This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Diabetic encephalopathy (DE), a complication of type 2 diabetes (T2D), causes cognitive impairment that increases the chance of death. Because DE has no cure, investigating its mechanisms and finding new therapies are crucially important. DE has similar symptoms to Alzheimer's disease (AD), and both involve elevated β-amyloid peptide and hyperphosphorylated tau protein, so finding new therapies for DE could involve using what's already known about AD. The autophagy-lysosomal pathway (ALP) breaks down persistent proteins in cells and helps clear the neurofibrillary tangles and senile plaques characteristic of AD, and upstream genes called transcription factor EB (TFEB) and mechanistic target of rapamycin (mTOR) regulate ALP. Researchers used both cultured cells and a mouse model of T2D to investigate whether TFEB activation could help alleviate DE. T2D mice showed cognitive impairment and AD-like pathology, which were alleviated when TFEB was activated by either mTOR inhibition or TFEB overexpression..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Chronic brain hypoperfusion (CBH) is caused by decreased blood flow to the brain and is considered a key predictor of neurodegenerative diseases such as Alzheimer’s disease and vascular dementia. CBH can indirectly lead to cognitive decline by altering the expression of proteins at synapses, where neurons communicate through neurotransmitters released from presynaptic vesicles and recognized by postsynaptic receptors. Researchers recently linked this decline to the microRNA miRNA-153. FM 1-43 experiments showed that overexpression of miRNA-153 impairs presynaptic vesicle release, and in a CBH rat model, overexpression of miRNA-153 decreased the expression of multiple proteins involved in vesicle release. Conversely, knockdown of miRNA-153 rescued these synaptic defects and attenuated cognitive decline in the rat model..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

We asked people diagnosed with Alzheimer's to tell us memories they never want to forget.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Micro-RNAs are small, non-coding molecules no bigger than a couple dozen nucleotides in length. But don’t let their size fool you. While they may not code for proteins, themselves, these molecules play an important role in many biological processes by regulating the expression of genes. Recently, they have been implicated in neuron development and neurodegenerative diseases such as Alzheimer’s. Now, a recent study published in the journal, _Molecular Neurodegeneration_, has identified a previously unreported association between the amount of a particular microRNA and the accumulation of toxic proteins that characterizes Alzheimer’s disease. Late-onset Alzheimer’s is characterized by structural changes in the brain and a decline in cognitive abilities, such as memory loss, that worsens with age. Despite the high prevalence of this disease and research efforts, its precise causes are still being worked out. Recent research, though, suggests altered gene expression by non-coding RNAs may play a role..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.