Alzheimer’s tagged posts

Does Herpes cause Alzheimer’s?

Researchers found large amounts of viral DNA in key areas of the brains of Alzheimer's patients CREDIT: REDHEAD ET AL

Researchers found large amounts of viral DNA in key areas of the brains of Alzheimer’s patients CREDIT: REDHEAD ET AL

Decades of research show a striking correlation between Alzheimer’s disease risk and infection with Herpes Simplex Virus 1 (HSV1) in people carrying a specific gene. Now, newly-available epidemiological data provide a causal link between HSV1 infection and senile dementia – raising the tantalizing prospect of a simple, effective preventive treatment for one of humanity’s costliest disorders.

Professor Ruth Itzhaki. Her latest paper presents a lifetime of research evidence that the herpes virus responsible for cold sores can also cause Alzheimer’s – and new data which show antiviral drugs drastically reduce risk of senile dementia in patients with severe herpes infections...

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Source of Cell-specific Change in Alzheimer’s disease

mRNA expression analysis of EWAS-related genes in AD CA1 pyramidal neurons AD CA1 astrocytes and AD CA1 microglia. Only two of the seven identified transcripts in the EWAS study were significantly differentially expressed, BIN1 in AD neurons and SERPINF2 in AD microglia. * indicates p < .05.

mRNA expression analysis of EWAS-related genes in AD CA1 pyramidal neurons AD CA1 astrocytes and AD CA1 microglia. Only two of the seven identified transcripts in the EWAS study were significantly differentially expressed, BIN1 in AD neurons and SERPINF2 in AD microglia. * indicates p < .05.

ANK1 gene expression change found in brain’s microglia cells associated with neuroinflammation. Researchers led by Arizona State University (ASU) and the Translational Genomics Research Institute (TGen) have identified altered expression of a gene called ANK1, which only recently has been associated with memory robbing Alzheimer’s disease, in specific cells in the brain...

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Combating Iron in the Brain: Researchers find anti-aging micromolecule

1. Schematic model of miR-29 action in brain aging. During aging an accumulation of iron in neurons occurs. This induces expression of miR-29 that in turn represses expression of IRP-2 thereby limiting iron uptake. This mechanism counteracts aging-related damages. MiR-29 may also counteract effects aging-related phenotypes by additional mechanisms, for example modulation of pro-apoptotic BCL-2 family members 2. MiR-29 is up-regulated with age in neurons. a Genomic organization of miR-29 family in N. furzeri. Three different clusters were isolated (pri-mir-29 1, 2, 3) encoding four different mature members miR-29a, b, d, e. In red, seed sequence is reported, single nucleotide differences in blue. b Age-dependent expression of miR-29 primary transcripts (Pri-miR-29-1, 2, 3) in the brain of N. furzeri. The relative expression was evaluated by RT-qPCR, data were normalized on TATA binding protein (TBP), pri-miR-29-2 results much more expressed than the other clusters and shows a clear age-dependent up-regulation (1 way ANOVA with post-test for trend: R = 0.5285 P < 0.0001, n = 4 animals for age group). c Correlation of miR-29 with its predicted targets. Blue bars show the distribution of Pearson’s correlation coefficients between miR-29a and its predicted target. Light-blue bars show the distribution of correlation values extracted from a bootstrap (P = 10–14, Kolmogorov–Smirnoff). d, e Pri-miR-29-2 expression pattern in N. furzeri brain. d Pri-miR-29-2 signal (red) and HuC/D expression (green) in the optic tectum (TeO). Pri-miR-29-2 shows a nuclear staining and a co-localization with neuronal marker HuC/D along the periventricular gray zone (PGZ), white arrows show neurons in the optic tectum (TeO) negative for pri-miR-29-2. Scale bar = 50 μm. Cerebellum overview picture (e) shows a clear and strong expression of pri-miR-29-2 just in the granular cell layer (GCL), it is instead absent in the Purkinje cell (white arrow) and molecular layer (ML). Scale bar 100 μm

1. Schematic model of miR-29 action in brain aging. During aging an accumulation of iron in neurons occurs. This induces expression of miR-29 that in turn represses expression of IRP-2 thereby limiting iron uptake. This mechanism counteracts aging-related damages. MiR-29 may also counteract effects aging-related phenotypes by additional mechanisms, for example modulation of pro-apoptotic BCL-2 family members
2. MiR-29 is up-regulated with age in neurons. a Genomic organization of miR-29 family in N. furzeri.

The older we get, our brain ages. Cognitive abilities decline and the risk of developing neurodegenerative diseases like dementia, Alzheimer’s and Parkinson’s disease or having a stroke steadily increases...

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Single Protein may hold secret to treating Parkinson’s disease and more

Parkinson's disease

Immunohistochemistry for alpha-synuclein showing positive staining (brown) of an intraneural Lewy-body in the Substantia nigra in Parkinson’s disease. Credit: Wikipedia

New details learned about a key cellular protein could lead to treatments for neurodegenerative diseases, such as Parkinson’s, Huntington’s, Alzheimer’s, and amyotrophic lateral sclerosis (ALS). At their root, proteins misfold and accumulate in neurons, inflicting damage and eventually killing the cells. In a new study, researchers in the laboratory of Steven Finkbeiner, MD, PhD, at the Gladstone Institutes used a different protein, Nrf2, to restore levels of the disease-causing proteins to a normal, healthy range, thereby preventing cell death.

The researchers tested Nrf2 in 2 models of Parkinson’s disease: cells with muta...

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