Showing posts with label Alzheimer. Show all posts
Showing posts with label Alzheimer. Show all posts

Wednesday 14 September 2022

Learning a New Language Against Alzheimer's Disease – Part 2 - Alzheimer's 9

You may read previous post (Part 1):

- Learning a New Language Against Alzheimer's Disease – Part 1 - Alzheimer's 9



Image 1- Learning Spanish.

Brian Gold, a neuroscientist found that people who bilingual since childhood are better at the high order thinking than monolingual seniors.

Craik and his colleagues conducted research for 211 patients who diagnosed with probable Alzheimer's in clinics at Baycrest, Toronto, Canada.

They classified the patients in two groups as:

- bilingual (102 patients)
- and as monolingual (109 patients).



Image 2- White flower

He said “We found that the bilingual patients had been diagnosed 4.3 years later and had reported the onset of symptoms 5.1 years later than the monolingual patients. Bilingualism thus appears to contribute to cognitive reserve, which acts to compensate for the effects of accumulated neuropathology”



Image 3- Learn French from Google Play

The data confirm that lifelong bilingualism give a protection against the onset of Alzheimer's Disease.

How about learning a new language in adulthood?

Learning a second language increase the density of grey-matter” Michelli (2004) published his research in Nature. “The degree of structural organization in this region is modulated by proficiency attained and the age of acquisition”

To avoid cognitive decline, keep our brain healthy by applying “use it or lose it” with learning a new language.

Have you interested to learn a new language?

# Previous postings:

Thursday 1 September 2022

Learning a New Language Against Alzheimer's Disease – Part 1 - Alzheimer's 9

Can you speak more than one language?

Here, in my community, one of activities of churches and libraries is to facilitate communities to learn new languages.



Image 1- CD to learn several foreign languages, illustration only

This service is free, and everybody can join them. A chapel on campus serves not only English (English Second Language) but also:

- Spanish
- and Chinese.

How fun!

For children, many of them grow up exposed to two different languages from an early age.



Image 2 – Customers at a vendor



Image 3- A book cover, illustration

It does not hard for them to learn more than one language at the same time, even they tend to borrow one word from another.

We still remember the concepts in the past about bilingual. It said that bilingual was bad for brain.

By then, many scientists have conducted research about bilingual and multilingual.

The research had been done for bilinguals in all levels of ages, from bilingual in baby to bilingual in elderly. Many amazing findings about them.

# To be continued to Part 2

## Previous postings:

Monday 15 August 2022

Why does Gum Disease cause Alzheimer's?- Part 2 - Alzheimer's 8

 You may read the previous post (Part 1):

- Why does Gum Disease cause Alzheimer's?- Part 1 - Alzheimer's 8



Image 1- Gum infections (Credit: Shutterstock)

There is a wide range of bacteria in our mouth.One of them is Porphymonas gingivalis, causes the gum disease.

The big group of bacteria grow and forming a plaque, and the worse one they release toxins and cause inflammation.

Once the oral cavity is infected by P. gingivalis, they may access the brain through some pathway including: cranial nerves, monocytes, endothelial cell in the blood brain barriers.



Image 2- People, illustration only



Image 3- Plants sold in the market, illustration

When P. gingivalis enter the brain, they spread slowly for years and also damage neuron to neuron.

Gum disease or gingivitis is common and preventable. Symptoms include:

- swollen
- red
- and tender gums.

Regular dentist visits are important for gum disease prevention and treatments.

Treatment includes professionally cleaning around teeth to prevent bone damage. Prevention can begin at home by brushing and flossing twice a day.

# Previous postings:

Tuesday 2 August 2022

Why does Gum Disease cause Alzheimer's?- Part 1 - Alzheimer's 8

Tau or neurofibrillary tangles protein is one of landmarks of the Alzheimer's disease. It is abnormal accumulation of protein in the brain cells.



Image 1- Porphyromonas gingivalis, bacteria cause the gum disease.

The abnormal conditions of Tau could spread from one neuron to another neuron.

Their patterns are exactly the same with the spreading of infections in many diseases as we know.

