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Dementia seeds

Seeds of Dementia: Misfolded Proteins in Neurodegenerative Disorders

Alzheimer’s disease (AD), Lewy Body Dementia (LBD) and frontotemporal dementia (FTD) are characterized by the accumulation of specific proteins in the brain. The identification of these proteins is necessary to make a definite diagnosis of AD, LBD or FTD but, unfortunately, it can be performed only on post-mortem brain tissue. Recently, a trace amount of these pathological proteins was found in the olfactory mucosa (brain region that detects smell; OM) of individuals with dementia. Since collection of OM is safe and minimally invasive, we will set up a diagnostic test on OM samples which will help discriminate those with AD, LBD and FTD-tau at early stages.


Our aim is to demonstrate that the OM, collected from individuals at early stages of dementia, contains disease-specific pathological proteins that can be used to set up a diagnostic test which will help to discriminate between AD, LBD and FTD-tau.

Study Design:

Olfactory mucosa samples, collected from a well-characterized group of individuals with AD, LBD and FTD-tau, will be analyzed using an ultrasensitive test (RT-QuIC) that can detect the presence of a trace amount of specific pathological proteins, otherwise undetectable using conventional tests. Detection and identification of these proteins will allow us to identify the type of dementia at early stages when symptoms are not specific and might overlap. Results will be correlated with clinical, biochemical, neuropathological and MRI data.

Impact on Diagnosis/Treatment of Parkinson’s Disease:

Olfactory dysfunction is a common symptom in individuals with neurodegenerative disorders, especially those affected by Parkinson’s and Alzheimer’s disease. Such impairment might arise from the accumulation of disease-related proteins in the OM. The identification of these proteins will be of fundamental importance to make the correct diagnosis at early stages of dementia, when symptoms are not specific and conventional diagnostic tests do not provide a clear answer.

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Next Steps for Development:

If successful, this project could provide an innovative and strategic diagnostic tool to be used along with conventional tests that is characterized by higher specificity and sensitivity to help physicians identify pathology at early stages. Moreover, it could be used to design specific therapeutic intervention (when available) long before the brain damage occur.

Newcastle University

Providing end of life care for people with dementia with complex needs is often challenging and we need to understand how end of life care is currently delivered to people with dementia and their families. To achieve this we will use a range of methods including telephone and face-to-face interviews as well as observations of current practice.

We will interview professionals about their views and experiences of providing and commissioning end of life care to people with dementia in a range of services and settings. We will ask professionals, people with dementi‌a and family carers to define best practice, and identify factors that influence the extent to which this is actually achieved when providing care.

The aim of this research is to support providers and commissioners to identify and deliver good quality, community-based end of life care in dementia; this will be achieved through four phases.

The SEED programme is funded by the National Institute for Health Research (NIHR) under its Programme Grants for Applied Research Programme (RP-PG-0611-20005)

Detrimental effects of chia (Salvia hispanica L.) seeds on learning and memory in aluminum chloride‑induced experimental Alzheimer’s disease

Polyphenols and omega‑3 fatty acids are thought to have beneficial effects in Alzheimer’s disease, the most common cause of dementia. Seeds of chia (Salvia hispanica L.) are highly rich in these nutrients, and thus, the present study investigated the effects of chia seeds on behavior and cognition in an aluminum‑induced Alzheimer’s disease model in rats. Experimental animals received chia supplementation either during the generation of the model (i.e., pretreatment) or after the model was established (i.e., treatment). A battery of behavioral and cognitive tests were performed, including open‑field, elevated plus maze, Porsolt’s forced swim, and Morris’ water maze, to evaluate anxiety‑ and depression‑like behaviors, and learning and memory. Results showed that chia supplementation was ineffective against Alzheimer’s‑related anxiety, whereas depression‑like behaviors were attenuated with both pretreatment and treatment. There was no improvement in learning and memory with chia treatment. Rather, cognitive performance in chia‑pretreated animals was remarkably worse as compared to their non‑treated disease‑induced counterparts. Hippocampal concentrations of amyloid-β42, amyloid precursor protein, and total tau protein were similarly increased in all disease‑induced animals (despite chia supplementation), as compared to the controls. Based on these findings, chia supplementation during the progression of Alzheimer’s disease may exacerbate the disease. Although the results presented here emerge from an experimental/preclinical study, we suggest cautious and careful use of chia, especially in early‑stage Alzheimer’s patients, until future research in different experimental settings is conducted.

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