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ol to identify individuals at particularly high risk for future cognitive decline.The oldest-old, those 85 years and older, are the fastest growing segment of the population and present with the highest prevalence of dementia. Given the importance of neuroimaging measures to understand aging and dementia, the objective of this study was to review neuroimaging studies performed in oldest-old participants. We used PubMed, Google Scholar, and Web of Science search engines to identify in vivo CT, MRI, and PET neuroimaging studies either performed in the oldest-old or that addressed the oldest-old as a distinct group in analyses. We identified 60 studies and summarized the main group characteristics and findings. Generally, oldest-old participants presented with greater atrophy compared to younger old participants, with most studies reporting a relatively stable constant decline in brain volumes over time. Oldest-old participants with greater global atrophy and atrophy in key brain structures such as the medial temporal lobe were more likely to have dementia or cognitive impairment. The oldest-old presented with a high burden of white matter lesions, which were associated with various lifestyle factors and some cognitive measures. Amyloid burden as assessed by PET, while high in the oldest-old compared to younger age groups, was still predictive of transition from normal to impaired cognition, especially when other adverse neuroimaging measures (atrophy and white matter lesions) were also present. While this review highlights past neuroimaging research in the oldest-old, it also highlights the dearth of studies in this important population. It is imperative to perform more neuroimaging studies in the oldest-old to better understand aging and dementia.

Although it is known that the nutritional status among elderly persons and, in particular, patients with dementia, is compromised, malnutrition that results in insufficient uptake of several vitamins is often not diagnosed.

An elevated homocysteine level is a known strong risk factor for vascular dementia (VaD) and Alzheimer's disease (AD). Several B vitamins are involved in the metabolism of homocysteine. Therefore, we investigated the serum levels of vitamin B1, vitamin B6, folate, and vitamin B12 in 97 patients with mild cognitive impairment (MCI) or different forms of dementia and 54 elderly control persons without dementia.

Compared to aged non-demented people, vitamins B1, B6, B12, and folate were decreased in serum of patients with AD, and patients with Lewy body dementia had reduced vitamin B12 level. Vitamin B6 was diminished in VaD. Patients with frontotemporal dementia showed no alterations in vitamin levels. selleck chemicals Age was identified as an important factor contributing to the concentrations of vitamin B1 and B6 in serum, but not vitamin B12 and folate. Increased levels of total homocysteine were detected especially in MCI and AD. Homocysteine correlated negatively with levels of vitamins B6, B12, and folate and positively with Q Albumin.

Our data suggest that despite increased homocysteine already present in MCI, vitamin levels are decreased only in dementia. We propose to determine the vitamin levels in patients with cognitive decline, but also elderly people in general, and recommend supplementing these nutrients if needed.

Our data suggest that despite increased homocysteine already present in MCI, vitamin levels are decreased only in dementia. We propose to determine the vitamin levels in patients with cognitive decline, but also elderly people in general, and recommend supplementing these nutrients if needed.Alzheimer's disease and Alzheimer's disease-related dementias (AD/ADRD) disproportionally affect Hispanic and Latino populations, yet Hispanics/Latinos are substantially underrepresented in AD/ADRD clinical research. Diverse inclusion in trials is an ethical and scientific imperative, as underrepresentation reduces the ability to generalize study findings and treatments across populations most affected by a disease. This paper presents findings from a narrative literature review (N = 210) of the current landscape of Hispanic/Latino participation in clinical research, including the challenges, facilitators, and communication channels to conduct culturally appropriate outreach efforts to increase awareness and participation of Hispanics/Latinos in AD/ADRD clinical research studies. Many challenges identified were systemic in nature lack of culturally relevant resources; staffing that does not represent participants' cultures/language; eligibility criteria that disproportionately excludes Hispanics/Latinos; and too few studies available in Hispanic/Latino communities. The paper also details facilitators and messaging strategies to improve engagement and interest among Hispanics/Latinos in AD/ADRD research, starting with approaches that recognize and address the heterogeneity of the Hispanic/Latino ethnicity, and then, tailor outreach activities and programs to address their diverse needs and circumstances. The needs identified in this article represent longstanding failures to improve engagement and interest among Hispanics/Latinos in AD/ADRD research; we discuss how the field can move forward learning from the experiences of the COVID-19 pandemic.

Cerebrospinal fluid t-tau (CSF t-tau) is a measure of neurodegeneration in Alzheimer's disease (AD) and has been increasingly demonstrated to be a non-specific biomarker within the AD continuum.

We sought to test whether t-tau influences the longitudinal effects of amyloid-β (Aβ) and phospho-tau (p-tau) on memory and executive function (EF) in mild cognitive impairment (MCI).

319 MCI individuals from the Alzheimer's Disease Neuroimaging Initiative (ADNI) with baseline and 2-year CSF Aβ, p-tau, t-tau, and neuropsychological assessments were studied. Mediation and moderation analyses evaluated the role of t-tau in the effects of Aβ and p-tau on memory and EF over 2 years.

We found that high baseline p-tau but not Aβ was associated with higher t-tau and lower memory scores at 2 years follow-up. The association between p-tau and memory impairment was partially mediated by t-tau, whereby higher p-tau was indirectly associated with lower memory via higher t-tau. t-tau also moderated the association between p-tau and memory.