The researchers, Stephen Dominy and his colleagues, reported in ScienceAdvances (2019) that toxic enzymes from the bacteria Porphyromonas gingivalis were found in Alzheimer’s brain patients.



Image 2- A mask, just for illustration



Image 3- Flowers in the garden, illustration

Moreover, the percentage quite higher that about 99 and 96 percent of 54 human Alzheimer’s brain samples correlated with tau and ubiquitin pathology.

Porphyromonas gingivalis is Gram-negative anaerobic bacterium that produces virulence factor that we called gingipains, which is a protein-degrading enzyme.

This bacterium is well known for inflammatory diseases to cause destruction of tissues on tooth, and then make us loss our teeth.

The question then what is relationship bet ween teeth bacteria and Alzheimer’s diseases?

# To be continued to Part 2

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Friday 15 July 2022

Factors Causing the Late Onset Alzheimer's Diseases – Part 2 - Alzheimer’s 7

You may read previous post (Part 1):

- Factors Causing the Late Onset Alzheimer's Diseases – Part 1 - Alzheimer’s 7



Image 1- Astrocyte (Neuroscience, Purves et al).

In our brain, APOE is mainly produced by astrocyte. Then, diseases associate with APOE may include:

- Multiple Sclerosis
- Parkinson's Disease
- Vascular Dementia
- Type 2 Diabetes Melitus
- Ischemia Stroke
- Type III Hyperlipoproteinemia. 



Image 2- Cloudy in our city

In the late onset Alzheimer's disease, there are three type APOEs:

- APOE2 is associated with reduced risk of Alzheimer's
- APOE3 the most common variant and is considered neutral
- APOE4 is associated with a greater risk.



Image 3- A yard, illustration only

The function of APOE is to regulate lipid transport from one cell type or tissue to another.



Image 4- Morning view at the corner

In our brain, APOE is mainly produced by astrocyte and its function is to transport cholesterol to our nerve cell (neuron) in the brain.

Whenever an imbalance between the production and clearance of beta-amyloid peptide in our brain, thus, the accumulation and aggregation of beta-amyloid will be occurred. This become a toxic in our brain.

This toxicity also depends on the paired helical filaments of the microtubuli-associated protein tau.

So, in the in the late onset Alzheimer's disease, the toxic in the brain destroy the nice balancing of healthy brain, prominently the two proteins which are called beta-amyloid and tau.

# Previous postings:

Tuesday 5 July 2022

Factors Causing the Late Onset Alzheimer's Diseases – Part 1 - Alzheimer’s 7

In previous posts, several signs of the early onset Alzheimer's dementia had been covered.



Image 1- The cartoon above is an illustration about a relationship of Brain and Heart that I pulled from the awkwardyetidotcom.

Now, it is about the late onset, the symptoms appear when a person in the mid 60s and later of age.

The exact causes of late onset are remaining unknown. The scientists believe the cause could be a combination of three factors:

- life style
- environment
- genetic.



Image 2- Wild fruits in the park



Image 3- Crowd people in the park

Genetic markers related to the late onset form of Alzheimer's disease is associated with chromosome 19.

The mutation genes that cause increase Apoliprotein E (APOE). A person who inherit one copy of the APOE e4 has a big chance for developing this disease.

APOE primarily produced by liver and macrophages, and APOE4 is associated with:

- hyperlipidaemia
- and hypercholesterolemia.

Generally, the APOE is associated with various conditions of disease progression, not only Alzheimer's Disease.

# Previous postings:

Thursday 9 June 2022

The Mutant Genes in the Early Onset Familial Alzheimer's – Part 2 - Alzheimer's 6

You may read the previous postings (Part 1):

- The Rainbow Before Evening : The Mutant Genes in the Early Onset Familial Alzheimer's – Part 1 - Alzheimer's 6



Image 1- Meme from Google, just for fun

The mutant genes in another autosomal dominant forms of Alzheimer's disease were in:

- chromosome 1
- and chromosome 14.

This mutations lead to abnormal Presenilin 1 and Presenilin 2, which modified amyloid precursor protein so that increase amount of toxic form of Aß peptide.

Presenilins are kind of catalytic protease complexes that directly cleave the amyloid precursor protein.



