Explain how biological factors may affect one cognitive process.


  • State what you are doing in the essay 
    • This essay will attempt to give a detailed account including reasons or causes of how biological factors may affect the cognitive process of memory in Alzheimer's disease (AD) 
  • State interaction between cognition and biological factors 
    • Human cognitive processes have a biological basis. 
  • Define memory 
    • Memory is the cognitive process whereby information is retained and recalled from past experiences, in which memory processes are used to acquire, store, retain and later retrieve information from past information and knowledge. 
  • Define Alzheimer's disease 
    • AD is a serious and progressive degenerative brain disease, which leads to the loss of neurons and often leading to dementia. 
  • Outline AD 
    • The onset of symptoms is gradual but its progression is irreversible.
    • AD impairs the creation of new memories but procedural memory (how to die a bike or play a musical instrument) is largely unaffected.
    • Episodic memory (memory of events and personal experiences) is the most severely affected. Episodic memory problems are the earliest symptoms of AD
    • AD also causes a steady decline in the semantic memory – general knowledge about the world, concepts and language. 
  • State biological factors affecting AD 
    • Medial temporal lobe
    • Deterioration of neurons involved in the production of acetylcholine 
    • Amyloid plaques
    • Neurofibrillary tangles
    • Genetic predisposition 
  • Signpost
    • Therefore, to answer this question, the link between the biological causes and effects of Alzheimer’s Disease (AD) will be investigated in regards to the effect it has on a person’s cognition of memory processing.


Biological Factor 1: Medial temporal lobe
  • Introduce the Medial temporal lobe (MTL) 
    • One biological factor that may cause AD and then affect memory is the medial temporal love (MTL).
    • The MTL has been investigated because it is known to play a role in episodic memory and it is the first area to show pathological changes in the brain. 
Supporting Study 1: Schwindt and Black (2009) 
Introduction --> link to question: 
A study that shows how the MTL plays a role in AD therefore affecting memory is by Schwindt and Black (2009). 


  • To test the effect of episodic memory on AD. 
  • They conducted a meta-analysis of fMRI studies on episodic memory in AD patients, compared to normal & AD patients. 
  • There was greater brain activity in the MTL and frontal lobe in the control group. 
  • Compared to controls, the AD patients showed decreased activation in the MTL and increased activation in the prefrontal cortex. 
  • There were a number of consistent findings across the previous studies. 
  • It was well-established that AD patients show decreased activation in the MTL. 
Connection of study to question 
  • Schwindt and Black’s study supports the biological factor of the MTL in causing AD and thus, impairment in memory. 
  • Outline the series of stages that AD develops in so you could link it with the next biological factor: 
    • AD develops through a series of stages. First, the MTLs are affected, in particular the hippocampus, then the parietal lobes and other brain regions.
    • The symptoms of AD seem to be caused by the loss of brain cells and the deterioration of neurons. 
Biological Factor 2: Deterioration of neurons involved in the production of acetylcholine hippocampus
  • Introduce the next biological factor being explained: 
  • Therefore, another biological factor that can affect memory is the deterioration of neurons involved in the production of acetylcholine. 
    • This is particularly prevalent in the hippocampi area of the brain.
    • The hippocampus has been found to affect memory from cases of amnesia patients such as HM (Milner and Scoville, 1957) and Clive Wearing (Baddeley, 1997). 
Supporting Study 2: Mosconi (2005) 
Introduction --> link to question: 
  • A study that shows how biological factors occurring in the hippocampi play a role in AD therefore affecting memory is by Mosconi (2005). 
  • To test how the hippocampi region interacts with AD/To investigate metabolism in the hippocampus, which is when the neurons in the brain activate responses in the body and dies. 
  • Followed a sample of 52 normal participants for a period of 9 – 24 years (longitudinal). 
  • They used a brain scan based computer program that measures metabolic activity in the hippocampus.
  • Reduced metabolism in the hippocampus was associated with later AD. 
Connection of study to question 
  • Mosconi’s study supports the role of the hippocampus in AD. 
  • This can be explained by the fact that the hippocampus of normal people contains high concentration of acetylcholine (Squire, 1987). 
  • Low concentrations are found in people with AD. 
  • This results from severe brain tissue loss in areas of the forebrain, known to secrete acetylcholine.

