau accumulation in brain lesions. Recent studies have focused on toxicity caused by another post-translational modification (PTM), acetylation of the lysine (K) residues of tau protein. Because there are numerous acetylation sites, several studies have introduced mimics of tau acetylation using amino acid substitutions from lysine to glutamine (Q). However, human tau protein contains over 20 acetylation sites; thus, investigation of the effects of acetylated tau is difficult.

Here, we in silico evaluated acetylation effects using SIFT, PolyPhen-2 and PROVEAN which can estimate the effects of amino acid substitutions based on the sequence homology or protein structure in tau isoforms. In addition, we also investigated 27 acetylation effects on amyloid formation of tau protein using Waltz.

15 acetylation mimics were estimated to be most detrimental, which indicates that there may be novel pathogenic acetylation sites in human tau protein. Interestingly, deleterious effect of acetylation mimics was different according to type of isoforms. Furthermore, all acetylation mimics were predicted to be region of amyloid formation at the codons 274-279 of human tau protein. Notably, acetylation mimic of codon 311 (K311Q) induced formation of additional amyloid region located on codons 306-311 of human tau protein.

To the best of our knowledge, this is the first simultaneous in-silico evaluation of the acetylation state of 27 human tau protein residues.

Strategies for the Recruitment and Retention of Racial/Ethnic Minorities in Alzheimer Disease and Dementia Clinical Research.

Current Alzheimer Research

Racial/ethnic minorities have among the highest risks for Alzheimer disease and dementia, but remain underrepresented in clinical research studies.

To synthesize the current evidence on strategies to recruit and retain racial/ethnic minorities in Alzheimer disease and dementia clinical research.

We conducted a systematic review by searching CINAHL, EMBASE, MEDLINE, PsycINFO, and Scopus. We included studies that met four criteria: (1) included a racial/ethnic minority group (African American, Latino, Asian, American Indian or Alaska Native, and Native Hawaiian or Other Pacific Islander); (2) implemented a recruitment or retention strategy for Alzheimer disease or dementia clinical research; (3) conducted within the U.S.; and (4) published in a peer-reviewed journal.

Of the 19 included studies, 14 (73.7%) implemented recruitment strategies and 5 (26.3%) implemented both recruitment and retention strategies. Fifteen studies (78.9%) focused on African Americans, two (10.6%) on both African Americans and Latinos, and two (10.5%) on Asians. All articles were rated weak in study quality. Four major themes were identified for recruitment strategies: community outreach (94.7%), advertisement (57.9%), collaboration with health care providers (42.1%), and referral (21.1%). Three major themes were identified for retention strategies: follow-up communication (15.8%), maintain community relationship (15.8%), and convenience (10.5%).

Our findings highlight several promising recruitment and retention strategies investigators should prioritize when allocating limited resources, however, additional well-designed studies are needed. By recruiting and retaining more racial/ethnic minorities in Alzheimer disease and dementia research, investigators may better understand the heterogeneity of disease progression among marginalized groups. PROSPERO registration #CRD42018081979.

Therapeutic strategies targeting amyloid-β in Alzheimer's disease.

Current Alzheimer Research

Alzheimer's disease (AD) is a neurodegenerative disorder linked to protein misfolding and aggregation. AD is pathologically characterized by senile...

Retinoic acid and the gut microbiota in Alzheimer's disease: fighting back-to-back?

Current Alzheimer Research

There is growing evidence that the gut microbiota may play an important role in neurodegenerative diseases such as Alzheimer's disease. However, how these commensals influence disease risk and progression still has to be deciphered.

The objective of this review was to summarize current knowledge on the interplay between gut microbiota and retinoic acid. The latter one represents one of the important micronutrients, which have been correlated to Alzheimer's disease and used in initial therapeutic intervention studies.

A selective overview of the literature is given with the focus on function of retinoic acid in the healthy and diseased brain, its metabolism in the gut, and the potential influence that the bioactive ligand may have on microbiota, gut physiology and Alzheimer's disease.

Retinoic acid can influence neuronal functionality by means of plasticity but also by neurogenesis and modulating proteostasis. Impaired retinoid-signaling therefore might contribute to development of diseases in the brain. Despite its rather direct impact, retinoic acid also influences other organ systems such as gut by regulating the residing immune cells but also factors such as permeability or commensal microbiota. These in turn can also interfere with retinoid-metabolism and via the gut-brain-axis furthermore with Alzheimer's disease pathology within the brain.

Potentially, it is yet too early to conclude from the few reports on changed microbiota in Alzheimer's disease to a dysfunctional role in retinoid-signaling. However, there are several routes how microbial commensals might affect and might be affected by vitamin A and its derivatives.

Does intraneuronal accumulation of carboxyl terminal fragments of the amyloid precursor protein trigger early neurotoxicity in Alzheimer's disease?

Current Alzheimer Research

Alzheimer's disease (AD) is associated with extracellular accumulation and aggregation of amyloid β (Aβ) peptides ultimately seeding in senile plaques. Recent data show that their direct precursor C99 (βCTF) also accumulates in AD-affected brain as well as in AD-like mouse models. C99 is consistently detected much earlier than Aβ, suggesting that this metabolite could be an early contributor to AD pathology. C99 accumulates principally within endolysosomal and autophagic structures and its accumulation was described as both a consequence and one of the causes of endolysosomal-autophagic pathology, the occurrence of which has been documented as an early defect in AD. C99 was also accompanied with C99-derived C83 (αCTF) accumulation occurring within the same intracellular organelles. Both these CTFs were found to dimerize leading to the generation of higher molecular weight CTFs, which were immunohistochemically characterized in situ by means of aggregate-specific antibodies. Here, we discuss studies demonstrating a direct link between the accumulation of C99 and C99-derived APP-CTFs and early neurotoxicity. We discuss the role of C99 in endosomal-lysosomal-autophagic dysfunction, neuroinflammation, early brain network alterations and synaptic dysfunction as well as in memory-related behavioral alterations, in triple transgenic mice as well as in newly developed AD animal models.

This review summarizes current evidence suggesting a potential role of the β-secretase- derived APP C-terminal fragment C99 in Alzheimer's disease etiology.