Image 2- Handmade jar, illustration



Image 3- Here, my fav lady who always make me smile (credit to Google)

A person who carrying Presenilin mutation shown an alteration different of variant of amyloid beta peptides in the cerebrospinal fluid.

Mutation of presenil 1 and presenil 2 modify processing of amyloid precursor protein the increasingly of particular toxic form of Aß peptide.

This mutation suspects a heritable form of Alzheimer's disease.

So, the signs of mutant genes that lead to early onset Alzheimer's disease is prominent amyloid deposit in the brain.

The abnormal process of amyloid precursor protein lead to what is called as: extracellular deposit.

The amyloid deposit is characteristic fibrils of amyloid beta peptide.

# Previous postings:

Thursday 2 June 2022

The Mutant Genes in the Early Onset Familial Alzheimer's – Part 1 - Alzheimer's 6

Previously, I posted about chromosomes related to the Alzheimer's disease and gene mutations as the genetic marker that believe to lead to this pathological disease.



Image 1- Simple talks of Alzheimer's patients


You may read previous postings (Part 1 and Part 2):

As we might know that the progressive declined in cognitive functions in Alzheimer's disease are associated with depositions of aggregated protein in form of extracellular plaques and neurofibrillary tangles in the brain.



Image 2- Plants, just for illustration



Image 3- Dialogs of normal and Alzheimer’s person.

Early-onset Alzheimer's disease appears about in the thirties and mid-sixties of the age which are characterized by the mutation of single gene in any chromosome in chromosome 1, chromosome 14 and chromosome 21.

Long investigations about the mutant gene that causes abundance of amyloid plaques were conducted.

Then the scientists found that this gene, the gene encoding amyloid precursor protein (APP), sits in chromosome 21.

It's an autosomal dominant.

# To be continued to Part 2

## Previous postings:

Thursday 12 May 2022

In what chromosomes are the gene mutation related to Alzheimer's Disease? - Part 2 - Alzheimer's 5

You may read previous posting (Part 2):

Image 1. Chromosome 19 
 (Image from US National Library of Medicine)

Despite of the late onset Alzheimer's dementia causes are still unknown, but the scientists tend to say that it could be by a combination of:

- lifestyle
- environmental
- and genetic.

The specific genes that directly cause the late onset Alzheimer's disease is from Chromosome 19 (Please see Image 1).



Image 2- Walking Iris



Image 3- Red flower, just illustration

The genetic marker of Alzheimer's disease on chromosome 19 is APOE. The mutation in this chromosome cause increases Apolipoprotein E (APOE) that plays a big role in memory ability in aging.

For the early onset Alzheimer's disease comes about a person between thirties and mid-sixties is caused by genetic mutation.

The mutation was in the any one of number of different of single gene in any chromosome with number 1, 14, and 21.

In my opinion, this is one of interesting parts to understand Alzheimer's disease.

Isn’t it?

# Previous postings:

Wednesday 4 May 2022

In what chromosomes are the gene mutation related to Alzheimer's Disease? - Part 1 - Alzheimer's 5

In the postings (part 1 and 2), I have two images about chromosomes that related to Alzheimer's disease.



Image 1- Human chromosome with a combination of fluorescence dyes.

The image 1 above is an artificial line up of chromosome.

There are always in a pair to indicate one chromosome is from mother and another one is from father.

Every pair of chromosome is arranged based on their number and become a full set of 46 chromosome.

This arrangement is called karyotype. 



Image 2- Walking path, just illustration



Image 3- A bottle, just for illustration



Image 04- A little library at the corner

Karyotype arrangement to help to identify if there is variation in the specific chromosome (pair of chromosome)

Then, relevant scientists will try to find out whether variation refer to disorder or just normal.

The chromosomes are packages of long string of genes. A gene is a segment of DNA that contain the code for making a particular protein.

To identify for human chromosomes, we can see from the unique banding pattern. Some abnormalities or diseases can be learned from the bands.

# To be continued to Part 2

## Previous postings:

Is Meat Not a Main Food of Fox? - Nature 129

We have talked briefly about a fox crossing street at our neighborhood recently at previous posting.  Image 01 - A fox, sitting on the stree...