  • Outline the series of stages that AD develops in so you could link it with the next biological factor: 
    • Autopsies reveal two characteristic abnormalities in these acetylcholine-producing neurons. 
    • These neurons in AD patients also show abnormal levels of amyloid plaques and neurofibrillary tangles. 
Biological Factor 3: Amyloid plaques 
  • Introduce next AD Factor: 
    • AD is caused by deposits of amyloid-B protein which accumulates in spaces between neurons and damages the membranes of axons and dendrites (Lorenzo et al., 2000)
    • The amyloid plaques are formed from the degenerating axons and dendrites and contain a dense core of amyloid-ß protein, in which the plaques accumulate in the spaces between neurons. 
    • Most AD patients accumulate amyloid plaques before onset of AD (Selkoe, 1990). 
Supporting Study 3: Murphy and Levine (2010)
Introduction --> link to question:
  • A study that shows how amyloid plaques interact in causing AD is by Murphy and Levine (2010). 
  • To investigate whether is a relationship between default activity patterns in cortical regions in early adulthood and amyloid deposition in elderly AD patients. 
  • Eighteen older participants were enrolled from the longitudinal sample of the Washington University  Alzheimer’s Disease Research Centre and screened to exclude neurological illness, psychoactive medications and medical conditions that may produce cognitive impairment. 
  • Presence of amyloid-B protein 42 in early AD starts a chain of events that leads tAD. 
Connection of study to question 
  • Therefore, the results of this study support the biological factor of amyloid-B protein in AD. 
Biological Factor 4: Neurofibrillary tangles 
  • Introduce AD Biological Factor: As well as amyloid plaques, another factor which plays a role in the degrading of neurons that is significant for the onset of AD is neurofibrillary tangles. 
    • The tangles are microtubules found in the cell body and dendrites of neurons, which forms abnormally and causes the microtubules to tangle (neurofibrillary tangles).
    • When they tangle, the neuron loses its structure and no long has support, thus shrivels up and dies. 
    • The inhibition of the movement of neurotransmitters across the synapse prevents electrical messages to be passed from one neuron to the other; therefore, certain actions in the body are unable to be activated.
    • It is caused by the accumulation of an abnormal form of tau protein around the support structure of neurons that causes them to collapse. 
  • AD is thought to be affected by amyloid plaques and neurofibrillary tangles that degrade neurons in the brain, which causes atrophy of areas of the brain (hippocampus). 
Biological Factor 5: Genetic predisposition 
  • Introduce AD Biological Factor 
    • Another important biological factor in causing AD is our genetic predisposition to diseases such as AD. 
  • Outline the factor 
    • Research has found that genes play a role in producing amyloid-B protein. Research by... 
      • Lott (1982): Demonstrate and early onset Alzheimer’s linked to chromosome 21 (down’s syndrome) 
      • Levy-Lahad eta al (1995): Early onset Alzheimer’s gene found on chromosome 1 
      • Schellenberg et al (1992): Early onset Alzheimer’s gene found on chromosome 14 
      • Ertekin-Taner et al (2000): Gene for later onset Alzheimer’s found on chromosome 10 
    • But genes do not provide a full explanation of AD, which is demonstrated by: 
      • St George-Hislop (2000): Half of all Alzheimer’s patients have no relatives with the illness
      • Hendrie (2001): Yoruba people have Alzheimer’s genes, but much lower rates of the illness.


  • In conclusion, it is shown that the following biological factors...
    • Medial temporal lobe(Schwindt and Black, 2009)
    • Deterioration of neurons involved in the production of acetylcholine (Mosconi, 2005) 
    • Amyloid plaques (Murphy and Levine, 2010)
    • Neurofibrillary tangles
    • Genetic predisposition
      • ... all play a role in the development of Alzheimer’s Disease, affecting memory processing, which is a significant part of our cognition.
      • Therefore it can be assumed that biological factors affect memory in AD.

  • State its physiological basis
    • It can be seen that AD interacts directly with physiology because it is caused by biological factors such as a genetic predisposition to the disease; damage in brain; and the formation of amyloid plaques and neurofibrillary tangles; occurring mainly in the hippocampi region of the brain, which contributes to the degradation of the neurons developing the onset of AD.
  • State its cognitive basis
    • Therefore, the physiological effects of amnesia are what influences/affects cognition, in regards to memory processing.