Background: There is a lack of evidence to explain why patients with dementia are admitted to a general hospital. Methods: Main reasons for hospitalisation were investigated in all patients admitted to a multi-ethnic general hospital during 2002–2007, by analysis of type of admission and primary diagnosis on admission. Anonymised data from the Hospital Activity Analysis Register was used to trace these patients; 505 were diagnosed with Alzheimer’s disease (AD), 283 with vascular dementia (VD) and 1,773 patients were classified as unspecified dementia (UnD). Logistic regression analysis was used to compare these groups to 53,123 age-matched controls. Statistical significance of p < 0.001 was accepted. Results: More dementia patients were admitted as emergency cases compared to controls (AD = 95.8%, VD = 95.4%, UnD = 96.7%, controls = 54.4%; p < 0.001 for all comparisons). The proportion of patients admitted for dementia as their primary diagnosis was small (AD = 5.9%, VD = 10.6%, UnD = 6.0%). Primary diagnoses such as syncope and collapse, bronchopneumonia, urinary tract infection and dehydration were more frequent in all dementia patients than controls. Conclusion: Dementia patients are frequently admitted as emergency cases, but dementia itself is often not the primary diagnosis. Earlier detection of the specific conditions mentioned above may reduce emergency hospital admissions amongst dementia patients.
Patients with AD have a different pattern of co-morbidity, but die from the same diseases as other hospitalized patients. Infections including pneumonia and diseases that may occur secondary to neurodegeneration and cognitive decline may need special attention in patients with AD who may not be able to identify or report the early symptoms. Preventive measures may be helpful to reduce the high risk and fatal consequences of undetected disease in AD.
An emerging treatment for Parkinson's disease (
PD
) is cell replacement therapy. Authentic midbrain dopaminergic (
mDA
) neuronal precursors can be differentiated from human embryonic stem cells (
hESC
s) and human induced pluripotent stem cells (
iPSC
s). These laboratory‐generated
mDA
cells have been demonstrated to mature into functional dopaminergic neurons upon transplantation into preclinical models of
PD
. However, clinical trials with human fetal mesenchephalic cells have shown that cell replacement grafts in
PD
are susceptible to Lewy body formation suggesting host‐to‐graft transfer of α‐synuclein pathology. Here, we have used
CRISPR
/Cas9n technology to delete the endogenous
SNCA
gene, encoding for α‐synuclein, in a clinical‐grade
hESC
line to generate
SNCA
+/−
and
SNCA
−/−
cell lines. These
hESC
lines were first differentiated into
mDA
neurons, and then challenged with recombinant α‐synuclein preformed fibrils (
PFF
s) to seed the formation for Lewy‐like pathology as measured by phosphorylation of serine‐129 of α‐synuclein (
pS
129‐αSyn). Wild‐type neurons were fully susceptible to the formation of protein aggregates positive for
pS
129‐αSyn, while
SNCA
+/−
and
SNCA
−/−
neurons exhibited significant resistance to the formation of this pathological mark. This work demonstrates that reducing or completely removing
SNCA
alleles by
CRISPR
/Cas9n‐mediated gene editing confers a measure of resistance to Lewy pathology.
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